COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDAHD HX641 30827 RC667 .Sa82 1905 Diseases of the hear Columbia ©inibersJitp in tfje Citp of iBcto ^orfe COLLEGE OF PHYSICIANS AND SURGEONS Reference Library Given by /'^ -^^ Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/diseasesofheartaOOsatt St0?aa^a of tl|^ l|^art nnh Anrta BY THOMAS E. SATTERTHWAITE. M. D. PROFESSOR OF MEDICINE IN THE NEW YORK POST-GRADUATE MEDICAL school; consulting physician to the POST-GRADUATE, ORTHOPEDIC AND BABIES' HOSPITALS; PRESIDENT OF THE MEDICAL ASSOCIATION OF THE GREATER CITY OF NEW YORK 'Progre *is the Law of Life*' — BROWNING E. R. PELTON, 19 EAST 16th STREET. NEW YORK CITY Copyrighted 1Q05 BY 'I'hcimas v. Satterthvvaite, iM.D New York CONTENTS. CHAPTER I. PAca Diagnosis of Heart Diseases ^ CHAPTER H. Endocardiopathies 27 CHAPTER HI. Acute Endocarditis 43 CHAPTER IV. Mitral Insufficiency 50 CHAPTER V. Mitral Obstruction ce CHAPTER VI. Aortic Diseases 67 CHAPTER VII. Pulmonary Valve Affections 82 CHAPTER VIII. Tricuspid Diseases ........,......,..'...,. gj CHAPTER IX. Myocardial Affections ro2 CHAPTER X. The Fat Heart 112 CHAPTER XI. Fatty Degeneration of the Heart 124 CHAPTER XII. Syphilis of the Heart 136 CHAPTER XIII. Displacements of the Heart , 142 CHAPTER XIV. Pericardial Diseases 159 Contents CHAPTER XV. PAGE Functional Cardiac Diseases 170 CHAPTER XVI. Pulsus Infrequens 181 CHAPTER XVII. Graves' Disease 194 CHAPTER XVIII. Angina Pectoris 207 CHAPTER XIX. General Treatment of Heart Diseases 220 CHAPTER XX. Nauheim Methods with American Adaptations 230 CHAPTER XXI. Prognosis in Heart Diseases 243 CHAPTER XXn. True Aneurisms of the Larger Vessels 251 CHAPTER XXIII. Aortitis 263 CHAPTER XXIV. Arteriosclerosis 273 CHAPTER XXV. Surgery of the Heart 285 APPENDIX. I. Congenital Heart Affections 287 II. Tumors of the Heart 288 in. Aneurism of the Heart 288 IV. Parasites of the Heart 289 V. Treatment of Chronic Heart Diseases at Franzensbad 289 VI. Regimen in Chronic Heart Diseases 29? VII. The Modified Riva Rocci Sphygmanometer 293 PREFACE. The author of this volume has tried to place before the gen- eral practitioner a brief, simple, but practical, presentment of cardiac and aortic affections, chiefly from the standpoint of his personal experience. Unusual opportunities for seeing the clinical and pathologi- cal aspects of these diseases have furnished him with the material illustrating the relation of clinical signs to post mortem appear- ances. Over a hundred cases from his individual records are given at some length. But the book is not an encyclopaedia. Little space is given to the Anatomy or Surgery of the Heart or Aorta, to Congenital Anomalies or Tumors, or to Parasites of the Heart. And there are obvious omissions of subjects that are sometimes treated at length in books on Heart Disease. For example, only brief men- tion is made of the Sphygmograph, because it is thought to mis- lead rather than help at the bed-side or in the consulting room. The practical value of the Sphygmanometer, however, is recog- nized. Nor do theories or metl^ojds of treatment that have little, or merely a historical value, receive; much notice. At the same time it is believed that the exceptional quantity and character of the data made use of, will give proper emphasis to the newer views expressed. From this point of view, the comparative values of diagnostic signs, and the relative frequency and gravity of valvu- lar diseases are subjects that may enlist special interest. A good deal of space is given to modern methods of treatment. The volume is based on a series of articles that originally ap- peared in our Medical periodicals, but have been revised, while new chapters have been written. The majority of the cuts are original. With all its failings, for which the author must be responsi- ble, it is hoped that the general practitioner will find it a useful addition to his store of handy-books, helping him to manage his heart cases more intelligently, and therefore with more satisfac- tion to himself and his patients. March, 1905. "That writer does the most, who gives his readers the most knowledge, and takes from them the least time." — Colton. Dedicated TO I. B. S. Chapter I. THE DIAGNOSIS OF HEART DISEASES. Success in the diagnosis of heart diseases calls for method, thoroughness and a proper consideration of objective and sub- jective symptoms. But method is of the first importance, and in fact is absolutely essential. Both positive and negative condi- tions should be recorded in a systematic manner. For this pur- pose a blank such as is given on page 8 should be used. It is comprehensive enough for ordinary clinical use, and if filled, will tell its own story. Then it should be put aside for subsequent ref- erence. After noting the date and the patient's name and age it may be necessary to determine the height, iveight and even the measure- ments of the body or limbs. Such data are very important, as for example, in the management of the fat heart, which is closely related to general obesity, where scales and measurements are essential aids in diagnosis and treatment. But measure- ments are hardly less useful when wasting diseases, such as tuber- calosis and carcinoma, complicate the cardiac trouble. The meas- urement chart on page 9 is adapted for these cases. First in order among physical signs is the pulse. It may be frequent or infrequent, according to the number of pulsations per minute, the normal being placed at y2, or from 70 to 75 for an adult male. However, quick and frequent are not synony- mous, for the word quick means merely that each expansion of the vessel is brief, in point of time. The word large, applied to the pulse, implies that the vessel is well distended during cardiac systole. On the other hand, in the small pulse, the systolic dis- tention is less than normal. The pulse usually gives important indications in heart disease. Oppolzer, it is said, would make a diagnosis of aortic insufficiency before his hospital class, after merely placing a hand on the posterior tibial. For he held that the trip-hammer rhythm is pathognomonic.^. In arterio-sclero- sis a diagnosis may be made from the resistance felt in the walls ^ It probably is, excepting in aneurism and anaemia. Diagnosis of Heart Diseases Examination Blank. Name Date Age Weight Pulse Resp. Height Temp. Palpitation Head Symptoms Pain Apex Prscordium Liver Elsewhere Other Sul)jective Symptoms Phys. Appearance Impulse Bloodvessels Thrill Aortic Direct Aortic Regurg. Mitral Direct Mitral Regurg. Pulmonary Direct Pulmonary Regurg. Tricuspid Direct Tricuspid Regurg. T., , f Pulse Rhythm •< ^ ,. (Cardiac Liver Spleen Lungs Digestion Urine Notes Treatment Medicines Exercises Diet L Baths Diagnosis of Heart Diseases Measurement Chart. CALF ANKLE Fig. I. WRIST Name ...Age... Height.... p 1 u 4_, +J j= QJ j= not very uncommon to have a pulse of 60 or even less, in chronic degenerative cardiac changes. Occasionally during a prolonged attack of heart failure, a pulse may remain continuously in the 30's for weeks at a time. I had such a case in 1900. Recovery ensued, at least so far as that the patient was able to go about and enjoy life much as before the attack. Then there is the pliysiologically infrequent pulse. Napoleon is said to have had' a pulse of 40. I saw a patient in 1901 w^ho had just suffered from an a]^oplectilorni attack. His pulse, also, was 40. Two years later when I examined him it was from 36 — 40. He was in fairly good condition. There has been no change since then, so far as I know. A patient I saw in 1903 with Dr. Swasey of New Britain,. Connecticut, has had a pulse of about 28 for the past year (1904). and at last accounts was attending to an active business, and had recently returned from a trip to Europe^ ■ In these cases it is important, however, to distinguish between the infrequent pulse due to infrequent cardiac action, or mere failure of the blood waves to reach the wrist. In a lady recently un- der my care, where the heart contractions averaged 80, only 30 pulse beats were felt at the wrist, when she first came under my observa- Diagnosis of Heart Diseases II tidn. She had been under a severe nervous strain, but made a successful recovery. Some of the more important varieties of pulse are worthy of mention. The allernating pulse is indicated by a fulness or diminution of every alternate beat. In the intermittent pulse some of the heart weaves fail to reach the wrist, as was the character of the pulse in the case just given. In the deficient pulse the "missed heats" are diie to failure of the heart to contract. In the bigeminal and tri- geminal pulse the second and third beat respectively fails to reach the wrist. The arhythmic pulse is one of the signs of heart failure. When there are three even or similar heart beats, the pulse is said to have the triple or gallop rhythm, similar to the rat-tat- tat of a galloping horse. Sometimes as in delirium cordis, which is apt to occur in profound heart failure, the pulse is wholly irregular in force and frequency, and as regards the intervals be- tween beats ; and yet as we all know, recovery is possible. This matter will be further considered in connection with heart sounds. It is always well to note the rate of respiration in heart diseases, because it is often hurried or embarrassed. In the Cheyne-Sfokes variety the patient stops breathing. Then shallow respirations begin slowly, increasing in depth and rapidity, until they reach a certain point, after which they decline, getting slower and more superficial until they finally stop. This cycle is then repeated and occupies from a half a minute to two minutes. In acute heart diseases and in complications, the temperature also gives import- ant information. As palpitation is one of the cardinal symptoms of heart disease no examination is complete without a record of its existence or non-exiStence. Head symptoms should also be noted. They are apt to be marked in aortic disease. Pain should also not be overlooked. Pain at the apex is common in endocarditis. The subjective pain of angina in the precordial region in distinctive. Praecordial pain on pressure may be due to pericarditis. Pain over the ensiform is also one of the signs of pericarditis. Pain over the liver is common in loss of compensa- tion, owing to the congestion of the organ. Pain in the left arm arid' shoulder is also common in heart disease and arterio- sclerosis. It is important to determine whether there is an im- pulse. This is apt to be wanting in myocardial affections. Fail- ure of the impulse is a warning that heart failure may suddenly 12 Diagnosis of Heart Diseases supervene. A ilirill indicates obstruction at a valve or in a vessel. It is one of the most important signs in mitral stenosis. In listening to the heart, one should make note of what is heard at each valve, both during systole and diastole. The fail- ure to discover the more uncommon heart lesions, has been largely due to neglect of this precaution. According to the pres- ent scheme, the character of the direct and indirect sounds at each of the four valves should be recorded. In cases of irregular pulse the cardiac rhythm should be noted as distinguished from the pulse-rhythm. In chronic affections, the liver, spleen and liDigs are pretty sure to be engorged with blood at some time or other, and the en- gorgement may become permanent. In the lungs, chronic inter- stitial thickening and embolic deposits are also to be found, with bronchorrhea, if not chronic bronchitis. The digestion, too, should be considered. It is apt to be disordered in chronic heart diseases. The last few years have seen important modifications in our views of the normal position and shape of the heart. Before the X-ray was used in clinical medicine, the teachings of Luschka and Spalteholtz ( 1900) were successively accepted as guides for students of topographical anatomy, because their drawings from frozen sections w^ere thought to represent living conditions. Now, however, it is realized that these represent only the relations of the organ to its environment, as seen in death. Besides better mehods of manual percussion, with skiagraphy, fluoroscopy' or fluorography have so combined to confirm the inac- curacies of the anatomists that corrected diagrams of the heart wath its relations to the other thoracic and abdominal or- gans have become necessary (Figs. 3 and 4). This fact has been recognized in some of the more recent text-books. Until a comparatively recent date, various plans w^ere in use for mapping out the heart. Some examiners were able to out- line it fairly well by percussion, while others relied on dul- ness and flatness. Believers in the latter plan make the areas of cardiac dulness and flatness fall within two tri- angles, the larger including the smaller ; the larger triangle hav- ing for its vertical side a line let fall perpendicularly from the episternal notch ; for its base, a horizontal line drawn to meet it from the upper border of the sixth left costal cartilage at its ■ First brought to the attention of the profession by Dr. H. Campbell Thompson, of the Middlesex Hospital, in The Lancet, of Oct. 10, 1896, and Dec. 12, 1896. Diagnosis of Heart Diseases 13 junction with the rib. The hypothcnuse connecting their extrem- ities is drawn from the vertical line at the level of the upper border of the second left costal cartilage to the point usually oc- cupied by the heart's apex. The lesser triangle is formed of the same vertical and same base line ; but the hypothenuse, leaving the vertical line at the level of the third left costal cartilage, passes downward, paralleling the other hypothenuse. The areas of dul- ness and flatness are presumed to be found within the larger tri- angle, flatness within the smaller. This conception is manifestly erroneous. Besides, flatness is no proper guide for the dimensions of the heart. The flat areas change with every breath, as the to- and-fro movements of the lungs alternately diminish and en- large them. Further, the heart neither corresponds to angles, nor has them during life. Another class of practitioners does not at- tempt to delimit the heart, but simply indicates by vertical lines the extreme right border and extreme left border and the apex. In women and in stout people there is, of course, manifest difficulty in all these matters, and yet fluorography shows that in a male of ordinary build, the heart can be mapped out in its entire contour up to the origin of the great vessels with sufficient accuracy for practical purposes. For, by the X-ray, the whole inferior border of the heart is brought plainly into view ; indeed, as the diaphragm descends it leaves a vacuum between itself and the heart. This line cannot be delimited, however, by any kind of percussion. But inasmuch as X-ray work is not often available in the office or at the bedside, it is well to know that in ordinary practice enough of the cardiac borders can be determined by percussion for practical purposes, and in the following way: With a dermatographic penciP draw on the skin a horizontal line from nipple to nipple, defining each by a circle (Fig. 2) ; next draw a vertical line from the episternal notch to the point of the ensiform appendix. Then trace by percussion the right and left borders of the heart. This can be done nearly to the inter-mammillary line. Designate the apex by an X. Con- nect the two lines at the apex by continuing the curved lines on the same arcs of circle, as have been already drawn above the hor- izontal line, and the contour of the heart will be indicated with sufficient accuracy. Except in stout people, or women with flabby breasts, the nipples are reliable landmarks. ^ Faber's is not so good as the Express zvax crayon used in marking express packages. A tracing made with these crayon on a sheet of French vegetable fibre paper laid on the skin may be kept for subsequent reference. 14 Diagnosis of Heart Diseases By these two simple lines the relation of the heart is shown to the middle line of the body, and the dilatation of the several chambers of the heart brought into contrast. Fig. 2 is the car- diogram of a patient who was under my care in 1891. It shows clearly the contractions that took place between ]\larch 1st and April 1 2th and how a record of thcni was kept. Of course, this was an unusual case, the patient being a neurotic subject, with mitral regurgitation and sub-acute dilatation of the heart. With the aid of these recent discoveries, the position and con- tour of the heart may be outlined as follows: The heart's dulness commences in the second right intercostal space, at the edge of the sternum, just abo\'e the 3d rib. Curving outward to the right it follows the line of a segment of a circle from this point to the apex. The line crosses the cartilages of the 3d. 4th and 5th ribs, reaching the sternum at the fifth right costo-sternal junction ; l)Ut the line is never more distant from the sternum than the breadth of a rib, and the most distant point is on the 4th rib. (Fig. 3). On the left side the line of dulness commences in the second interspace, just below the 2d costal cartilage, and, curving to the left so as to form a segment of a circle, joins the curve of the right side, at the apex, in the 5th space. This curved line crosses the third costal cartilage at about the breadth of two ribs inside the chondro-costal junction, and the 4th rib a little more than the breadth of a rib from the margin of the nipple, crossing the carti- lage of the 5th rib about two ribs' breadth inside its costal articu- lation. The apex should be the breadth of i^ to 2 ribs inside the inner line of the nipple. The heart in life is ovoid in shape, its right and left borders comprising regular arcs of circles which meet at the apex, form- ing, of course, not an acute angle, but a rounded point. In determining the contour and position of the heart, feel for the apex beat. In a doubtful case (as in myocardial disease) iden- tify the point at which the heart sounds are best heard by the stethoscope. If the sounds are still obscure let the patient walk briskly around the room, a few times, so that the organ will act with more energy. In spare people there should be little difficulty in mapping out the outline of the heart on the right side by percussion, at least from the 2d right interspace as far as the 4th right interspace, or possibly the 5th right costal carti- lage, and certainly to the inter-mammillary line (see Fig. 3). Diagnosis of Heart Diseases 15 However, it is not essential to map out the entire contour by percussion, for j:;^ivcn the apex and the arc of a circle r;^^^^^^^ X^ \ A /r\ ^^ ^ 1 i ■■ ■ ■■'.-..■ ,■'■., ■■;■ ■ :, :!??, . . ■ :;:--.„.^^--J- Vill2 '"""^--,.,..._ _...^i' March 1 Fig. 2. Cardiogram. Fig. 3- Relation of the heart to the viscera. 1 6 Diagnosis of Heart Diseases between the 2d right interspace and 5th rib, the remainder of the arc can be estabHshed by simply extending its known portion to the apex. (Fig. 2.) Percussion can not delimit the contour between the 5th right sterno-costal junction and the apex, because of the interposition of the liver and stomach. However, this is not very ma- terial, for the reasons just given. On the left side it is easier to define the heart's margin, because the greater resonance of the lungs makes the percussion note (owing to its greater dis- tance from the sternum) contrast more sharply on the left than on the right side. Usually we can delimit the heart as far as the 4th rib, sometimes as far as the inter-mammillary line (Fig. 3), occasionally a trifle lower. But on either side we have determined the line of curve, and we have but to continue both and they will intersect at the apex. It is true, as Gerhardt says, (Lchrb. d. Aiisc. and Perc. Tuebingcn, 1890) that the heart is capable of displacement to one side or the other from 1^4 to 2^ inches ; but this displacement is exceptional, or due to changes in posture. In the case of one of my patients (Case XLVIII) with spinal curvature, the apex was displaced beyond the nipple by the curvature, and subsequently brought 2^ inches inwards, by correct- ive treatment. Emphysema crowds the heart downwards ; tumors and effusions displace it laterally; dilated abdominal viscera push it upwards. Sometimes, though rarely, when there is a general de- scent of the viscera as in Glenard's disease, the heart falls. But notwithstanding these facts, the heart has a standard position in the chest, and in healthy average patients the contour is such as has been described. Certainly the heart is so fixed that it does not ascend or descend with the diaphragm, as Gerhardt has claimed. Owing to the fact that the four valves are so close to one another that the extremity of a Bowles' stethoscope can be made to cover all of them, more or less, at one time, the ear cannot dis- tinguish between the various sounds distinctly, if placed imme- diately over any one of them. But as the sounds are convey^xl by the blood current, they can be heard and differentiated with con- siderable accuracy, if we listen somewhere along the course of the several currents. The location of the valves is shoAvn in Fig. 3- As seen from the front, the mitral valve is behind the 3d left interspace, the breadth of a rib from the edge of the sternum. The aortic valve lies behind the left margin of the sternum, adjoining Diagnosis of Heart Diseases 17 the 3d interspace. Tlic pulmonary lies between the two, on about the level of the aorta. The tricuspid lies behind the sternum, a little to the left of the median line, and opposite the junction of the 4th left costal carti- lage with the sternum. All of the valves are somewhat to the left of the median line. These statements as to the shape and posi- tion of the heart and the location of the valves, vary from some that have been given ; but they are the results of careful personal study. Fig. 4. The heart as seen from behind. In this connection the following note from Holden's Anatomy* is apropos. It says, "Anatomists dififer much in the descriptions they give of the relations of the valves to the thoracic walls, ii» fact, no two agree in all the details." And yet it is proper to say here, that my statements agree pretty closely with those giveit in Holden, which are that the left auriculo-ventricular valve is opposite the 3d left intercostal space and about one inch to the left of the sternum. The pulmonary valve lies immediately behind the junction of the 3d left costal cartilage with the sternum ; the aortic valve is on a level with the upper border of the 3d left inter- costal space, just at the left of the middle line of the sternumu The position of the aortic and pulmonary valves as given by Holden I regard as too high, but the difference in our views is not, after all, a very material one. * Edition of 1901, p. li l8 Diagnosis of Heart Diseases Seen from behind, the npijcr level of the heart corresponds •\\ ith the center of the 4th dorsal vertebra, and the lower margin of rtlie 5tli rib, on the left side; the ni:)per margin of the 6th rib on the right side. The apex is opposite the Sth left interspace, abont midway between the spines of the vertebra; ami the free border of the ribs. The mitral valve is opposite the 6th interspace, close to the left margin of the 6th dorsal vertebra. The aortic lies to the left of the median line, opposite the point where the 5th dorsal «pine overlaps the 6th ; the pulmonary lies between them ; the tricus- ]iid covers the median line, though slightly more to the left than the right, and is opposite the root of the spine of the 6th dot sal verte- t.ra (Fig. 4). In considering heart murmurs the physiological action of the 'heart must be taken into consideration. The movement of the 'blood is caused by the contraction of the auricles, ventricles and vessels. The blood enters the auricles by the veins, and then is ■ex])elled by the auricles through the auriculo-ventricular open- ings or valves into the ventricles; when the ventricles are filled, they contract and force this blood back into the vessels, the left ventricle driving a column of blood through the aorta into the .greater or systemic circulation : the right \entricle driving an- •other column of blood into the lesser or pulmonary circulation. 'Then follows a contraction of the great vessels, the aorta and pulmonary artery. In health the action of the ventricles in clos- ing is attended with a sound or tone, due to three principal causes; i. The closure of the auricular-ventricular orifices. 2. The muscular action of the ventricles. 3. The vibration of blood in the ventricles. Roth auricles and great vessels contract during the filling of the ventricles (diastole) and hence any sound produced during this period is called diastolic, but they are not synchronous, the vessels contracting at the beginning of diastole, and the auricles at the end. A systolic sound is produced during the contraction of the ventricles (systole), and the word presystolic is accepted as indicating a sound produced at the end of diastole, or during the contraction of the auricles : or in fact, any sound not produced during the time for the contraction of the aorta. The second sound is chiefly due to the closure of the aortic and pulmonary valves, and the vibration of blood in the aortic and pulmonary arteries. "Valves, muscular action, chordse tendinge, vessels and the vibration of the blood, produce heart sounds. Now, supposing the time occupied by these actions were di- • vided into eighths, one-eight would be occupied by the contrac- Diagnosis of Heart Diseases 19 tion of the lari;-c vessels and auricles, three-eighths by the contrac- tion of the veiilt icles ; the remaining- four-eighths or one-half, by the filling of the auricles and ventricles. The following diagram illustrates the rhythm of the heart under normal conditions: D S D S Fig. 5. Vicrordt. When we listen at the apex or at the ensiform cartilage the first sound will be more accentuated, as in Fig. 6. S D S D S D S Fig. 6. Vierordt. On the other hand, if we listen at the base, the second sound will be most accentuated, as in iMg. 7. S D S Fig. 7. Vierordt, In health the sounds are modified, as to intensity, by the elas- ticity of the chest, thickness of superimposed tissue, especially by fat, and in women by the breasts, and in all by age. Sharp accent- uation of the second sound is, if continuous, a very sure sign of hyper- trophy of the corresponding ventricle. And it is particularly impor- tant as related to the second pulmonary sound, which, if accen- tuated, means dilatation and hypertrophy of the right ventricle. In arterio-sclerosis of the aorta, the second aortic sound may be slightly resonant or bell-like. And yet when there is heart fail- ure the accentuation of the second sound fails. But all heart sounds are more or less faint in heart failure, pericardial afTec- 20 Diagnosis of Heart Diseases tions and emphysema. In valvular affections the heart sounds are replaced by nnirmurs. The tick-tack rhythm is known as the embryo cardial or pendulum rhythm, and is abnormal in the fcetus. The heart sounds may be doubled or trebled, as is shown in the following dia.c^ram ( Fig. 8) : Fig. 8. Vierordt. Sometimes there is a triple rhythm as in Fig. 9. s s Fig. 9. Vierordt. I heard a triple rhythm as in Fig. 10 S S Fig. 10. W'ith Dr. Dudley in 1901, when the patient was in a very weak state after laparotomy, and when there was a short beat followed by a long one, in the radial pulse. Or we may have a gallop rliyihiii, as shown by the following diagrams, but this is not always a pathological condieitn. S s S s s Fig. II. Vierordt. Diagnosis of Heart Diseases 21 Potain claims that some divisiun of the sounds occurred in 20% of persons he examined. In 99 of his cases the first sound was divided in 61 instances ; the second sound in 30 ; in 8 both were divided. He thinks division is caused by respiration ; that the di- vision of the first sound is associated with the end of expiration and the beginning of inspiration ; division of the second with the end of inspiration and the beginning of expiration. A murmur either supplants a tone (sound) or co-exists with it. Sometimes murmurs replace both tones. Occasionally mur- murs are so loud that they can be heard at a distance from the patient. Others can only be heard with the greatest dif^culty. In fact, very slight murmurs may only be elicited by movements of the body ; or if the patient runs around the room. Patients should, if practicable, be examined both in the recum- bent and upright positions. Sometimes, murmurs cannot be heard in the upright position, and only if the patient lies on the right or left side. Mitral lesions are often best heard when the patient is recumbent. Murmurs are divided into : 1. Vakmlar and 2. Accidental. Under the latter are included those that are disconnected with valves, papillary muscles, and chordae tending. They are due to altered conditions of nutrition in the heart muscles, or alterations in the quality or constitutents of the blood, and are found exclu- sively during systole, and at any single valve ; often at all valves together ; usually with slighter murmurs in the vessels of the neck, of a light blowing character. But most important, from a diagnostic point of view, is that all the consequences of valve de- fects are absent in these accidental cases. The exciting causes are chiefly anaemia, or some form of blood deficiency, fever, cancer, consumption, or pressure of neighboring organs on the heart. In pernicious anaemia the murmurs are very loud. Any kind of diminution in heart pressure also causes accidental murmurs. Less often they are caused by transitory disturbances of the functions of the m3^ocardium, or the papillary muscles, causing temporary insufficiency of the valves. Other accidental sounds may be caused by the act of respiration. Corresponding to the four valves of the heart there are nor- naally four tones or sounds, and as each valve ma}' leak, we have four additional sounds, making eight in all. 22 Diagnosis of Heart Diseases A iininmir is tlie name given to an atlvontitious sound heard in connection w itli the heart sound, when there is \ alvuhir endo- carditis or valve distortion. Aluruiurs vary in fyitcli, quality, duration and intensity. They are charactertistic of valvular diseases, but may be absent, and are not always heard (5 per cent.)''. Endocardial murmurs must be carefully disting^uished from j^ericardial and respiratory sounds. Respiratory sounds are limited to inspira- tion, so that in order to eliminate them, the patient should hold his breath. An endocardial murmur is synchronous with systole or diastole, and is deep seated. A pericardial murmur is heard over any part of the heart, but is best heard at a distance from the valves or apex. It is a sound that is very near the ear. Pressure by the stethoscope increases pericardial friction sounds, but does not affect the endocardial. None of the valve sounds are best heard immediately over the valves, because the sound is conducted in all cases to the sur- face, along the line of the flowing blood current ; but the pulmon- ary, being nearest the surface, is heard best at points just above or below the valve, and so the tricuspid ; while the aortic and mi- tral, for similar reasons, are best heard at points remote from the valves. We find, accordingly, that the pulmonary obstructive murmur is best heard at the junction of the 26. left interspace with the sternum. Fig. 12. According to my figures. Fig. 13. Diagnosis of Heart Diseases 23 or above its actual position, and is conducted upwards. (y^g. 15.) The pulmonary regurgitant murmur is heard a little below this point and is conducted downwards ; but as the pulmonary valve is the most superficial of all, the sounds are always near the ear. (Fig. Fig. 14. Fig. 15. 14.) The aortic obstructive murmur (Fig. 12) is best heard over a somewhat larger area than the pulmonary and at the junction of the 3d right cartilage with the sternum, and the sounds are conducted upwards chiefly. The aortic regurgitant murmur is- also best heard somewhat below the normal position of the valve and at the junction of the 4th left costal-cartilage with the ster- num. This murmur is conducted chiefly towards the ensiform cartilage, nipple and apex, but to a slight extent also in the re- verse direction (Fig. 13). I'he mitral obstructive murmur is heard best at a still more remote distance, viz., over a limited area above the apex, usually about midway between the ensiform- appendix and the nipple. The area of mitral stenosis, however, is not always well defined. Occasionally, but still rarely, the murmur of mitral obstruction may be heard over any part of the shaded area marked M (Fig. 15). The mitral regurgitant murmur (Fig. 14) is heard at the point farthest from the valve of all, viz., over the apex." But the murmur is conveyed to the left, not uncommonly to the axilla, and sometimes to the scapula, a matter not hard to under- stand by aid of Fig. 4 ; for not only in dilated hearts may the bor- 24 Diagnosis of Heart Diseases der of the heart reach to the scapula, hut the hlood current, from the position of the mitral in the back of the thoracic cavity, and the direction of its current must necessaril}' cause the. murmur to be carried to the back. The mitral area is indicated by the large letter M (Fig. 15). In tricuspid obstruction the murmur is usually heard best along the left border of the ensiform appendix at the points in- dicated by the small letters (Fig. 15). The regurgitant murmur is best heard over the sternum, mostly at the junction of the 5th left costal cartilage with the sternum, but occasionally also on the opposite side. It is indicated by the small letters r r r (Fig. 15). The fricitsf'id area, however, is a large one, and in- definite. It is indicated by the shaded area over which is the large letter T (Fig. 15). But it must be remembered that while the base of the heart is tolerably fixed by the great vessels and structures that compose its root, the heart itself is apt to be dilated and hypertrophied both in endocardial and myocardial diseases, so that the relation of the sounds to the bony landmarks of the thorax will vary correspondingly. Accord- ingly, the meaning of these sounds must be read in connection with other objective and subjective phenomena, in order to be properly appreciated. No examination of the heart should be made without at the same time an examination of the lungs, liver and spleen. Patients are often seen by the consultant where tuberculosis of the lungs is the main disease, and the cardiac a secondary affair ; most of the symptoms of the latter depending on the lung disease. On the other hand, spitting of blood, which is common in some forms of cardiac disease, ma}- be wrongly attributed to a non-cardiac lung disease. The liver should be examined for size, position and tender- ness. In cardiac diseases it is apt in the later stages to extend below- the free borders of the ribs, and may even reach the um- bilicus. It may be tender to the touch. Sometimes, especially in very advanced cases, a hob-nail surface can be felt. In one of my cases of enlarged liver the left lobe pushed uj) the heart so that the apex was above the nipple. The spleen is also apt to be enlarged when the liver is. It is often the seat of embolism, and as in case No. V, may have suppurative infarcts. It is needless to sav that the urine should ulwavs be examined. Diagnosis of Heart Diseases 25 Attention to the digestion is also imperative in the management of cardiac diseases, especially in persons of middle life and beyond. Indigestion alone is not an infrequent cause of death. In anaemia there is the venous hum, or "bruit de diable." This is a continuous murmur heard over the internal jugular veins at .the root of the neck, but it is not pathognomomic of anaemia, as in 50% of the cases where it has been observed there has been none. , It is often of a musical quality, and usually more distinct on the right side. The intensity of the murmur is increased by the upright position ; by turning the head away from the side which is being auscultated; and by a deep inspiration. It is also modified by the pressure of the stethoscope. The cause appears to be some alteration in the calibre of the vein,'' due to com- pres'sion or adhesions attaching it to surrounding parts ; or it may be due to a diminished flow^ of blood. It has been claimed in some of these cases that the vein is "pouched," which would account for the murmurs. The venous hum is not heard in all cases of anaemia, and the intensity of the murmur is not propor- tionate to the alteration in the quantity or quality of the blood. In .anaemia a bruit is also heard over otherveins. A continuous murmur, described as being like the wind "blowing through the rigging of a ship under bare poles," is also sometimes heard on either side of the xiphoid cartilage, and it is thought to indicate constriction of the inferior vena cava. In anaemia there is sometimes a sys- tolic murmur in the pulmonic area. It is most distinctly heard in the 2nd left intercostal space, close to the sternum, and is the most constant of the mvirmurs associated with anaemia. This is said to be due to dilatation of the right ventricle, owing to mal- nutrition, without change in the pulmonic orifice, so that it is relatively narrowed, and therefore capable of producing a mur- mur, as in organic stenosis. The same theory holds good if the heart is diminished in size, as it often is in anaemia. For in such case the orifice would be relatively dilated and equally capable of producing a murmur. There are other theories, such, for example, as that the murmur is due to pressure on the pulmonary artery by a distended left auricle. It has also been claimed that the murmur is due to dilatation of the conus arteriosus and pul- monary artery, and that this condition is to be found at the post- mortem examination of patients who have had this functional murmur during life. This view seems at the present time to be ° Colbert, Dis. of the Heart, London, 1901, p. 72. 26 Diagnosis of Heart Diseases icasonablc, but it rccjiiires substantiation. Tbe mitral systolic )iiiin)ittr beard in some cases of anjemia, at tbe apex, and carried to tbe left, even to tbe angle of tbe scapula, is due to regurgita- tion from relaxation of the muscular fibres about tbe mitral ori- fice, so that the valve leaflets do not come into proper apposition. This is either due to malnutrition of tbe myocardium, to the musculi papillares, or to simple dilatation of tbe left ventricle. The tricuspid systolic niunuur in aniemia is beard in tbe tri- cuspid area. It is due to dilatation of the right \(.ntrick\ If the anjemia is slight, the miu'nnn- may be absent. Tbe aortic systolic )inir}inir in anjemia is beard in the aortic area, and is thought to be due to relative narowing of tbe aortic orifice from dilatation of the left ventricle. In these so-called licDnic imtrjiiurs the position and direction of tbe murmurs cor- respond with those of the organic variety ; but they are usually soft, and are not conducted so far as in the latter variety. Exocardial sounds may be mistaken for cardiac murnnirs. Of these there are several varieties. In health there is no soimd produced by the heart pressing against the pericardium, but when either surface is roughened by disease, a friction sound is pro- duced. It is usually best heard over the right ventricle and the base of the heart. The sound is limited to this particular area, and is like that of two bodies rubbing against one another. It is described as "grating, creaking," etc., and is intensified by pressure with the stethoscope, deep inspiration, or changes in pos- ture. It also changes its position from time to time. Tbe sounds correspond to the contraction and relaxation of the ventricles. A pleural friction sound may also be produced b}- tlic move- ments of the heart, but it ceases when the breath is held. CllAl'TKK IT. ENDO-CARDIOPATHIES.^ Endocardial diseases are usually, though not always, localized about the valves, and may or may not be inflammatory. Conse- quently, the word endocarditis,- sometimes used as synonomous with endocardial diseases, is not sufficiently comprehensive. A better term is endocardiopathies, which adequately includes all endocardial affections. Though endo-cardiopathies were alluded to as early as 1684 by Thomas Willis in his "Practice of Physick," and attracted the attention of Merkel, Senac and John Hunter in the century fol- lowing, physicians gave them little attention, until exploited by Cor- visart in 1808. During the remainder of the century, however, they were studied from almost every available point of view by such men as Kreysig, Andral, Corrigan, Bouillaud, Virchow, Walshe and Stokes, American physicians contributing in later years valuable material. Affections of the endocardium constitute about one-half of the total of cardiac diseases, and as the inflammator}- differ materially from the non-inflammatory in etiology, prognosis, and treatment so we may classify them on this basis ; or, on the other hand, ma} divide them into the primary (i. e., inflammatory), under which fall the vegetative, infiltrative, ulcerative, stenotic or sclerotic varie- ties, as distinguished from the secondary {i. e., non-inflamma- tory), where the changes are secondary to the former, and are such as are caused by the mechanical stretching of the muscular or fibrous tissues. Some have adopted the plan of classifying them on the basis of their alleged causes. Thus Litten (Phila. Med. Jour., May 5th, 1900) has distinguished a rheumatic, scarlatinal, typhoid and pneumonic endocarditis, etc., but lately we have discovered that endocarditis follows, and appears to be caused by, a number of dis- eases of less moment, such as coryza, diseases of the skin, and gas- tro-intestinal disorders. A more simple method is to separate endo- cardiopathies into the acute, sub-acute and chronic. ^Originally published in the Virginia Aled. Semi-Moitthly. April 26. 1901. ^Introduced by Bouillaud in 1841. 28 Endo-Cardiopathies The coincident relations of tlie various i)iicro-organis}iis to the endocardial inflammations have been frequently noted, and cultures have produced endocarditis in the rabbit. But the va- riety of these organisms is confusing;. In 1886 Weichselbaum distinguished tw^o varieties, the staphylococcus pyogenes aureus, and the streptococcus. Netter found the diplococcus of Frsenkel ; others have found the bacterium coli ; others the gonococcus of Xeisser, etc. But Michaels (Phil. Med. Jour., May 5th, 1900), opened a number of rheumatic joints and found no micro-organ- isms. Still, notwithstanding this divergence of opinion there i.s reason to believe that some forms of endocarditis are of microbic origin. Acute rheumatism is generally taken to be the chief cause of endocarditis. In fully 40 per cent, of my cases there was an ante- cedent history of rheumatism, and as many as one-third of the cases of acute rheumatism I have found were followed by endocardi- tis. These are conservative figures in the light of statistics that follow. And }et, figures do not always have much significance when rheumatism is concerned, because the word, both with the laity and physicians, is loosely applied. However, Latham found that in 136 cases of acute rheumatism the valves were affected in seventy-four, or 54 per cent., Gibson in 184 out of 325 cases, or 56 per cent. (Gibsoiis Diseases of the Heart, 1898, p. 397). In this connection it is interesting to observe that chorea has a close genetic relation with acute articular rheumatism and that Fagge found few fatal cases of chorea without organic valvular changes similar to those of rheumatic endocarditis. There is also a manifest relation between the age of a patient and the initial attack of rheumatic endocarditis. For example, when infants or children have an acute attack of rheumatism, they are liable to endocarditis, perhaps in 70 per cent. ; and yet acute rheumatism is rare in infancy and young life, though com- paratively common in the decenniums between 30 and 50. After this period it rarely develops. There is no rule as to the date at w^hich endocarditis appears in acute articular rheumatism. It may occur at any time during the attack, or may precede it. After rheumatism, pneumonia fol- lows as one of the most frequent causes of endocarditis. The loxin of the pneumococcus, however, administered to rabbits ■bv Carnot and Fournier {Arch, dc Med. Exp., XII, p. 357, Endo-Cardiopathies 29 Schmidt's Jahrbuch), was followed by acute inflammation of the heart muscles, intestinal haemorrhages, dej^eneration and fragmentation of the voluntary muscles, while the valves were not affected. Gibson, on the other hand (Edinb. Med. Jour., Nov., 1900J, has reported a case of diplococcal infection resulting in pleuro pneumonia. At the autopsy the aortic segments were seen to be ulcerated, and in a thrombus adherent to the aortic valves there were found diplococci, leucocytes and fibrin. Endocarditis is quite often found in tuberculosis, but the cause of the disease has been usually attributed in these cases to a streptococcus, staphylococcus, Fraenkel's pneumococcus, or Friedlander's cap- sule bacillus. Endocarditis is also frequently associated with surgical dis eases, such as osteomyelitis, erysipelas, dysentery, pyaemia and septicaemia, puerperal fevers, and furunculosis : and the staphy- lococcus pyogenes aureus has been most frequently found asso- ciated with the lesions of these affections. In erysipelas, an asso- ciated endocarditis has been traced to a streptococcus, and with it endocarditis has been produced experimentally by a number of workers. In gonorrhoea! endocarditis Leyden found the gono- coccus of Neisser in the valvular deposits. They had the dis- tinct biscuit form, and were colored satisfactorily by Gram's method. In scarlatina, endocarditis was seen to develop by Trousseau^ and others. It may occur at any time during the disease or with its sequelae. But a characteristic micro-organism has not been found, as yet, in this form. Influenza afifects the heart in many ways, but chiefly attacks the muscular substance, through the poisonous influence of the toxins ; though endocarditis has been attributed to influenza. Endocarditis occurs occasionally in var- iola, but if the primary disease is severe, the cardiac affection is (as often happens in endocarditis) associated with other affec- tions, such as a myopathy or pericarditis. Endocarditis occurs occasionally in measles, but syphilis rarely attacks the valves, though the myocardium is occasionally involved. While, as al- ready stated, many different sorts of micro-organisms have been found in the ulcerated valves, the etiological relation they hold to the diseased condition is still doubtful. This problem may eventually be settled by determining whether or not the micro- Trousseau, Clin. Med., vol. 2, 1869, p. i{ 30 Endo-Cardiopathies i^rg^anisms arc to be found in the Initial lesions of the valves. There is a close relation between endocarditis and some fvuin> of Brig;ht's disease. Inasmuch, however, as. according- to my in- vestigations.'' Htlu-emia is a causal factor of Bright's disease in from 50 per cent, to 75 per cent., the close relation between rheuma- tism and endocarditis is plainly shown. But Bright's disease is apt to be a late phenomenon in endocarditis. Endocarditis is most frccjuent after ten and before forty, but there is a manifest relation between the age of the patient and the seat of the disease. In the foetus, the right side of the heart, doing the most work, is most frequently aflfected ; in extra- uterine life it is the left heart, for similar reasons. Accordingly, age and the character of work to be done must be considered in es- timating the liability to endocarditis. In extra-uterine life, dis- ease affects the mitral or aortic valves b}' preference, next the pulmonary and tricuspid valves, but these latter in a compara- tively small number of instances. There is little difference in the tendency to endocarditis between men and women, though it is generally held that mitral disease is more common in women and aortic in men. The beginning of an endocarditis is marked by an invasion of the substance of the valves by toxins, micro-organisms and in- flammatory exudates, wdiile on their surfaces the shining endothe- lium becomes opaque and gives birth to minute rounded flesh colitred papillary bodies, which are one or two millimeters in height when first seen, and situated near the free edges of the valves. On the mitral they develop on the auricular surfaces at a distance of 2-3 millimeters from the free edge, while on the aortic they form on the ventricular surfaces. They are at the point of maximum contact. To these excrescences are at- tached particles of fibrin from the blood, and these, together with ulcerated portions of the valves, may be carried into the general circulation and cause embolism. There are all degrees of infdtra- tion in these valves, with or without ulceration, and the disease may extend and involve the myocardium. But wherever ulcera- tion takes place, there is at the same time a sclerotic chang-- coincident with it, so that destructive and constructive processes go hand in hand, nature attempting to repair as disease destroys. Pathologically, the changes consist, first, in a thickening of the small vessels, with hyaline degeneration and perhaps partial sclerosis of the smaller arteries, followed bv a small-celled infiltra- *.Y. )'. Med. Rec, March 7, 1889. Endo-Cardiopathies 3 1 lion and proliferation of connective tissue, with eventual destruc- tion of muscle cells. The process may be so extensive that the greater part of a valve is destroyed or even converted into an aneurismal sac. I have seen an example of the latter accident. In the chronic forms, there is often a deposit of the salts of lime in the valves, or along their attached margins, and the pro- cess extends down over and into the chordae tendinse, contracting and stiffening them, while the papillary muscles are also apt to undergo fatty and calcareous degeneration. Such stiffened por- tions of the endocardium occasionally rupture. Endocarditis develops insidiously, as a rule. It may not be discovered unless looked for. Years often pass before it is recog- nized. Much depends on the situation. If confined to the walls •of the heart it seldom shows any signs. I have seen a few such cases. It is interesting to know exactly what is found in valvular ■diseases at autopsies, and the tables of Sperling prepared from the Records of the Berlin Pathological Institute between i868-'70, are the best I have met with. They may be compared with my •own tables of a smaller number of cases arranged on the same plan. Sperling's Tables.'^ 300 Cases of Endocarditis. 1868-70. 268 cases :rr 89 per cent, left side of heart. 3 cases z=^ I per cent, right side of heart. 29 cases =z 10 per cent, both sides of heart. 300 100 Affections of One I'akx Only. 200 Cases =; 66.7 per cent. Mitral valve only 157 cases r= 78.5 per cent. Aortic valve only 40 cases :=: 20. per cent. Tricuspid valve only 3 cases z= 1.5 per cent. Pulmonary valve only o cases = 0.0 per cent. 200 loo.o per cent. Combined J\ilvular Lesions. 100 Cases = ^3.3 per cent. Mitral and aortic... 71 cases z=z 71 per cent. Mitral and tricuspid 9 cases 1= 9 per cent. Mitral and pulmonary 2 cases r= 2 per cent. Aortic and pulmonary i case zz: i per cent. f Aortic and tricuspid o case z= o per cent. Mitral, aortic and tricuspid 16 cases z= 16 per cent. Mitral, aortic and pulmonary o case izz: o per cent. -Tricuspid, pulmonary and mitral o case ^= o per cent. Tricuspid, pulmonary and aortic o case =r o per cent. All four valves i case z= 1 per cent. Gibson's Dis. of the Heart and Aorta. 1898, p. 413. TOO 100 per cent. 32 Endo-Cardiopathies Einholisin. 84 Cases = 28 per cent. ;() with left side disease — 8 with right side disease. Kidney, 57. Spleen, 39. Brain. 15. Digestive organs, 5. Skin, 4. Author's Tables. 6s Cases of Endocarditis, 1872- 1888. 56 cases rr 86 per cent, left side alone affected. o cases =z o per cent. ri}.;ht side alone affected. 9 cases =z 14 per cent, both sides affected. 65 100 per cent. Affections of One Valve Only. 18 Cases = 27 per cent. Mitral valve only 6 cases nr 33.33 per cent- Aortic valve only 12 cases r= 66.67 P^r cent. (Including diseases of ascending portion of arch) Tricuspid valve o case zzz 0.0 per cent. Pulmonan,- valve o case zzn 0.0 per cent. 18 loo.o per cent.. Combined I'aii'ular Lesions. 44 Cases = 67 per cent. Mitral and aortic 31 cases zzr 70.5 per cent. Mitral and tricuspid 2 cases ^: 4.5 per cent.. Mitral and pulmonary case ;rr CO per cent. Aortic and pulmonary o case zz: 0.0 per cent.. Aortic and tricuspid 2 cases zr 4.5 per cent. Mitral, aortic and tricuspid 4 cases ^ 9.4 per cent. Mitral, aortic and pulmonary i case = 2.2 per cent.. Tricuspid, pulmonary and mitral.... i case :=z 2.2 per cent. Tricuspid, pulmonary and aortic o case :=: 0.0 per cent. All four valves i case =z 2.2 per-cent. Pulmonary and tricuspid 2 cases =z 4.5 per cent. 44 100 per cent. Embolism. 1 1 Cases z= 16 per cent. All occurred in connection with left side disease and as- follows : Kidney, 6 times. Spleen, 4 times. Brain, once. Liver, twice. It will be noticed that there is a general agreement between' the two tables, except as to the comparative frequency of aortic and mitral diseases. Probably in my tables a larger number of cases would have altered this relation. If, however, in my 65 cases we throw out the affections of the first part of the aorta, the incidence upon the valves stands as follows: Endo-Cardiopathies 33 .. Aortic insufficiency 49 times 2. Aortic obstruction 39 3. Mitral insufficiency 38 4. Mitral obstructions 33 5. Tricuspid insufficiency 8 6. 'Jricuspid obstruction 4 7. Pulmonary insufficiency 4 175 But as single valve lesions were rare, the total foots up 175, a« average of from two to three valve lesions in each case. The fol- lowing is the order of frequency, as recorded in my office cases : Aortic disease 56 per cent. Mitral disease 35 per cent. Tricuspid disease 6 per cent. Pulmonary disease 3 per cent. 100 per cent. On the other hand, in 50 cases from my clinic, as taken by imyself and assistants (not verified by post-mortems), the inci- dence was put down as follows : 1. Mitral insufficiency. 2. Aortic insufficiency. 3. Aortic obstruction. 4. Mitral obstruction. 5. Tricuspid insufficiency. 6. Pulmonary insufficiency. This is not very unlike the order of Walshe (Diseases of the Heart, London, 1873, P- ^^05), which is — 1. Mitral insufficiency. 2. Aortic stenosis. 3. Aortic insufficiency. ,4. Mitral stenosis. 5. Tricuspid regurgitation. 6. Pulmonary incompetency. 7. Tricuspid stenosis. Dr. George S. Middleton,'' of Glasgow, puts the order of fre- .quency from his dispensary cases (unsupported by post-mor- tems) as — 1. Mitral insufficiency. 2. Mitral stenosis. 3. Aortic incompetenc}'. 4. Aortic stenosis. 5. Tricuspid disease 6. Pulmonary disease. "Lancet, Oct. 26, 1889. 34 Endo-Cardiopathies And yet I should prefer not to take any purely clinieal evi- dence as a basis of statistics, for the following reasons : In my 65 cases with clinical histories and post-mortems, while endocardial disease was recognized by those who had charge of the patients' in 95 per cent., 37 cases of aortic disease were only noted in 27,, or 62 per cent. ; while in 31 cases of mitral disease, it was detected in only 19. or ()i ])er cent. In other words, there was a positive failure to locate in 39 per cent, of actual lesions. This revelation of the results of actual experience in hospitals, where the physicians were among the best we have had, shows how futile it is to base conclusions on clinical evidence only. And yet up to this time it has been the main stay of clinicians. On the other liand, it is expecting too much to require a physician to differentiate •every valvular lesion at the bedside, or in the consulting room. As the best clinicians often fail to recognize them now. so the}- will con- tinue to do for all time. The reasons are threefold. In many in- stances they give no sign, or if they do, attendant circumstances prevent them from being appreciated. I have even heard a dis- tinguished diagnostician say that a diagnosis of a specific valvular disease made at a first examination had little value. The truth is that in well-established forms of organic valvular disease a specific diagnosis can usually be made correctly at a single examination ; while in less pronounced cases several examinations may be necessary. As Stokes said, in 1855, "The difficulties of special diagnosis are still infinitely greater than many might be led to expect." But of course we shall gradually overcome some of these difficulties, as we frame better rules for diagnosis. On the other hand, the diagnosis of endocardial disease, on the post-mortem table, is comparatively easy, and rarely liable to misinterpretation, though clinicians do not all take this view. The chief difficulty lies in determining whether or not valves are sufficient. However, the ordinary water test is, I think, satis- factory, if applied by an experienced pathologist ; and the latte^ can also determine whether the valve affected has been the seat of inflammation, or has been dilated or distorted by muscular action, etc. ; in other words, whether the endocardial disease is primary or secondary. The symptoms of an acute benign endocarditis are variable and inconstant, and may escape detection. On the other hand, it may be announced by unmistakable signs. A patient is seized Endo-Cardiopathies 35 ■with intense priecordial pain, dyspntx;a, arrhythmia or rapid pulse, perhaps with some fever or even cyanosis, and the ear applied to the chest detects a rough, loud or harsh murmur. Occasionally, the suspicion that the patient is having an acute exacerbation of the chronic disease leads us to apply the car. More rarely a, sud- den strain ruptures a valve that has been previously softened by infiltration, or made brittle by atheroma or senile changes. Such an event is usually announced by a musical murmur. An acute attack will be more readily detected by keeping in mind the var- ious affections that appear to cause endocarditis. In the actite septic form there are irregular chills and sweats, with fever. •Other signs have already been noted as belonging to the benign form, to which should be added pretty uniform tenderness and ■enlargement of the spleen, with sometimes similar conditions of the liver and kidneys. The urine should be dark colored ; i. e., .bloody, if a kidney develops an infarct. According to my hospital tables, as I have said, endocarditis has recognizable murmurs in 95 per cent, of the cases, and the three most prominent signs, following the auscultatory, are dysp- noea in about 50 per cent., palpitation in about 25 per cent., and prsecordial pain in about 10 per cent. Other less constant symp- toms are cough, weak or irregular action of the heart, dizzi- ness, epigastric pulsation, orthopnoea, cyanosis, delirium and oedema. In only 5 per cent, there were no characteristic signs during life. But as I have said, it is one thing to be able to distinguish endocarditis, or in fact any endocardiopathy, inflam- matory or not. and quite another to locate the precise lesion ac- curately. Of the endocardial murmurs there are two kinds. First, the organic; second, the functional. The former are heard when there is a mechanical hindrance to the flow of the blood from ulceration, sclerosis or rupture of the valve. The functional mur- tnurs are caused by relative — i.e., muscular — insufficiency, which •occurs when the orifice is dilated so that the valve margins do not come together accurately ; or, when from degeneration oT weakness of the papillary^ muscles, the valves are not held in place ; also, when as in anaemia, especially in convalescence from long continued illness, there is an alteration in the composition or amount of the blood. An irregular pulse with praecordial pain and dyspnoea, or even a systolic murmur at the apex, does not necessarily indicate that the murmur is due to organic disease ; but a systolic 2,6 Endo-Cardiopathies mnrniur at the base is likely to be functional, if it is liniiteil to the left side of the sternum, and there is no thrill. Orijanic nnirniurs durini^ the tlevclopment of an endocarditis are usually harsh and loud. The I'rench talk about the sawing nnirmurs (bruit du scic). the raspinc^ murnuir (bruit du rape), the musical luurmur {bruit d'oboe), the bellows nmrmur (bruit du souffle). These are usually organic; functional murmurs are low, soft and ahuuiys systolic. But a single examination luay not suffice to distinguish between the two. The organic murmur will be more apt to continue ; while the functional will disappear under tonic treatment or rest. The point of greatest intensity of a murmur is somewhere in the course of the blood current beyond the obstruction, and is usually due to the breaking up of the cur- rent. Just as in the stream of water flowing through a narrow orifice, it is not at the point of greatest obstruction where the noise is loudest, but where the water expands beyond the ob- struction, and is broken up into diverse currents. When a blood current passing over a rough surface, or through a narrow pas- sage, can be felt, the sensation is called a "thrill," sometimes a "purring thrill." {fremissement cataire) , because it is like the thrill felt by the hand pressing on a purring cat. In endocarditis we do not always need to be alarmed if the pulse is frequent or infrequent. Neither condition should be treated as a disease. A pulse of 50 or 60 may be characteristic of the man, and so a pulse of 100. It is not at all a rare thing to find a patient with an average pulse of 60 ; but it is uncommon to find a pulse of 100 or more. We should first inquire if these abnormal rates of the pulse are not individual or family charac- teristics. I have known the most serious mistakes to be made in such cases. A man with a pulse of 50 to 60, or even 120, may not reailize that there is anything peculiar about the action of his heart, and may be quite as able to do his daily work as the next man. And yet physicians are quite apt to treat these conditions, by trying to bring the rate to the recognized average of seventy- two. In such cases, drugs should be the last remedies resorted to. The frequent pulse sometimes follows surgical operations, or injuries to the thorax or neck. The rhythm is usually afifected in endo-cardiopathies, both in the acute and chronic forms, and always in broken compensation. If the pulse is large, it generally indicates cardiac hypertrophy; the hard pulse, rolling under the fingers, means arterio-sclerosis. Endo-Cardiopathies 37 the feeble pulse is found in the fatty heart, the soft pulse in anaemia and in fevers. Pulsation of the jugulars suggests tricus- pid regurgitation ; the capillary pulse aortic regurgitation. The pulse may be unequal — that is, more easily felt in one radial than in the other — but this peculiarity may be congenital or due to arterio- sclerosis, or other causes. The sphygmo graph, is a pretty instrument, but it is less used than formerly, because it is apt to mislead. It is of value in clinical experimentation, but its uses at the bedside are few. Clinicians are using it less and less in this country. It should not be relied upon for differential diagnoses in valvular diseases. In endocarditis there are, not infrequently, attacks of tumultu- ous action, with distressing palpitation, the impact extending over a considerable area. In the intervals between these attacks, the action of the heart may be quite regular, the apex beat inap- preciable to the finger, and a "thrill," which was distinctly felt, ■may disappear. Auscultation yields the most important information. Suppos- ing a valve, say the mitral, is obstructed to a considerable extent, so that it cannot close perfectly, the blood will necessarily leak Iback into the left auricle, during the contraction of the left ventri- 'cle. In such case the first sound, which is due chiefly to the closure of the mitral valve and to muscular action, is replaced by a murmur caused by the leaking or regurgitant blood passing through the obstructed opening, and this sound is best heard between the apex and the axilla or spine of the scapula, where it is conveyed, in accordance with the rule's governing the conduction of sound. If the new deposits in the valve are soft and smooth, the murmur is soft ; if very rough or irregular, it is loud or harsh. This is provided the heart's action is strong; if it is weak, there may be no appreciable murmur. Sometimes a harsh murmur suddenly disappears, while the action of the heart continues the same. Some portion of the obstruction has then been swept away. There are not the hard and fast areas in which to hear the several murmurs, as laid down in some books, and there is quite a little dift"erence of opinion as to the locality of these areas among teachers of physical diagnosis. The truth is that the point of maximum intensity for determining mitral regurgitation is be- tween the apex and the axilla or scapula ; but in mitral stenosis the point of maximum intensity extends from the apex upwards and downwards perhaps as much as an inch or more, and a less distance ^S Endo-Cardiopathies to the right. In aortic obstruction tlic obstructive unirniur is beard'. best over the right 3d costo-sternal junction, or at the junction of the second right interspace \vith the sternum, or even as far over as the correspon(Hng space on tlie left side; while the aortic regurgitant may be well heard along a broad area spreading like a fan from the aortic area to the ai)ex, or even to the cnsiform appendix. As the point of maximum intensity for the tricuspid is located at the junction of the left fifth interspace with the sternum,, it is not far from the mitral area, ami its munuurs may be conveyed to that area : hence it may be difficult to make a diagnosis between these two lesions, rulmonar} lesions are so rare that they are curi- osities ; most of them are due to congenital malformations of the heart. In general, the murmurs indicative of the greatest danger are the diastolic. Percussion is at first negative, but, as endocarditis progresses, the contour of the heart gets larger and more ovoid. This enlarge- ment is the most important sign of organic heart disease, because it is unequivocal. The heart swings like a pendulum in the cavity of the chest, sus- pended by its great vessels ; so that the apex is carried well outside the nipple in some cases, especially in lateral curvature, where the spinal concavity is generally to the left. It may also be displaced" to the right by fluid in the chest, and by lying on the right side. Still, as we only examine in the upright or recumbent positions, it is relatively fixed, and we find the apex in the fifth space, the left border of the heart the breadth of a rib inside the nipjile, and about twice that distance below it. The right auricle is al)0ut the only part of the heart outside the right border of the sternum. Two- fifths of the heart lies to the left of the median line. -Ingina pectoris is not uncommon in endo-cardio]:)athies. Both forms, which are best classified as the mild and the severe, are usu- ally brought on by mental or moral excitement, indigestion, over- exertion, and a number of minor causes, especially those that in- fluence the special senses. They are always, in my experience, capable of being controlled by suitable remedies, though drugs may prove ineffectual when rest, massage, electricity, baths or a change of scene will succeed. Endocarditis gives rise to various symptoms in other organs, for there may be hypersemia of the lungs, embarrassed respiration, engorgement of the kidney and chylopoetic tract, and even general' dropsy. Endo-Cardiopathies 39 •^ A distinct picture is produced iu these cases l)y embolism, where ,;articles detached from the diseased endocardium, or clots formed about the valves, in the auricular appendages, or about the papillary muscles, arc carried to distant organs. These accidents may cause few symptoms, and yet may involve the brain, causing alarming re- sults, and even sudden death. But if the collateral circulation is rap- idly established, little or no functional disturbance will be produced. As terminal arteries, however, are found in the brain, lungs, spleen, kidneys and heart, the occlusion of large vessels in these organs is apt to be followed by severe symptoms, such as chills, vomiting, pain and haemorrhage. Benign emboli may cause only arrest of function, but the malignant or septic will certainly produce abscesses that in turn will furnish foci for others. Embolism of tlie brain occurs most frequently along the line of the branches of the left carotid, the trunk of which lies directly in the course of the circulation. The embolic masses find their way through this carotid to a branch of the Sylvian artery, and if there is occlusion of a large branch, loss of consciousness, hemiplegia and aphasia usually follow. In young or middle life, embolism is the rule ; in advanced life, apoplexy. Embolism of the lungs has characteristic features. If a vessel of any considerable size gets plugged there is apt to be pain, vomiting, cough, dyspnoea, haemorrhage, and expectoration of frothy mucus; perhaps cyanosis, suffocation and syncope. Etnbol- i.wi of the liver may be ushered in with chills, pain, swelling, tender- ness and icterus. Embolism of the spleen also shows itself with a chill, fever, and severe pain in the organ, which should be en- larged and tender to the touch. Embolism, of the kidneys similarly may be ushered in by chills, fever, pain and albuminous, perhaps bloody urine. Embolism of the mesenteric arteries is revealed by colicky pain in the abdomen, diarrhoea and discharges of black blood. Embolism of the retina is sometimes seen with the ophthalmoscope. If septic, it causes inflammation and destruction of the globe. Em- bolism of the skin may cause purpura or gangrene. In fact, embolism arrests the function of the part where the in- farct is lodged, and if septic, produces destruction of tissue. So long as compensation is imperfect, there are also other com- plications. For whenever the heart begins to labor, congestion of the veins and capillaries of the lungs immediately results, and then the bronchial mucous membrane, alveoli and passages become swollen and oedematous ; with eventual desquamation of epithelium, and transudation of mucus, serum and blood. Embarrassment of 40 Endo-Cardiopathies respiration ensues, and it is heightened b) the increased efforts of the lungs to aerate the abnormal quantity of blood in the pulmonary vessels. Such a condition may be only temporary, constituting pulmonary oedema ; but if it become chronic, the character of the lung tissue is changed, for the continued venous engorgement is followed by deposits of pigment matter. This leads to what is known as brou'n induration of the lungs, and even rupture of pul- monary vessels ; indeed, pulmonary hccmorrhage is not uncommon in chronic heart diseases. The liver also becomes enlarged from a similar cause, and pig- mented. In fact, there is a congestion of the entire chylopoetic sys- tem, which continues so long as the heart is embarrassed. As soon as there is congestion of the venous system, it is shown by a bluish color of the skin or visible mucous membranes. Thrombosis may also occur, and cases have been described by Welch, A. A. Smith, and MacGregor. (See Amer. Medicine, May 25, 1901, and Brannan, Med. Rec., Feb. 22, 1902.) For a similar reason the kidneys become swollen, and later tough and firm. The urine is diminished, but the specific gravity is in- creased ; it may contain blood, and usually a little albumin ; some- times a little sugar, varying from ^ to 23^ per cent. Oedema, due to prolonged distention of the veins of the peripheral system, he- patic or renal implication, deserves attentive consideration. But all cases of oedema about the ankles, hands or face need not alarm us. They may occur from lack of exercise or anaemia, or temporary compensatory failure, and will disappear under appropriate treat- ment. Accumulations of fluid, however, in the abdominal cavity, or oedema ascending gradually from the ankles to the trunk, are very serious matters, pointing to a fatal issue at an early date. If the valvular disease is at all serious, dilatation and hypertro- phy of the right or left ventricle will supervene. Hypertrophy is essentially a compensatory change, enabling the heart to do the work required of it, notwithstanding the valvular disease, and to re-estab- lish the proper balance between the arterial and venous systems. In aortic disease compensation produces the long heart, due to dilatation and hypertrophy of the left ventricle. On the other hand, in pulmonary stenosis, which is rare, of course, the right ventricle dilates and hypertrophies. As soon as the former cardiac balance has been restored by the means just described, we say that com- pensation has been established, for then the consequences of the valvular disease have been overcom.e, for the time at least. While, Endo-Cardiopathies 41 however, compensation is being established the patient is short- winded, cannot walk any distance, has precordial pain owing to the dilatation, perhaps fainting fits, and feels physically exhausted at the end of the day. But after compensation has been established all these symptoms disappear, and he feels as well as most persons, except if called on for some extra exertion, or upset by some emo- tional disturbance. Enlargement of the liver helps to detect lack of compensation. It indicates dilatation of the right ventricle and right auricle as well. If there is obstruction in the pulmonary cir- culation, the right auricle is pretty certain to be dilated. But it is a mistake to think that compensation calls only for dilatation and hypertrophy of particular chambers of the heart, corresponding to certain valves. If the valvular lesions are at all serious, both ventricles and both auricles are eventually more or less dilated and hypertrophied, owing to the close relation they hold to each other. Chapter III. '\CI;TK ENDOCARDITIS: BENIGN AND MALIGNANT.^ l-'or convenience sake acute endocarditis may be said to have two prominent types, the benign or non-suppurative, and the ma- lij^^nant or suppurative. The latter variety has also been known as the mycotic, infective, etc., but as both contain micro-organisms in the endocardial dei)Osits, and are associated with systemic in- fections, these terms are inappropriate. Nor has the word ulcera- tive, as a])plied to endocarditis, an\ distinct value, because all forms tend to ])roduce ulceration. The acute benign form is by far the most frequent. In an analy- sis of forty-eight cases of endocarditis, verified by post-mortems, some years ago- I found that it was rarely produced by an injury, but more often resulted from systemic poisoning, such as rheumatism, scarlatina, measles, etc., though in about half my cases I did not discover the cause. In the light of our present knowledge, how- ever, we may attribute it also to a large number of minor ailments, mcluding gastro-intestinal alTcctions, tonsillitis, etc., which are now known to immediately precede the attack. I saw such an instance in 1901 at the New^ York Orthopedic Hospital, with Dr. Hibbs, in an otherwise healthy boy of seven, who entered the hospital to be operated on for congenital dislocation of the hip. After the opera- tion, from which there was at first no unfavorable reaction, he devel- oped an obstinate diarrhoea, in the course of which there was a sharp attack of endocarditis. In this case the gastro-intestinal tract appears to have been the source of the infection. I am inclined to think that various systemic poisons, many of them still unknown to us, produce the disease. But it is an incident of systemic affec- tions, rather than a separate entity. In most cases endocarditis selects those portions of the endocardium which are at or about the valves. The first gross evidences of disease consist in the formation of minute reddish excrescences near the free valve margins. In ihe mitral leaflets they are on the auricular surfaces, in the aortic leaflets on the ventricular surfaces. Soon after these soft excrescences appear they are covered ' Published originally in the Medical Times. Mav. 1901. '.V. Y. Medical Record, Feb. 27, 1886. Acute Endocarditis 43, with layers of fibrin, hence the term diphtheritic. 'J'wo processes are now possible, either a healing, with thickening- and puckering of the leaflets, or a degeneration that leaves broken surfaces or ul- cers. And yet, when this degenerative process goes on there is about it a regenerative process by which Nature attempts to heal the part and restore its function. At all times micro-organisms, in greater 01- less number, are found in the fibrin or granular debris of the ulcer- ating surfaces. The degenerating matter, or the fibrin attached to it, may produce infarcts in various parts of the body. In extra-uterine life the left side of the heart is most frequently attacked; in congenital disease the right. Patients seldom suffer much from the simpler forms of endo- carditis in their early stages. They often complain of some prae- cordial pain, though symptoms such as this may be due to an asso- ciated pericarditis, the irregular action of a hypertrophied heart, or pulmonary complications. In a large number of cases there is a noteworthy frequency of the pulse (a rate of 120 to 140 is not un- common at first). Dyspnoea, orthopnoea and palpitation also are of pretty regular occurrence. But it is the accidents and complica- tions that are most dangerous to life. In a disease which in nine out of ten cases lasts for years (sometimes twenty and thirty, and even more) it is natural that these accidents should at times occur ; and we find them in the shape of infarcts in the kidneys, lungs,, spleen or brain, etc., in one-third of the patients. The danger therefore increases as the disease becomes chronic. For in the great majority of cases patients survive the acute stage,, though embolism may occur, even at that time, as we have seen. Often the acute or benign form eludes observation. However,, we should be on the lookout for it in acute rheumatism, especially when the temperature rises to 100° or 102° F. ; and also in pneu- monia and scarlet fever. It is less frequent in typhoid, erysipelas^ bronchitis and gastro-intestinal afifections. The diagnosis is beset with some difficulties, or otherwise it would be recognized more frequently. The signs include palpi- tation, dyspnoea, prascordial pain, insomnia, often rapid and irreg- ular pulse, headache, and anxiety. In the first attack there may be no enlargement of the heart, and therefore no dislocation of the apex. In adults we have to deal most often with acute exacerbations of a chronic malady, or the recrudescence of a latent endocarditis. In the majority of cases the disease is either in the mitral or aortic valve. One of the main difficulties encountered, however, in making a 44 Acute Endocarditis diagnosis, is that the acute attack is apt to be engrafted on a chronic, or at least a latent, condition ; or. the lesion may be masked by a pericarditis. In acute endocarditis the tirst requisite is rest in bed. As far as possible we should avoid drugging ; and stimula- tion by alcoholics may also be harmful. But the diet should be care- fully regulated. Starchy and saccharine substances should be pro- hibited. For children, milk is the best food, and it is also good for adults, if it agrees with them." It may be diluted with one-third to one-half lime-water in children ; with Seltzer and Vichy in adults. The patient should also be kept in a quiet room and free from all annoyances. As soon as practicable, efforts should be made to combat the systemic disorder. If it is rheumatism, the salicylates should be given with caution, in 5 to 10 grain doses^ every two to four hours, with an alcoholic or diffusible stimulant ; but not in sufficient quantity to produce vertigo, ringing in the ears, or constitutional symptoms. A little pal- pitation may be let alone. If, however, the heart acts tumultu- ously, a cold compress may be put to the prgecordial region, and bro- mides, such as the bromide of sodium or monobromate of camphor, giv^en. The latter is an excellent remedy, in 2 grain doses. Two or three grains of Dover's powder every two hours is also excellent. Aconite, in i minim doses every two hours, is soothing if there is fever. Phenacetine may also be given to adults, in 3 to 5 grain doses, with a stimulant at bedtime, if the effects of the drug can be watched. Digitalis should not be given, or, if at all, with great caution. It is a dangerous remedy in these cases. In intense arrhythmia stro- phanthus may, however, be tried cautiously, because it is soothing ; but it is apt to be unreliable and, like digitalis, it should be given in emergencies only, and for a very short time. The milder reme- dies should be tried first. The following two cases illustrate the benign type. Case I. Acute Benign Aortic Endocarditis Engrafted on the Chronic Form. — E. B., twenty-two, colored, was admitted to hospi- tal December 11, 1880. Three weeks previously he had been taken with prrecordial distress, palpitation and dyspnoea, slight cough with white sputum, orthopnoea ; at times nausea and vomiting. On physical examination the heart was ' found hypertrophied, with apex to left of nipple. Wavy movement of the epigas- trium. Expiration prolonged, and high-pitched behind. Murmur at apex with first sound. Pulsation of jugulars. The murmur, Acute Endocarditis ^5 supposed to be mitral regurgitant, was carried to the left, but was better heard above the scapula than below it. The patient died of pneumonia. At the autopsy an abnormal amount of fluid was found in the pericardium, and some in the pleural cavities. Both hmgs were solidified at their bases, and pigmented. Nutmeg liver. Kidneys and spleen congested. The heart was hypertrophied. Pul- monary opening dilated. Right heart dilated. Mitral valve nor- mal, but aortic valve the seat of fresh vegetations, and posterior cusps thickened and inflamed. This case was an acute benign aortic endocarditis with hyper- trophied heart. The murmur at the apex, supposed to occur with the first sound, heard best behind and above the scapula, proved to be 'One of those instances where the murmur of aortic regurgitation is conveyed to the apex from the aortic. And it opens the question w'hether the regurgitant murmur was conveyed to the apex by the sternum, the solidified lung or the heart walls. It also illustrates the importance in these doubtful cases of noting that in the aortic regurgitant the murmur may be conveyed above the scapula ; and farther, that the second sound may be mistaken for the first. The pulmonary, though dilated, appears to have been sufficient. Case II. Acute Benign Mitral Obstruction; Pericarditis. — C. W., twenty-one, single, was admitted to hospital January 25, 1884. He believed himself in good health up to five weeks before admission, when he had an attack of acute articular rheumatism. On physical examination a systolic murmur was heard at the apex. Liver enlarged ; albumin and casts in the urine ; oedema of legs. These symptoms improved, but at the end of four weeks there was an increased oedema, which reached to his scrotum. About this time a "purring thrill" was noticed at the apex and a double murmur at both apex and base. The patient died a few days later, in coma. At the autopsy the pericardial sac was found to contain a large amount of serous fluid, with fibrin in flakes. Both visceral and parietal layers of the pericardium were covered with a fibro- plastic material. On the mitral valves were villous granulations sufficient to produce obstruction. The other valves were normal. I.Amgs congested and oedematous. This case illustrates how an associated pericarditis mav obscure an endocarditis. The "purring thrill," however, pointed to mitral ob- struction. Septic or suppurative endocarditis is a comparatively rare dis- ease. In a series of forty-eight cases of endocarditis I found it in 46 Acute Endocarditis only three, or about 6 per cent. And from a review of others of my cases to date, I think it is even less common than these figures would imply. In fact, it is an unusual form of purulent infection. The lesions in the valves ma}- be vegetative or ulcerative, but always suppurative ; "so that the emboli are necessarily sei)tic. eventually producing metastatic abscesses. So rare is the disease that it often escapes notice, but there are certain signs which should attract our attention. They are those of anaemia, embolism and metastatic abscesses, in conjunction with theother subjective or objective phenomenaofendocarditisandsepsis. If. in a case of pueri)eral fever, pneumonia, suppuration from bones or joints, gonorrhoea, or any form of infection, or in trauma- tism, signs of endocarditis develop, we should suspect the septic or suppurative form, especially if there are chills and fever (even though periodic) with an enlarged and tender spleen, and bloody tirine. In suspected malignant endocarditis the blood should always be examined. Sometimes a pyogenic coccus can be cultivated, indi- cating that there is a septicaemia ; or the gonococcocus may point to the cause of the disease, just as the pneumococcus suggests the lung, and the colon bacillus the intestines as the gates of infec- tion. Usually with the anaemia there is marked leuocytosis, to- gether with destruction of red blood cells, which may be reduced to J, 000,000. (Ewing.) If blood examinations in a suspected case fail to react for ty- phoid, malaria or tuberculosis, a diagnosis of malignant endocardi- tis may be made by exclusion. (Cabot.) In a case of gonorrhoeal endocarditis, however, reported by Stein {Wien. Klin. IVoch., Nov. 22, 1900), Weichselbaum found strej!)- tococci, the inference being that the gonococci simply made the soil favorable for other bacteria, and that the case was one of mixed infection. I am inclined to think that there are several micro- organisms concerned in the production of this acute infection. >• The diagnosis is manifestlyy difficult, and yet is not impossibfe, if all the phenomena are taken into consideration. The signs in- clude precordial pain, dyspnoea, headache, insomnia, irregular chills, sweats and fever, anxiety, rapid and irregular pulse, and the phys- ical signs of endocarditis, with septic or pygemic manifestations ; in short, the signs of endocarditis, with a tendency to metastatic ab- scesses. Inasmuch, however, as in most cases the acute form of the disease is engrafted on an old one, we should also inquire as to Acute Endocarditis 47 whether there have been previous signs of endocarditis. Therefore, we should expect to find some dilatation of the heart, with a dislo- cation of the apex outwards or downwards, or both. The organic murmurs of septic endocarditis are, so far as my experience goes, confined to the aortic and mitral valves. The disease is usually fatal in a few days, but cases have been reported where it has lasted for months. Recoveries must be very rare. In my opinion most of the cures reported have been in cases where there has been embolism, with chills and sweats, but the em- boli have been benign. Personally I have never known a case of recovery in malignant endocarditis. 1 have, however, known re- covery to follow gonorrhoeal rheumatism with metastatic deposits, and I have also seen one recovery in pure pyaemia. Septic endo- carditis should not, therefore, be altogether hopeless. The following are illustrative cases : Case III. Acute Malignant Endocarditis; Caries of the Carpal Bones. — A. C, colored, aged forty-six ; was admitted to hospital November 5, 1878. He was first taken sick on October 25th, but had never before been seriously ill. At first he had pain in the left knee, and about the same time there were chilly sensations, followed by headache, fever and backache. He took to his bed, and remained there until removed to hospital. On admission, there was found to be pain on the left side (spleen?), and in his left leg. His wrist also was swollen, tender and intensely painful. No fever, but great prostration. On November 28th, after showing no signs of improvement, he passed blood per rectum. Probably there had been an evening rise of temperature for some time. It re- mained between 101° and 102° until December 3d. Towards the last it rose to 104°. pulse to 116 and respiration to 46. At the post- mortem examination no cardiac hypertrophy was observed, but at the aortic orifice, beneath one of the cusps, w^as a verrucose growth the size of a small chestnut, while the valve was ruptured. On remov- ing the brain, pus was found in the meshes of the pia mater. At the wrist (left?) the first row of carpal bones was found necrotic or carious. Duration of the disease, six wrecks. In this case the evidence pointed to necrosis, or caries, of the carpal bones as the source of the acute endocarditis, though the evidence connecting it is not as satisfactory as one might wish, because at the time no special attention was directed to the endocarditis. Case IV. Lobar Pneumonia; Malignant Endocarditis. — The history of this case was sent me from St. Francis Hos- 48 Acute Endocarditis pital. A patient of alcoholic habits, aged forty-one, was ad- mitted in November of 1882^ with a lobar pneumonia. There was high temperature, but no cardiac murmurs were detected. Other and apparently more important conditions obscured the car- diac disease. At post-mortem examination the aortic cusps were found extensively diseased, each segment exhibiting vegetations, while one carried a growth the size of a hickory-nut, and was rup- tured and ulcerated. An abscess was also found in the course of the coronary artery, and a sinus led from it to the fungating mass in the aortic valve." The spleen contained an infarct. Duration of the illness, about five weeks. The malignant endocarditis was probably closely related in etiology to the pneumonia. Case V. Malignant Endocarditis; Sufypurativc hifarcts. — A gentleman of this city was taken sick with an attack of fever that confined him to his room for four or five days. He then felt bet- ter and went downstairs, but soon returned and took to his bed. JDuring the first two weeks of his illness the temperature ranged from 98° to 100° F., his pulse from 140 to 150, sometimes reach- ing 160. During the last two weeks of his life it had a wider range (120 to 150). At an early period the diagnosis of obstructive en- docarditis was made out. The respiration was never embarrassed, except when the patient sat up. There was never any impairment of motion or sensibility, nor did he experience any pain, except on one occasion when his physician attempted to turn him over on his left side. He then cried out suddenly, "You have killed me," and placed his hand over the region of the spleen, groaning with pain. He recovered from this attack, but died subsequently with suppression of urine. The post-mortem examination revealed a stenosis of the aortic, which would hardly admit the passage of the first joint of my little finger. The surfaces of the cusps were marked by calcareous con- cretions and vegetations. The heart, and especially the left ventri- cle, was dilated and hypertrophied. The kidneys presented the usual appearances seen in the large variety of chronic diffuse nephritis, and also contained both recent and old infarcts. The lungs also had infarcts. The spleen and the meninges, however, showed the most important lesions. The first-mentioned organ measured about nine inches in length, and was the seat of numerous infarcts of various ages, some red, others brown and others yellow, while one had been the point of origin for an abscess from which a pint to a pint and a half of dirty, grumous, oflFensive matter was discharged. Acute Endocarditis 49 Emboli were also found in the meshes of the pia, with attendant suppuration. This acute attack was plainly engrafted on an old rheumatic endocarditis, but why the emboli were suppurative was not determined. Chapter IV. MITRAL INSUFFICIENCY.^ Mitral insufticiency, regurgitation or incompetency is a com- paratively common valvular affection, and the least serious of any, so long as it is uncomplicated. But it is seldom the only valvular lesion. From my tables it appears that in 86 per cent, it was asso- ciated with aortic, pulmonary or tricuspid disease, the combination with aortic being the most common. The most frequent cause of insufficiency is endocarditis, which is also most frequently caused by litha^mia. Under the influence of this and other constitutional vices vegetations form along the borders of the leaflets, which thicken and then retract, wdiile the tendinous cords and papillary muscles also become infiltrated and, contracting, hold the leaflets back. Another cause of inorganic insufificiency is the rupture of a leaflet. All of these phenomena I have seen. Finally, the orifice ma}' be involved in a new growth, or atheroma may prevent closure. Usually, however, the latter infiltrates a leaflet without interfering with its closure. Of the inorganic or relative form there are many varieties, and it may be a temporar}- or permanent condition. One of the most common causes is violent physical exercise, such as young men are subjected to, in training for athletic sports. In one of the physical culture schools of this city I have been told by the manager, who is also a physician, that most of the prominent athletes under his tuition are affected wath mitral regurgitant murmurs during their training. Or an aneurysm of the arcli causing the large heart so common in aortic disease is pretty apt to entail some relative, that is. inorganic, dilatation ; or in plainer language, stretching of the mitral orifice. This is because the whole left heart must dilate and the tendinous cords and papillary muscles stretch (the leaflets usu- ally failing to enlarge in size, so as to fit the enlarged orifice).^ In a somewhat similar way the fatty heart may dilate, the leaflets failing to enlarge proportionately. Now, it is quite apparent that this form of insufficiency is capable of remedy, provided the condi- tion governing it is removed. ^ Published originally in the A''. Y. Med. Journal, Feb. 12. 1902. ' In some instances the valve leaflets do actually enlarge to compensate for the enlarged valvular openings. Mitral Insufficiency 5^ Probably it is quite common as a temporary affair — for example, after a set at tennis, a boat race or a running match, in recovery from fevers, or after an infection or in cardiac neuroses. At autop- sies we are not likely to see very many of these accidents, because they do not cause death. On the other hand, we not infrequently find at autopsies an artificial mitral insufficiency where post-mortem softening has set in. This condition is less often seen now than formerly, owing to the system of post-mortem refrigeration that is at present in vogue. In mitral insufficiency there is such an imperfect closure of the mitral leaflets that, during systolic contraction of the left ventricle, more or less blood leaks back into the left auricle, already partly filled with blood coming from the lungs. Necessarily the left auri- cle dilates and then hypertrophies, because it has more blood to be driven into the left ventricle. And inasmuch as the left ventricle has to use more force in order to supply the aorta with its proper quantum of blood, it also hypertrophies after dilating. But over- filling of the left auricle dams the blood back on the lungs and offers such resistance to the column coming from the right ventricle that this also hypertrophies and gives way, causing dilatation of the right auricle, whenever the tricuspid yields. The most characteristic sign of mitral insufficiency is a systolic murmur between the apex and the axilla or scapula, due to the leakage of the mitral during the contraction of the left ventri- cle. This murmur will vary in quality ; it is usually rough and loud, rarely musical. Inorganic murmurs are softer and have more of a blowing character. Regurgitant murmurs are also intensified by slight exertion. Accentuation of the second sound over the pulmonary artery is another sign which is due to the sudden closure of the pulmonary leaflets, caused by the strong resistance ahead of them in the auricle. The right ventricle gets to be hypertrophied rather than the left when compensation is accomplished, so that we look for greatly increased transverse dulness ; for the left border of the heart may extend from an inch or two to the right of the sternum as far as to and beyond the left nipple. In the early development of mitral insufficiency, of the organic form, the compensatory symptoms usually go hand in hand with the lesion, so that although a systolic murmur is present, the affection may not be appreciated by the patient or those about him. Yet there will result some embarrassment of the pulmonary circulation, 52 Mitral Insufficiency ^vhich will be shown by a little shortness of breath on exertion, per- haps by an increase in the pulse rate, ^vith more or less irregularity. There may also be spitting of blood, for at this period the pul- monary vessels are all dilated and cause some bronchorrhoea. When compensation is fully established it is at first through the hyper- trophy of the left ventricle, but eventually and chiefly by the right, and then the pulse will be slow, full and regular. Compensation may last a long while, with patients who are fortunate enough to combine both a knowledge of their condition and the ability to con- trol adverse incidents. In my records 1 have not a single instance of uncomplicated mitral insufficiency in which death w'as attributable to it ; though it may certainly cause death when complicated with some other valvular trouble. With laboring men and those exposed to unusual vicissitudes there will necessarily be lapses, the breakdown at the end coming earlier; and yet during all this time the systolic murmur may con- tinue to be loud, while its quality, w^hether rasping, fiUng, blowing, etc., or even musical, will depend upon the physical character of the orifice and adjacent parts. In my opinion, however, organic insufficiency passes over even- tually into stenosis or obstruction. Acute relative insufficiency is a temporary condition that will mend with rest and systemic treatment ; while the forms that re- sult from muscular weakness, as from the poison of diphtheria, the continued fevers and infections generally, from faulty innervation or fatty degeneration, will improve synchronously with improvement in the conditions producing them. And yet in the mitral insufficiency of day laborers, and in adher- ent pericardium, there is less likelihood of compensation, because the conditions that cause it are apt to be permanent. In uncomplicated cases the prognosis is good, but complications are to be expected. Ruptures or lapses of compensation are ushered in by relaxa- tion of the ventricular walls, causing venous congestion, first of the pulmonary system and then later of the systemic. At the end the systolic murmur grows faint and may even become inaudible, owing to the deficient force of the left ventricle. The second pulmonary sound also will become progressively weaker, owing to the yielding of the right ventricle. Venous ptilsation, or certainly a wavy motion in the veins of the neck, indicates giving way of the right ventricle. The surface be- comes livid, there is palpitation, with a weak and intermittent pulse. Mitral Insufficiency S3 and the cardiac impulse grows faint or disappears. The liver may be swollen and tender ; the urine scanty and albuminous. About this time dropsy may be expected, perhaps delirium cordis, and death is a natural sequence. Or death may result from asystole, though uraemia or pulmonary haemorrhage may close the chapter. Up to the period of breaking compensation the three cardinal signs are: i. A systolic murmur between the apex and the axilla. 2. Accentuation of the second pulmonary sound. 3. Increased trans- verse dulness of the heart. In and after breaking compensation the diagnosis must be based on the previous history, because the ab- normal transverse dulness may be the only one of the three cardinal physical signs left from which to construct a diagnosis. If obstruction coexists, as it does in from 70 to 80 per cent, of the cases, we must expect a systolic thrill at or near the apex in from 15 to 60 per cent., and a presystolic murmur in at least from lo to 30 per cent. In children or young people there may be a bulging of the prsecordia. Mitral insufficiency is, as I have said, comparatively easy to diagnosticate in uncomplicated cases, as the following instance will show: Case VI. Mitral and Tricuspid Insufficiency. — L. A., a cabinet- maker, born in France, seventy years old, was admitted to hospital January 3, 1881. Eight days previously he was taken with short- ness of breath, wheezing, slight cough and spitting of blood. Soon his legs began to swell. On examination fluid was found in the pleural cavity. Patient cyanotic ; heart sounds indistinct. A few days later, a mitral systolic murmur was made out, wath increased heart dulness and diffuse heart beat. A cardiac murmur, loudest over the ensiform cartilage, was attributed to tricuspid regurgita- tion. Later some lung consolidation was discovered. At the post- mortem examination the aortic and pulmonary valves were found normal, while the right cusp of the mitral was thick and contracted and bound up. Left auricle greatly dilated. Mitral admitted the tips of seven fingers. Valves of tricuspid thickened and restricted in movement ; weight of heart, 23 ounces. Both lungs contained red infarcts. Right chest full of serum ; left chest nearly full. This case was examined by several of our best clinicians, the result being an absolutely correct diagnosis in essential particulars, the chief point of interest to us being that both the mitral and tricuspid lesions were noted. But though mitral regurgitation is comparatively easy to diag- 54 Mitral Insufficiency nosticate, it is unsafe to pin our faith too exclusively on ausculta- tory murmurs, as indicative of organic disease. For occasionally functional mumuirs are produced at the apex, by the patient's pos- ture or other causes. These murmurs, however, are not apt to be accompanied by an accentuated secondary pulmonary sound. They may also be due to impoverished blood or muscular vibration. Ow- ing to the extreme rarity of a tricuspid insufficiency (according to my records about 4 per cent.), it is apt to be disregarded in practice. It may, however, be combined with mitral insufficiency, as in Case VI. It is, however, difficult of diagnosis, not only because the centre of the tricuspid area is tolerably close to the mitral, but the two areas overlap to some extent. In uncomplicated cases of tricuspid insufficiency, however, there is no accentuation of the second pulmon- ary sound ; the systolic nmrmur is not conveyed to the left as much as it is to the right ; there is venous pulsation of the veins in the neck, and a dilated right heart. In instances where there are merely fresh vegetations on the valves sufficient to cause very slight insufficiency no murmur may exist. After all, mitral insufficiency is comparatively easy to de- termine, because the valve is to the left and behind, and as the mur- mur follows the regurgitant current, which flows more or less back- ward as it goes upward, it is carried somewhat towards the angle of the left scapula. In my experience the diagnosis of pure mitral insufficiency is made in three quarters of the cases. The treatment is coub-idered in Chapter XIX. Chapter V. MITRAL OBSTRUCTION.! Our conceptions of mitral obstruction originated with Corvisart, Napoleon's able physician, and the teacher of Laennec, who tells us that in 1819 Corvisart first called attention to the "purring thrill" of mitral obstruction, which he described as a "particular sensation, which in some cases is perceptible to the hand when this is applied to the region of the heart," and is a "sign of the ossification of the valves, and particularly of the mitral valve. Indeed, this phenom- enon is observed in almost every case in which there is some con- traction of the auricle of the heart." Leaving out of consideration Laennec's erroneous views about "ossification," it is enough to note that he clearly associated the discovery of the "purring thrill" with his distinguished teacher. He is also equally emphatic in attributing the discoverv of the diastolic bruit of mitral obstruction to his contemporary, Bertin, but the description of it is all his own. Alluding to one of his personal cases, he uses these words:- "The contraction of the auricle, which was extremely prolonged, was performed with a dull but strong sound, precisely resembling that produced by filing wood. This was accompanied by a vibration sensible to the ear, and is evidentlv the same as is felt by the hand. At the close of the contraction one could distinguish by a louder sound, accompanied by an impulse and perfectly synchronous with the pulse, the contraction of the ventricle, which w^as three-fourths shorter." Three cases of this kind, he tells us, had been described by Bertin, and were verified by autopsies. Twenty-four years later Fauvel first called attention to the sub- variety of diastolic bruit now known as the presystolic, which he defined as a "loud, rasping bruit" preceding the first sound or mur- murmur and ending with it. In English circles W. T. Gairdner.^' of Edinburgh, is usually credited with defining it, which he did under the name "auricular systolic bruit." According to Gairdner. it was a murmur preceding the first sound, running sharply up to it, then coming abruptly to a stop. ^ Originally published in the A^. Y. Med. Journal, May 10, 1902. ^Mediate auscultation, London, 1846, pp. 555 and 617. * Clin. Med., 1862, p. 598. 56 Mitral Obstruction Obstruction at the left auriclo-ventricular orifice, which for con- venience sake rather than because it is the best term, has been called mitral stenosis, is not a very uncommon lesion. Walshe* puts it fourth in his list which is as follows : 1. Mitral insufficiency. 2. Aortic stenosis (obstruction). 3. Aortic insufficiency. 4. Mitral stenosis (obstruction). 5. Tricuspid insufficiency. 6. Pulmonary insufficiency. 7. Pulmonary stenosis (obstruction). It also occupies the same position in one of my lists (sixty-five valvular cases) verified by autopsies, which is as follows: 1. Aortic insufficiency, 49 times. 2. Aortic stenosis (obstruction). 39 times. 3. Mitral insufficiency, 38 times. 4. Mitral stenosis (obstruction), 33 times. 5. Tricuspid insufficiency, 8 times. 6. Tricuspid stenosis (obstruction), 4 times. 7. Pulmonary insufficiency, 4 times. One hundred and seventy-five valve lesions in 65 autopsies. And in fifty cases taken from my clinic by myself or assistants (not verified, of course, by autopsies), the incidence as to mitral obstruction was the same, being: 1. Mitral insufficiency. 2. Aortic insufficiency. 3. Aortic obstruction (stenosis). 4. Mitral obstruction (stenosis). 5. Tricuspid insufficiency. 6. Pulmonary insufficiency.^ It may be laid down as a fact that mitral obstruction in general implies regurgitation, though the mitral regurgitant murmur is apt to be absent in the later stages of obstruction. In the sixty-five cases alluded to they coexisted in 45 or 70 per cent. In fact, advanced obstruction seems to be almost impossible without regurgitation ; certainly in stenosis, where the orifice or leaflets or their attach- ments are rigid. On the other hand, regurgitation not infrequently occurs with- out obstruction, as for example, in the early stages of organic in- * Diseases of the Heart, London, 1873, p. T05. ° Endocardiopathies, Virginia Med. Semi-monthly, April 26, 1901. Mitral Obstruction 57 sufficiency and in all cases of the relative variety. The relation of obstruction to regurgitation is sometimes close, according to my figures, and yet it is variable. There is clearly a sequential relation between the two, regurgitation being as a rule preliminary to ob- struction, and subsequently its associate. So far from the stand- point of pathological anatomy. Clinically, there is also a close relation between the two, but the in- terest of the physician turns chiefly on the determination of which is the predominating disease. On this point hangs the prognosis, for mitral regurgitation has a comparatively favorable outlook, while mitral obstruction seriously modifies the expectation of life. Well marked mitral obstruction is, however, somewhat rare. In seventy-one instances, complete as to clinical histories and autopsies, taken by myself from French, English and American authors (not including my own cases), advanced obstruction occurred in only thirty-eight, or about 53 per cent. In twenty-nine of my personal cases the severe ones were nine, or only 31 per cent. The larger ratio in the foreign cases is, perhaps, because rheumatic affections are more common abroad, especially in Great Britain, than in this country. So that, on the whole, the severe cases average some- what less than one-half the total. But it is in this class that we encounter the greatest difficulty in diagnosis, because the diastolic murmurs are apt to be faint. How great this difficulty has been may be judged from the records of the Massachusetts General Hospital, where, as late as 1900, in forty-eight cases of mitral obstruction, ;as proved by autopsies, but twenty -three, or 45 per cent., were rec- ognized during life. (Cabot, Phys. Diag., New York, 1900, p. 163.) Another reason for failure in diagnosis (other than the one ^iven) is, as was intimated at the outset, that the data on which to iDase rules for diagnosis have been defective. An instance is well shown by Fagge,*' who tells us that previous to 1871 there were but twenty-eight cases on record where presystolic murmurs had been found, on post-mortem examination, to have been associated with mitral obstruction. And yet this sub-variety of the diastolic murmur had been known for upwards of thirty years, in fact since 1843. Speaking broadly, there is a wide difference between the gen- •eral effect on the heart and system at large, between chronic ob- struction and chronic insufficiency. In the former systolic contrac- Guy's Hospital Reports, 31, Ser. 3, 16, 1871. 58 Mitral Obstruction tion of the left ventricle fails to force a requisite quantity of blood into tlie aorta, because part of it escapes through the leak in the mi- tral valve. To overcome this dilTiculty the left ventricle hyper- trophies and. remains hypertrophied as long as the leak is consider- able ; but as chronic insufflcienc}' passes over into chronic stenosis, so the hypertrophied left ventricle synchronously finds its task more easy until at length, if the patient survive, the orifice is so reduced as to represent nothing but a chink or cleft, and the leak is no longer considerable. But now the blood is very greatly delayed in its pas- sage from the left auricle, and an undue quantity is detained there. Dilatation and hypertrophy of the left auricle naturally ensue, for greater force must be used by the auricle to expel the blood during each diastolic interval. Assuming, then, that chronic insufficiency of the mitral precedes chronic obstruction, this change in the walls of the left auricle is the second of the series. The third is the arrest in the hypertro- phy of the left ventricle, or even an atrophy, due to the fact that the insufficiency has been succeeded by stenosis (obstruction). The accumulation of blood in the left auricle, and the consequent backing of the venous blood into the lungs, produce in turn hyper- trophy of the right ventricle, because more work is thrown on it. If, however, this ventricle finds itself incompetent for the task and dilates, the tricuspid valves will also stretch and hypertrophy, and dilatation of the right auricle will follow. The vicious circle is then complete. At and beyond a certain grade of obstruction, therefore, the in- sufficiency is relieved. Unfortunately a substitution of the one for the other does not improve the expectation of life. But it em- phasizes the importance of combatting the systemic disease at an early period by treatment directed to preventing continued infiltra- tion of the valves and their attachments, because there appears to- be no controlling influence in nature to counteract it. In this con- nection I believe I may say that the profession is hardly willing to seriously consider Balfour's suggestion of opening the heart and cutting the constriction. Even supposing this procedure were prac- ticable, it could not arrest the constitutional process which produced the stenosis. The following cases, taken from my records, illustrate some of the points I have made. Case VII. Aortic and Mitral Disease. — , aged thirty- one. Admitted to hospital October 23, 1885. The patient com- Mitral Obstruction 59 plained simply of dyspnoea and rheumatic pains. On examination the heart's action was found to be rapid and irregular. There was a systolic murmur at the apex conveyed to the left. Death took place after fourteen hours' stay in the hospital. At the autopsy the heart was found to weigh 18 oz. The mitral was dilated and the tendinous chords and margins of the valves were covered with vegetations. Mitral orifice dilated so as to admit three fingers Ttwo ^ngers being the ordinary size of the opening). Aortic valves thickened and the seat of vegetations, but sufficient. Pericardial sac contained 4 oz. of serum. Left ventricle hypertrophied and dilated. Right ventricle not hypertrophied. Lungs oedematous. Kidneys Di the large, white variety. Infarctions of spleen. Now, such a case as this I hold to be in a stage preliminary to obstruction (stenosis), though as a matter of fact the orifice was really dilated. But given a mass of vegetations about any valve, let them continue to develop, and the patient will surely have steno- sis if the disease continues and he lives long enough. In this case the aortic disease appears to have been insignificant as compared with the mitral, the aortic valves being classed as sufficient ; so that the hypertrophy of the left ventricle may be fairly charged to the mitral insufficiency. On the other hand, the following case. No. VIII, may be re- garded as one of tolerably advanced obstruction in which the re- gurgitant element was supplanted by the obstructive. We ob- serve that the heart in this case was small as compared to No. VII. There was no hypertrophy of the left ventricle, but the dilatation pf both the right auricle and right ventricle indicated that the anatomical changes had shifted over from the left to the right side, as was to be expected in this particular case of valvular lesion. Case VIII. Mitral Obstruction (Stenosis) and Regurgitation. — - , aged thirty-eight, teacher, was admitted to hospital Nov. 19, 1 89 1. About a month before admission she was taken with dyspnoea, weakness, dyspepsia and epigastric pain. On a first ex- amination, a bruit preceding the first sound was heard at the apex. and it was propagated to the middle of the axilla, so it was thoughts At any rate, a correct diagnosis of mitral regurgitation and steno- sis was finally made. About a week after admission she was taken with spitting of blood and rales, and cogwheel respiration was heard at the base of the right lung. On November 29th the patient's mind became affected. Pulse moderately strong, but irregular. 6o Mitral Obstruction Delirium ensued and then death. At tiie post-mortem examination 20 oz. of fluid were found in the peritoneal cavity. There were hemorrhagic infarctions in both lungs. Weight of heart 8 oz. Right ventricle dilated. Tendinous chords contracted. Mitral did not admit a single finger. No liypertrophy of left ventricle. Aor- tic normal. Pulmonary valve a little tliickened and dilated. Right auricle dilated. Nutmeg liver. This case is a good example of the changes that may be found in the heart and system at large, in the middle period of mitral obstruction, after compensation has been established. It is astonishing how small the orifice may become. I have occasionally seen it so reduced that it would not admit the little finger. During the first period where there is hypertrophy of the left ventricle, the apex is carried out to or perhaps beyond, the nipple, but as this ventricle contracts the apex recedes within the nipple line, usually remaining within it during the course of the disease, unless there is some complication, such as the common one, aortic Iarch 31st she was discharged improved, but was readmitted on May 22d with a return of symptoms. She died two days later, of erysipelas. At the post-mortem examination the right ventricle and auricle were found dilated and thin. Stenosis (obstruction) of mi- tral with extensive calcareous deposits. Aortic thickened, but not rough. Pulmonary and tricuspid normal. Weight of heart, 19 oz. l^ungs oedematous. Kidneys granular and pigmented. . The absence of murmurs when examination was made is com- prehensible, w^hen we consider her weak condition, and that she was in the final stages of mitral obstruction. To distinguish between the mitral obstructive and the aortic re- gurgitant, feel the carotid pulse and not the radial, which is later Mitral Obstruction 63 than the carotid ; then carry your stethoscope by successive steps from the base to the apex, and you are certain to determine which is the first and which the second sound. It is important also to note if there is a pecuhar quahty, pitch or duration or intensity in either murmur. If there is it will help to distinguish the one from the other. W. S. Thayer (American Journal of the Medical Sciences, No- vember 19, 1901, p. 538), however, from a study of 74 cases of aortic insufficiency, where the lesion was determined by post-mortem examinations, has concluded that "in uncomplicated cases of aortic insufficiency a rumbling, echoing, presystolic or mid-diastolic mur- mur, limited to the region of the apex," occurs in fully half these cases (Medical Record, January 18, 1902), from which it would appear that the value of the presystolic or diastolic murmur as a sign of mitral obstruction is not so great as has been held. There are other signs of aortic disease, such as the "long heart," Corrigan pulse, and dilated aorta, that assist in the diagnosis of aortic insufficiency, while the aortic direct murmur is carried up- ward into the vessels of the neck. From my two series of cases I gather that a purring thrill exists in from 10 to 35 per cent. Samways, in 196 cases, found the thrill in less than 33 per cent. It is usually noted in the fourth left space, sometimes in the fifth or sixth, again in the fifth, sixth and seventh. The thrill in this situation probably always denotes stenosis of the mitral or implication of some other valve, usually the aortic. So far as the mitral is concerned, it means that the opening is small. The thrill continues through the period of effectual compensation ; indeed, a strong thrill means good compensation, and loss of thrill heartweakness. The accentuation of the second sound over the pulmonary is a very important sign. It indicates that the left auri- cle is over-filled, the extreme back pressure from the blood in the auricle against the pulmonary valve causing the accentuation of the second pulmonary sound. Epigastric pulsation is a late symp- tom. It is usually associated with a large, tender and pulsating liver, and is an unfavorable sign, indicating that compensation is failing and the right side of the heart becoming involved, so that dropsical efifusions are not ofif. Embolism is a special feature of mitral obstruction, as Cases X and XI show. Case X. Mitral Obstruction; Embolic Pneumonia. — , aged twenty-eight, widow, was admitted to hospital Dec. 20, 1877. She had suffered from cough for five years, and seven years from 6/ Mitral Obstruction heart trouble. Eight }ears previously had an attack of inflamma- tory rheumatism. The patient was found on admission to be anaemic and much emaciated. Breathing short and rapid, cough with frothy expectorations, pulse 120, temperature 101.2° F. On exam- ination, she was found to be in the third stage of phthisis. Heart's action weak, but not out of proportion to her general debility. No organic lesion discovered. Patient developed uraemia suddenly and died Dec. 22d. At the autopsy the heart was found to weigh 14 oz. and was stated to be normal, except as to the mitral, which had a button-hole opening three-quarters of an inch long, in its longest diameter. The lungs were the seat of embolic pneumonia. Liver atrophic and nutmeg. Cause of death, embolic pneumonia. But cerebral embolism may also cause death, as in the following case: Case XL Mitral Obstruction; Cerebral Embolism. — , aged fifty, clerk, was admitted to hospital Dec. 12, 1883. He had suffered from many attacks of inflamma- tory rheumatism. In 1882 there appeared symptoms of slight cere- bral embolism as shown by aphonia, which lasted two days. On en- tering the hospital he was found to have dyspnoea and abdominal pain with consolidation at the apex of the right lung. There were also murmurs at the apex of the heart with the first sound, and at the base with the second sound. Albumin and granular casts. Pulse strong and regular, later becoming weak and irregular, dur- ing an intercurrent attack of rheumatism with uraemia and pulmon- ary oedema. At post-mortem examination the heart was found to weigh 27^ oz. Hypertrophy of both ventricles. The mitral had a button-hole opening and was insufficient. Oedema and brown induration of the lungs. Chronic diffuse nephritis. Enlarged and pigmented liver. Death was attributed to cerebral em- bolism. In 18 per cent, of my first series of 100 cases the rhythm was irregular. In 20 per cent, of my second series it was also irregular. In one there was a double rhythm ; in one a quadruple rhythm. In several there was a gallop rhythm. The cardiac impulse may be ill defined or diffuse, heaving or strong, and the impulse may be carried to the epigastrium. In well established compensation the heaving is due to hypertrophy of the right ventricle. A noteworthy sign of mitral obstruction to which little attention has been given is the pretty constant relation of a strong cardiac impulse to a weak radial pulse. Mitral Obstruction 65 There has been some effort to divide mitral obstruction into three stages based on auscultatory signs (Broadbent, 3rd edition, T900), though as these signs are not closely associated wtih the stages it is a difficult task. It is more in accord with present meth- ods to divide this affection into stages on an anatomical basis. This is not altogether satisfactory, but 1 have endeavored, somewhat roughly, in the cases used for illustration, to indicate that there may be a preobstructive stage, and early, middle and late stages. In fact, I have already described the anatomical changes which take place in the evolution of a case of uncomplicated mitral ob- struction. According to this view we have at first simply the signs of mitral insufficiency. Then when those of insufficiency give way to those of obstruction the right ventricle becomes hypertro- phied and the impulse is "thumping" or strong. In a certain pro- portion of cases there is a thrill and a diastolic murmur, perhaps a presystolic ; and a sharp, "tapping" first sound at the apex. In the last stage, when compensation fails, the presystolic murmur disap- pears, because the auricle has no longer strength to drive its col- umn of blood into the left ventricle. The right auricle becoming di- lated through the giving way of the tricuspid, causes pulsation in the veins of the neck. Dyspncea, dropsy, and pulmonary cedema then supervene. This last stage is well shown in the following case: Case XII. Mitral Obstruction; Pulmonary Oedema, etc. — , aged thirty-seven, plasterer, was admitted to the hospital May 20, 1879. Three weeks before admission his feet began to swell. General anasarca followed, with debility, scanty urine, and pulmonary oedema. The heart was hypertrophied, but no signs were noted expect those of mitral insufficiency. No second sound was audible. Pulse 40. Under appropriate treatment he im- proved and was discharged. Bvit in less than a month he was re- admitted with a recurrence of the symptoms, culminating m sup- pression, of which he died. At the post-mortem examination there was found general anasarca, with 12 oz. of fluid in the pericardial sac. Heart hypertrophied, weighing 22 oz. Aortic and pulmonary ^/alves free. Mitral a mass of atheroma, with a small button-hole opening, causing both obstruction and insufficiency. Lungs oede- matous. Kidneys enlarged and congested. Liver atrophic, but pigmented. In mitral obstruction there is great danger of embolism, not so much from the diseased valves as from clots that become entangled in ()lo Mitral Obstruction the interstices between the tendinous chords and papillary muscles during imperfect cardiac action. The following- points appear from my tables : 1. Mitral obstruction is usually fatal before the age of forty is reached. 2. Females are little more prone to it than males. 3. There is apt to be a marked contrast between a strong car- iliac impulse and a feeble radial pulse. 4. The true presystolic murmur occurs in 15 per cent. It •comes and goes ; but it is usually inaudible in the last stage. 5. It is apt to have a loud, rasping or sawing quality, but may he "gushing" or "whirring." It may also be faint. 6. In about 40 per cent, there is some sort of a diastolic murmur. 7. These murmurs are best heard over a rather limited area, somewhat oval in form, having for its centre a point about over the middle of the 5th left intercostal cartilage, and about midway be- tween the nipple and the ensiform appendix. The breadth of this area may be two to three inches and its vertical length five to seven. The murmur is sometimes heard best as low as the fifth, sixth or €ven seventh left space ; more rarely it is heard as high as the second left rib. 8. In 10 to 35 per cent, there is a thrill over this area. 9. The first sound at the apex is short and abrupt. 10. The second pulmonary sound at the base is usually intensified. 11. Occasionally a murmur with the second sound at the base is heard over the left auricular appendix. 12. At first there is dilatation and hypertrophy of the left ven- tricle. Then atrophy of it, with dilatation and hypertrophy of the left auricle ; then follow dilatation and hypertrophy of the right heart. 13. ]\Iitral insufficiency must to some extent precede or accom- pany mitral obstruction. 14. In distinguishing the presystolic murmur of mitral obstruc- tion from the Flint murmur of aortic insufficiency we should rely on the "long heart" and the strong impulse, or the "Corrigan" of insufficiency, rather than auscultatory signs. In case there is both aortic insufficiency and mitral obstruction a differential diagnosis is impossible, with the means we now have at our command, unless we can recognize some distinguishing qualities in the murmuri: at the two openings. Chapter VI . DISEASES OF THE AORTIC VALVE. Of all cardiac valves the mitral and aortic suffer most in endocarditis, but there has been a divergence in opinion as to which of these is most often affected. According to Sperling's tables, however, in 200 affections of single valves, the aortic was involved in over 40 instances, or 20 per cent. ; while the mitral was affected m 157, or 78.5 per cent. On the other hand, in 100 of his combined cases the incidence on the aortic was 88, or 88 per cent. ; on the mitral 98, or 98 per cent. So far as my own statistics, in combined cases, are concerned, they tally pretty well with Sperling's. In 44 combined cases the incidence on the aortic was 39, or 86.8 per cent. ; on the mitral 40, or 90 per cent. From these statements it appears, therefore, that mitral disease preponderates in frequency over aortic disease, both in single and combined cases. But as aortic disease is apt to be a rather late phenomenon in general endocarditis, which attacks the mitral first, as a rule, we look for implication of the aortic in advanced mitral disease. In my 44 cases this conjunction occurred in 37, or 84 per cent. If the tricuspid is involved, it is apt to be still later in the endocardial cycle. Aortic disease gives rise to both insufficiency and obstruction, the latter often erroneously regarded as synonymous with stenosis. For obstruction may exist without stenosis, as shown in Case XVII. Insufficiency is the more common. Insufficiency of the aortic was first noted, it is said, by Mor- gagni, but a satisfactory explanation of it was not given until 1830, when Corrigan, of Dublin, gave his masterly description of it. It is more frequent in males than in females. There are two forms of insufficiency, (i) organic and (2) inorganic or relative, each capable of giving the characteristic signs of the disease. Of the organic variety one of the prominent causes that has been given is congenital malformation, but judging from my ex- perience this condition must be extremely rare. In the congenital cases that I have seen, closure of the valves was usually perfect, not- withstanding their defective construction. Furthermore, the claim made that congenital malformation is an etiological factor is apt to 68 Diseases of the Aortic Valve he associated with the statement lliat the Icatlets had undergone inflammatory changes. But these changes ma\ have occurred in- dependently of the anomalies. In fact, there is no reason why mal- formed segnients should incite cither inflammatory or degenerative changes. In this connection it nia\ be said that the small fenestra- tions so commonly seen in the leaflets do not produce insufiiciency, though large ones, the result of rupture, may do so. A more common cause is endocarditis, which may be of the benign or malignant variety. The latter, due to acute infective processes such as gonorrhoea, etc., is usually fatal, but the former, which is more common and usually the result of rheumatism or the continued fevers, is a slow, subacute process, originating with vege- tations on the valves, which either grow into tuberous masses that v/ill eventually snap off, or undergo fatt}- degeneration, or harden down into calcareous nodules causing obstruction. Again, adhesions may take place between the cusps, or between the cusps and the adjacent walls. In one of my cases a calcareous body was found attached to the edge of a leaflet, and it must have been carried back- ward and forw^ard in the blood current. In another a tumor the size of a chestnut lay beneath one of the leaflets, preventing its closure, A cause often assigned is arteriosclerosis, and it is the most serious. Occurring in early middle or advanced life, it is a general systemic disturbance implicating other important organs, and in- deed the whole arterial system. At first it is merely a slow scle- rotic change, but with advancing age and under certain conditions it assumes a degenerative character, from which there is little hope of amelioration, but only a prospect of progressive destruction. The first of the causes of arterio-sclerosis is to be found in the strain or tension of severe exercise. This condition is met with not only in the toiler (laboring man), but also in the athletes training for feats of strength or endurance. Alcohol is another of the causes. A third is syphilis, which produces at first hyaline changes in the vascular tunics and then thickening of the walls. Another cause is lithaemia, which produces changes in the vessels somewhat simi- lar to those resulting from syphilis. Rupture of a valve is another. This is a rarity, but I have seen it at post-mortems. It may occur in health as the result of a fall or severe concussion ; but a slight accident, such as a hurried walk, may produce it, when the valve is infiltrated and brittle. Relative insiifUciency is of comparatively infrequent occurrence. Diseases of the Aortic Valve 69 It may occur in any form of hy])crtrophy of the left ventricle, but is unusual, unless associated either with a sacculated aneurism of the arch, or the fusiform dilatation sometimes found in its ascend- ing portion (Hodgson's disease). This form of insufficiency, there- fore, is of late occurrence in life, while organic insufficiency may occur at any time. In the endocardial forms occur the usual indications of that flisease, which do not differ materially from the endocardial lesions of other valves ; though the intense rigidity that is seen in the mitral and the infiltration of the adjacent parts is not so common. But a very small amount of valvular infiltration may produce in- sufficiency, by shortening the cusps. In fact, there may be great relaxation of the ling at the base of the valves. This is seen in the relative insufficiency that is apt to attend the dilatation of the aorta from either the fusiform or sacculated aneurism. In arterio-sclerosis, which is in most cases associated with endo- carditis, there may be deposits at the base of the valves without in- sufficiency; or a spiculum or plate projecting out may cause insuf- ficiency, so that a considerable amount of arterio-sclerosis may exist without insufficiency. As in endocarditis, it is the location and configuration of the deposit rather than its size which determines the insufficiency. There are great differences in its degree. In moderate cases there may be only a triangular defect ; in advanced instances it may take the form of a slit or cleft. Occasionally the opening may be widely dilated ; but there may be an enlargement of the leaflets to compensate for the widened opening. In aortic insufficiency the changes in the heart, in the progressive evolution of insufficiency, are as follows in an uncomplicated case : Owing to the leak in the aortic valve some of the blood in the aorta regurgitates during diastole into the left ventricle, and meeting there the normal quantum of blood coming at the same time from the left auricle, causes dilatation of the ventricle. The latter, in order to expel this increased amount of blood, hypertrophies. Now if the insufficiency is progressive, or if stenosis is combined with insufficiency, there will be a progressive increase of blood in the left ventricle. But the increased collection of blood in the left ventricle will embarrass the left auricle, and through it the current of blood flowing into it from the lungs will be delayed, so that the right ventricle will also dilate and hypertrophy. But even if the right ventricle should enlarge when a sudden call is made on the heart, it may diminish in size w^hen the strain has been taken yo Diseases of the Aortic Valve off. Hence the enlargement of the left rather than the right heart is a measure of the success of compensation. This aortic lesion makes the big and Icvig heart where dilatation and hypertro- phy are very prominent. In one of my cases with obstruction and marked insufficiency the heart weighed 29 ounces. The early development of aortic insufficiency is so insidious that it is apt to be overlooked. Indeed, at first no physical signs may be present, and the attention of the patient is first called to it b\- subjunctive symptoms, such as precordial oppression, palpitation, fulness, roaring in the head, sparks before the eyes (denoting an irregular supply of blood to the head), or anginoid attacks. Occa- sionally these symptoms are only evoked by a strain or excitement of some kind, or when the hypertrophy does not keep pace with the growing insufficiency. If arterio-sclerosis is at fault, there may be the fades arterio- sclcrolica. In endocardial cases, however, the face is often pale, In arterio-sclerosis there will also be general systemic changes, and it is in these cases particularly that there is apt to be pain. On inspection in well established cases there is a broad area of cardiac pulsation. In children and young people there may be a bulging of the praecordium, and occasionally systolic contraction of the soft parts owing to the flexibility of the walls of the chest and the pressure of the enlarged heart, which often displaces the lungs. The apex may be found in the 7th or 8th space instead of the 5th, and may extend to the line of the nipple, or in very rare cases to the axilla. In well developed cases the impulse will be strong and heaving. Sometimes there is a thrill when obstruction is pres- ent ; it may be systolic or diastolic. Percussion will demonstrate that this is the large and long heart, and as dilatation and hypertrophy are largely confined to the left ventricle, the heart will assume a more vertical position than usual. But during the temporary dilatation and hypertrophy of tbe right ventricle, that may occur before compensation is established, after excitement or strain, or in failing compensation, the dulness may extend an inch or more beyond the right margin of the sternum. On auscultation a prolonged murmur is heard in diastole over the aortic area, w-hich corresponds to the second right or left inter- space and intermediate space, and the bruit is propagated down towards the ensiform cartilage, but it is usually heard with greatest intensity in the middle sternal region, extending sometimes to the Diseases of the Aortic Valve 71 right, but ordinarily to the left, of the sternum. Occasionally it is continued to the apex and even beyond it, the "Flint murmur." Indeed, it may closely simulate the murmur of mitral obstruction and be produced by the blood impinging on a leaflet of the stiffened mitral, for in more than half the cases aortic insufficiency is com- bined with mitral disease. In dilatation of the ascending arch of the aorta (or Hodgson's disease), which is common in advanced ar- terio-sclerosis, the murnmr may be carried far to the right, but the dilated arch will not necessarily be dull on percussion. The mur- mur may occur at any part of the diastole, and may entirely super- sede the second sound. The bruit is often described as "gushing," "swishing" or "whir- ling," but it may be so faint as to be overlooked. It may also be rough, or even musical. The intensity of the bruit depends on the size of the opening, and the force of the contraction of the ventri- cle. When extreme stenosis exists or in extreme dilatation there may be no murmurs. Other lesions of the valves may also mask them. The piilse is large and quick because the arteries are dilated by the powerful cardiac impulse, which has to be short in point of time to drive the requisite quantity of blood, during the interval allowed it. But this quick discharge of blood at the aortic is fol- lowed by a sudden leak or backward regurgitation into the ventri- cle. Hence the characteristic pulse first described by Corrigan in 1830 and known as the "cannon hall," "pistol shot," "trip havuner," "water hammer," or "Corrigan." It was for a time thought that the sphygmograph alone could furnish a ready diagnosis of this condition, but it is now known not to be pathognomonic, for a similar pulse has been occasionally found in aneurism and anaemia. Another sign is the capillary pulse. Rub the patient's fore- head with a towel until it is red and then note how the systolic action of the heart increases the ordinary redness, especialh- at the border of the reddened area. This capillary pulse, however, due to the left ventricle's forcing a column of blood directly into the capillaries, is seen in all hypertrophied hearts. Nor is the venous pulse of Quincke pathognomonic. It merely indicates that the blood is forced through the capillaries into the veins. In aortic insufficiency there is apt to be visible pulsation of the arteries. There is also pulsation of the jugulars when compensa- tion is incomplete. Pressure with the stethoscope on the femoral will sometimes 72 Diseases of the Aortic Valve produce a short systolic sound ("f^istol-shot"). Such pressure in health will produce a systolic murmur, but if a diastolic is also pro- ducetl {Diirocicz's sign) it is a pretty sure sign of aortic regurgita- tion. Still it is not often met with. Attacks of angina are more frequent in aortic insufficiency than in any other valvular lesion. The other symptoms often noted are headache, dizziness, palpitation, thrill, and pain transmitted up the neck and down the arm. S ltd dot death is more frequent in this lesion than in any other form of valve disease ; and it is here that neurotic disturbances are so prominent. In fact, such dis- turbances should be expected, though they may be merely of the hysterical variety. As in all other forms of valvular and non-valvu- lar disease, there are three stages. During the first stage, in organic cases, as the dilatation and hy- pertrophy of the heart keep pace with the advance of the insuf- .Hciency. there may be no subjective symptoms, unless the patient imdergoes emotional excitement, or strains his heart in some way. Then the hypertrophied heart finds itself unable to cope with the increased load, and the lungs fill up with blood, causing dyspnoea and palpitation ; and such attacks are always liable to occur. In tlie second stage compensation will have been established, and. barring such incidents as have just been described, there will be no subjective signs. This stage may last many years, fifteen or twenty, perhaps more. When compensation is about to fail, its approach will be her- alded by shortness of breath and dyspnoea, especially at night, cough and acceleration of the pulse. The pulse will be rapid, no to I20. or more. A new sign is at hand as soon as the systemic cir- culation is involved: we now note pulsation in the epigastrium, due to dilatation of the vessels in the liver. Aortic insufficiency is recognized with comparative ease. In my 37 cases it was noted in 23, or 62 per cent. In 65 proved by post- mortems at the Massachusetts General Hospital, only 44 \vere rec- ognized, or 67 per cent. The diagnosis is based on five principal points. We have the large and long heart, because in it dilatation and hypertrophy are prominent, but the dilatation and hypertrophy are mainly confined to the left ventricle. The position of the heart is apt to be somewhat vertical. In consequence of the enlargement of the left ventricle this displaces or compresses the lungs, so that it comes nearer to the Diseases of the Aortic Valve 73 sternum than usual, and its pulsation is better communicated. For the same reason the beat is more diffuse anrl heaving. The murmur is usually soft, but not neces.sarily so ; it may be rouo;h or musical, while it is conveyed downwarrl, and is apt to be heard best in the mid-sternal reg-ion along the left sternal border ; occasionally at the ensiform cartilage or at the apex. One should not pin too much faith on the murmur, however, for it may be absent. The pulse is usually characteristic. It is full and quick, and is apt to be of the trip-hammer variety. A thrill is comparatively rare, but it may occur if through the distortion of a valve or some impediment, the current of blood is twisted. In general, a previous history of alcoholism, lead-poisoning or syphilis should lead to a suspicion of aortic disease, especially in middle life. If mitral disease has been previously well established, we should, in 70 per cent, of the cases, expect aortic disease. One of the greatest difficulties is the differential diagnosis be- tween aortic valvular disease and aortic aneurism. The following diagnostic points must be taken into consideration : Aortic insufficiency. Bruit Aneurism. Bruit and thrill and thrill in area to right of aflfect both arch and ventricle, sternum, increasing as we ap- and area to right of sternum, di- proach the aorta from above. minishing as we approach the No dulness necessarily over aortic valve from above, dilated aorta. Dulness widespread if aneu- May also be inequality of rismal sac contains fibrin. Ine- radial pulse, but "trip-hammer" quality of radial pulses, but variety the rule. never the "trip-hammer." Syph- In arterio-sclerosis may be a ilitic history usually. The X- history of syphilis. May be ray throws a shadow correspond- caused also by rheumatism, gout, ing to the sac. lead poisoning and infections. The X-ray throws no shadow. In general, the amount of the lesion is proportioned to the hyper- troph}- of the heart, except when obesity or Bright's disease co- exist. The prognosis depends on many considerations. If the insufificiency is of traumatic origin, such for example as is caused by a sudden strain, the prognosis may be good, but such accidents are extremely rare. Occurring: in the voung. before the usual degenera- 74 Diseases of the Aortic Valve tive changes liavc taken place, it lias a better outlook. It is also comparatively favorable, because compensation is established by the left ventricle, which alone is competent to rectify the bad effects of this lesion. But though compensation may last fifteen to twenty years or more, long life is seldom attained. In the man- ageinent of a case we should remember that compensation depends on the ability of the left ventricle to do its work. Hence its dilata- tion and hypertrophy are to be maintained. Whenever it shows signs of irregular action or feebleness, it should be quieted and sus- tained. Rest in the recumbent position is at first the sine qua non in an acute attack, while cold compresses may be applied to the chest, and the extremities massaged, so as to draw off as much blood as possible from the heart. T am in the habit of using in these cases the bromides, or the mono-bromate of camphor ; sometimes acet- analid in 2 to 5 grain doses ; also Hoffman's ether and the comp. tincture of valerian in drachm doses. When the acute stage is over 1 use carbonated baths and exercises. The following cases taken from my hospital records illustrate some of the ordinary varieties of aortic insufficiency : Case XIII. Malignant Endocarditis; Aortic Insufficiency and Obstruction. — , fifty-six, single, was admitted to hospital May 2ist, 1881. Patient had been a well man, according to his statements, up to four weeks before admission. At that time he was attacked with pain in all his joints, which were swollen and disabled. For the previous three weeks he had suffered from headache, epi- gastric distress, and nausea, without vomiting ; and during this time had irregular chills and sweats. In the week preceding admission he had increased dyspnoea, but without cough. Physical examination showed that the apex was in the fifth space, one-half an inch to the left of the nipj)le. A double mitral murmur was lieard. Pulse very irregular. Fine, moist rales at the bases of both lungs. Later a presystolic murmur was heard twice at the apex, but no double murmur. Later a double murmur was heard at the base. Orthopnoea. On May 31st signs of hypostatic congestion were recognized, and a diagnosis of probable ulcerative ''malignant) endocarditis was made. The patient died suddenly the same day. At the autopsy, which, unfortunately, was not very complete, it was found that the pericardium contained half an ounce of bloody serum, while the right auricle was attached posteriorly. There was a large vegetation at the aortic valve and an ulcer extended Diseases of the Aortic Valve 75 beneath the valves, from the aortic to the mitral. The spleen was irregularly spotted and puckered from old infarctions, but no recent ones were found. Here, then, was an instance of aortic insufficiency in an old be- nign endocarditis which had taken on a malignant character. Case XIV. Organic Aortic Insufficiency, with Relative Mitral In- sufficiency. , twenty-seven, was admitted to hospital April 2, 1887, with the history of an attack of acute rheumatism ten years earlier, and a recent recurrence one week before admission. On phys- ical examination a low-tension pulse alternating between the normal and 120 to 130 was noted. Apex in the fifth space. Heart enlarged. At the apex there was a soft systolic murmur quite diffused and an aortic direct and indirect murmur. Dyspnoea, palpitation and nausea followed one another in the course of his three visits to the hospital. During the last of these he developed pleuris}' with effu- sion, and thirty-two ounces of fluid were withdrawn. The apex had been found at one time in the seventh space. Heart enlarged. There was much praecordial pain with anginoid at- tacks. The patient died Nov. 3rd, 1887, with acute dilatation. At the autopsy there was found m.arked aortic insufficiency, but it was not thought that there was enough infiltration in or about the valves to indicate obstruction. There was marked mitral insuf- ficiency without organic changes (relative variety). Heart weighed twenty-one ounces. Cardiac tissues degenerated. Case XV. Aortic insufficiency, zvith Dilatation of the Orifice and Fusiform Aneurism of the Ascending Arch (Hodgson's dis- ease). — , sixty-four, was admitted to hospital July 8th, 1882. Patient admits having been a moderate drinker, and having had gonorrhoea and rheumatism. On admission he was found to have cedema of the upper and lower extremities. Double aortic murmur at base. Apex in fifth space, one-half an inch outside the nipple. Rapid and irregular pulse. Patient soon developed suppression with albuminuria, with noisy delirium and dyspnoea. He died in coma on October 28th. At the autopsy the following was found: Heart not markedly enlarged, but an adherent pericardium. CaVities dilated ; all valves sound except the aortic. The aortic segments were thickened and shortened, and the orifice was markedly dilated. The ascending aorta was also dilated and had atheromatous plaques, ulcerations and calcareous deposits. It constituted a fusiform aneurism {Hodg- son's disease). Kidneys granular, contracted and cystic. Liver 76 Diseases of the Aortic Valve slightly cirrhotic ; chronic meningitis. Death attributed to chronic diffuse nephritis. Casf Xl'I. Relative Aortic and Mitral Insufficiency Due to Car- diac Hypertrophy of Renal Orii^i)i. — , thirty-eight, was ad- mitted to hospital Aug. 22nd. 1887. He had suffered from acute articular rheumatism, and for the past three years from palpitation and dyspnrea, but swelling of the feet and abdomen had occurred, for tlie first time, about a week previously. On admission he com- plained of sparks before the eyes, cough and bloody sputum ; was pale, and had facial oedema. Pulse irregular. The heart w^as found tc be hypertrophied. Apex one inch below line of nipple and one and one-half inches outside it. Double aortic and also a mitral re- gurgitant iTiurmur. Urine sp. gr. 1012. Trace of albumin. The ursmic symptoms from which he had been suffering became aggra- vated, and he died about two weeks after admission. At the autopsy it was found that so far as the aortic and mitral valves were concerned there was no organic change, except a slight roughness in the aortic, and the insufficiency of both valves was attributed to the hypertrophy of the heart from renal implication. The following case shows incidentally how auscultatory signs may be misinterpreted : Case XVII. Aortic Insufficiency mistaken for Mitral InsufH- ciency. — B. — was admitted to hospital December nth, 1880. The pa- tient stated that he felt perfectly well up to three weeks previously, when he was taken with pr?ecordial distress and difficult breathing. Two weeks later he had cough and expectoration, orthopncea, general malaise, nausea and vomiting. On examination it was found that the heart was hypertrophied and that there was pulsation of the veins m the neck. Apex to the left and below nipple. Wavy movement of the epigastrium. Expiration high pitched and prolonged. Con- solidation of left lung posteriorly. Murmur at apex thought to be w'ith first sound. Murmur heard behind and better above than below the scapula. Diagnosis of dry pleurisy and of mitral regurgitation. Patient died with oedema of the lungs December 14th. At the au- topsy both lungs were found to be almost solid at their bases. The heart was enlarged. Pulmonary opening dilated. Dilatation of right heart. Fresh vegetations on border of aortic valve. Both cusps thickened. Obstruction, but no stenosis. Mitral normal. In the absence of mitral disease we see in this case how sometimes the murmur of aortic insufficiency may be conveyed to the apex and beyond, probably in this instance through the agency Diseases of the Aortic Valve TJ of the consolidated left lung, the result being an error in the diag- nosis. Aortic Obstruction. — In the choice between the words obstruc- tion and stenosis I select the former, because it has a wider signifi- cance, embracing all forms of stenosis, wliile the latter does not embrace all forms of obstruction. As in mitral disease, there may be obstruction without narrowing (stenosis). Aortic obstruction is a tolerably common valvular lesion. Walshe put it second in his list, and in 65 of my autopsies, in valvular dis- eases, I found it holding the same position. In a clinical series of 50 cases, however, I put it third. But while there is a general agreement that it is a common valvular lesion, it is not so well un- derstood that uncomplicated aortic obstruction is extremely rare. Several of our most prominent clinicians have seen no cases, and in the pathological records of the Massachusetts General Hospital, em- bracing 252 valvular cases, not a single one was recorded. In my 65 post-mortems I have but one. If there were any lingering doubt as to the rarity of simple obstruction, a search through the literature should dispel it. Certainly painstaking investigations on my part have discovered only a very few published cases of aortic obstruction without insufificiency. It well might happen that a practitioner with a pretty wide experience in heart cases would never meet wath a pure example of uncomplicated aortic obstruction. These cases will be referred to, however, for after all it is only from uncomplicated cases that we can frame rules for diagnosis. Indeed, the inference is positive that heretofore our diagnoses have for the most part been based on phenomena not con- firmed by autopsies, or on cases of aortic disease complicated by insufficiency. But while, practically speaking, obstruction is usu- ally attended by insufficiency, the converse is not true. And this w^as shown in my 65 cases, where in 11, or 17 per cent., there was aortic insufficiency without stenosis (obstruction), but of course relative insufficiencies were included. This point has a practical bearing, for given the signs of aortic ob- struction, and the chances are that in the great majority of instances obstruction is combined with insufficiency. These two forms are well contrasted in the following cases : Case XVIII. Aortic Obstruction and InsuMciency Associated with Aortic Aneurism. Syphilis. — J., thirty-eight, painter, was admitted to hospital January loth, 1883. The patient had contracted syphilis about seven years perviously, secondary manifestations, such 78 Diseases of the Aortic Valve as sore throat and alopecia, occurring four or live years later. He then complained of pain in the sternum. On physical examination direct and indirect aortic murmurs were distinctly heard. The patient died five days later, during a sudden attack of cyanosis with dyspnoea. At the autopsy the pericardial sac was found to contain 12 ounces of serum. The heart was very much hypertrophied, especially the left ventricle. Weight 24 ounces. The aortic valve was much thickened, and its segments were shortened by atheromatous deposits, there being insufficiency and obstruction. All the valves of the right side were normal. The arch of the aorta was the seat of what was regarded as ex- tensive syphilitic endarteritis, with ulcerations and cicatrices. At one point to the right of the aortic valve some of the arterial coats had given way and a sacculated aneurism had formed, about the size of a hen's egg. A small opening led into the sac. In the liver were small gummatous tumors. Case XIX. Aortic Stenosis without Insufficiency. — E., forty- eight, was admitted to hospital April 4th, 1878. The patient, whose only previous disease, so far as he knew, had been pneumonia, or pos- sibly scarlatina, learned that he had heart disease one year previously from a physician who was treating him for a cough and haemoptysis. Shortly afterwards he found that his lower extremities were begin- ning to swell. Two weeks before admission the oedema had reached his scrotum, and the urine had fallen to 15 ounces per day. On examination the apex beat was found to be diffused over a larger area than normal and was two inches below the nipple. On auscultation a systolic murmur was heard at the apex, not conveyed to the left or behind (tricuspid regurgitation). At the base w^as a double murmur supposed to be an aortic direct and indirect. Pulmonary oedema. The patient was put under active treatment, with digitalis and elaterium, and cupped ; but there was little reaction. Symptoms of ursemia supervened and he died twen- ty-four days after admission. At the autopsy his heart was found tobe very large, weighing 31 ounces. All cavities distended. Aortic perfectly sufficient, but leaflets contracted, while the free surface ex- hibited a small row of white, shining, translucent bodies. Left ventri- cle hypertrophied. Right very little hypertrophied. Tricuspid and pulmonary insufficient, a large stream of water passing through the former. Infarcts in both kidneys. Cysts in one. Nutmeg liver. Vessels at base of brain atheromatous. The cause of death in this Diseases of the Aortic Valve 79 case was uraemia, induced in part at least by renal embolism. In this case the only error committed was that pulmonary insufficiency was mistaken for aortic insufficiency. The extreme rarity of the former might be offered as an excuse for the failure to recognize it. Aortic obstruction in the vast majority of instances is caused by arterio-sclerosis, which in turn often means syphilis, and it is merely an extension of the disease of the aorta back into the valves, Or rheumatism may cause endocarditis, which invades the segments of the valves, the disease beginning at the free edges, generally with the development of vegetations or papillary growths and a contempo- raneous infiltration of the segments, and subsequently their contrac- tion or distortion. Again, the leaflets may become fused together by adhesive inflammation, leaving a triangular or funnel-shaped opening. This latter is not so common as in mitral stenosis. In health the opening should admit the little finger, but in stenosis it may become so small that it will only admit a small sound, or even the tip of a slate pencil, as in one reported case. Congenital aortic obstruction, which is a true stenosis, is only one of the numerous cardiac anomalies, the combination of which, as a rule, soon ends the infant's life. Very exceptionally, patients may live with aortic stenosis of the congenital type to advanced life, according to Eshner,^ who has reported one that lived to the age of 90 years. The duration of life, however, is probably measured by the insufficiency that accompanies the stenosis. Among the remoter causes are strain and injury, which almost necessarily lead to inflammation, adhesion and contraction. Other causes of obstruction are lateral pressure on the valves by something extra cardiac, as an enlarged gland. Aortic obstruction being a late event in valvular disease, it is found, as a rule, after middle life ; in exceptional cases it occurs in early life or even in infancy. The obstruction to the escaping blood throws extra work on the left ventricle, which hypertrophies and dilates, as seen in Case XIX, the heart becoming greatly enlarged. It has been claimed (Whit- taker) that it never assumes the magnitude of the heart in aortic insufficiency, but this is disproved by Case XIX, where the heart weighed 31 ounces, and this also disproves the statement of Potain that a scarcely appreciable hypertrophy with but slight displacement of the apex speaks for aortic (stenosis) obstruction, for the case given was one of pure aortic stenosis. The truth is that while the left heart hypertrophies invariably from a moderate degree to an 8o Diseases of the Aortic Valve enormous extent, it does not on the whole average so much as in aortic insufficiency. Basing tiie symptoms of uncomplicated aortic obstruction on tlie recorded cases* I have collected, including one of my own, I find the following symptoms : Thev are mostly in males, usually after middle life, though one of them was 19 years of age. The pulse is slow and weak, some- times irregular. Dyspncea, palpitation and syncopal attacks occur. The impulse is diffused over a wide area and the apex is to the left. Usually the murmur is absent ; always when stenosis is ex- treme. In two cases, systolic murmurs at the apex, or thereabouts, were attributable to tricuspid regurgitation. Among other signs are pulsation of the veins in the neck and in the interclavicular notch, cyanosis and dropsy. There was no thrill in any of the cases. Right ventricle moderately or greatly enlarged ; left less so. Embolism and oedema are other features. It will be noted (from the above summary) that no thrill was found, and this may be regarded as an important negative sign. We have seen that it is a positive sign in insufficiency. The impulse, of course, varies with the stage of the disease. It is diffuse, though not so strong and heaving as in insufficiency combined with steno- sis. The murmur is usually heard best in the second or third right intercostal space, is long-drawn, conveyed up the great vessels of the neck, and gradually diminishes in loudness as it asscends. Its quality depends on the character of the obstruction. If the orifice is smooth or small, there may be no murmur. A systolic murmur at the apex, due. according to Dickinson, to regurgitation from strong pressure through the mitral, w^as attributable according to Case XIX to tricuspid regurgitation. When there is a rough or musical mur- mur, there is roughness in the valve or just above it. It may be so loud that it is heard all over the heart, and cannot well be located. The apex will be low down to the left, and may even reach the sev- enth space, and extend two inches outside the nipple, but this is ex- ceptional. In all cases there will be an enlarged heart with the apex carried downwards and to the left. There must be, in the early and middle stages, certainly until the orifice has diminished to a mere ^ Farwell, Birmingham Med. Gac, 1830. Eshner, Path. Soc. of Phil., XIV.. p. 154. Ashton, Path. Soc. of Phil., XVII.. p. 103. Gibbons, Path. Soc. of Phil.. XVII., p. 134. Murray. Path. Soc. of London, XXL, p. 98. Owen, Path. Soc. of London, XXXIII. , p. 72. Diseases of the Aortic Valve 8l slit, a systolic bruit, heard best in the aortic area and carried up through the great vessels of the neck. When stenosis and insuf- ficiency are combined, as is usual, there will be the signs of insuffic- iency. Engorgement of the lungs due to commencing heart fail- ure will lead to tricuspid regurgitation, and will be evidenced by a. systolic murmur near the apex, increasing as the ear nears the ensi- form cartilage. Obstruction of the pulmonary artery is rare, but it. may lead to confusion, because the signs of aortic obstruction are sometimes best heard over the pulmonary valve. In pulmonary valve disease, however, the sounds are very superficial. Angina, embolism and vertigo are especially common in aortic stenosis. Owing to the diversity of causes, the prognosis is variable. In; congenital cases aortic stenosis is usually only one of the many car- diac anomalies which together soon end the infant's life ; so that the: consideration of this matter from the standpoint of the aortic lesioni is of comparatively little importance. And yet a man with acquired stenosis of an extreme type may live to ninety, as in Eshner's case. Considerable contraction of the orifice ma}' exist for a long time, if hypertrophy develops contemporaneously with the construction ; but unfortunately, as already said, we seldom have pure cases of aortic disease. As it is generally combined with aortic insuf- cicncy, the duration of life must be measured by the insufficiency^ and the rule laid down by Fagge is probably correct that in the see^ saiv of aortic disease the louder the first sound the better the prog-- nosis ; the louder the second sound, the reverse. But a short sec- ond sound is regarded as more unfavorable than a long-drawn sec- ond sound. When there is a loud systolic murmur the probability IS that there is a wide opening and little obstruction. If the patient has syphilis the prognosis, other things being equal, is worse than if he has rheumatism. And yet if he is under good management, and leads a careful life, it is better than in rheumatism. Unfortunately we are too apt to believe that a prolonged course of treatment ex- tending over two or three years, by mercurials and the iodides, will rid the system permanently of the poison. This is a very serious error. ClIAl'TER \'II. PULMOXARV \AL\E AFFECTIONS.^ Of all cartliac vahcs ihc pulnioiiary is least often affected. Very exceptionally it is a single lesion. Sperling {Cibson's Dis. of the Heart, London. 1898). with his large experience, has not recorded ii single case. Fortunatcl} I have brief notes of one. In association with other valvnlar diseases, pulmonary affec- tions occur in the ratio of 1 to al)(>ut 10 per cent. Si)erling puts it at 4 per cent. Insufficiencx is the form commonh- seen in adult life; stenosis in foetal life or infancy. Pulmonary valve diseases occurring in adult life, however, are usually consecutive to endocarditis or other valves, or to arterio- sclerosis, the ratio being, according to m\- tables, six in a total of 177 lesions verified by post-mortems. In my office cases the ratio v.as put at 3 per cent., and in fifty taken from my clinic by myself and assistants, pulmonary insufficiency was at the bottom of the list. Walshe {Dis. of the Heart, London, 1873, p. 105) from his list makes it occupy the sixth place in a total of seven varieties of lesions. But his clinical notes, not to any large extent confirmed by pathological data, are interesting rather than convincing. Five of the cases I now record are taken from my post-mortem records as former pathologist to the St. Luke's and Presbyterian hospitals. the neck on both sides. Diagnosis not made. No c\anosis. At the autopsy the puhuonary orifice was found one- third smaller than normal. Xo other cardiac lesion. It will be noted from this case that obstruction (stenosis) of the pulmonar}- does not necessarily produce cyanosis. Pitt (Albutt's System. \'ol. VII. p. 9) has collected fourteen cases of acquired stenosis. I have collected and verified fifteen, yet have failed to get access to at least one-half of the literature on this subject. The references to my cases I give here: Ebstein, Dcutsches Arch. f. klin. Med. Bd., VII.. s. 281. Peacock, Lancet, 1868, Vol. I. Rindrteisch and Oberneier, Deutsches Arch. f. klin. Med., Bd. V., s. 539. Mayer and Oberneier, Deutsches Arch. f. klin. Med., Bd. XXIV., s. 435. Whitley, Guy's Hosp. Repts., III., 1857, p. 255. Whitley, Guy's Hosp. Repts., III., 1857, p. 255. Paget, Med. Chir-Trans., 1844, p. 182. Crudelli, Riv. Clin. di. Torino., VII., 2 p. 37-68. Schmidt's Jahrb. 8, 1870. Berlin, Heart Diseases, 1821. Constantine Paul, Soc. Med. de Hop. de Paris, T. VIII. Schwalbe, Virchow's Archiv., Bd. 119, S. 2, s. 45, 1890. Schvvalbe, Virchow's Archiv., Bd. 119, S. 2, s. 45, 189a Schwalbe, Virchow's Archiv., Bd. 119, S. 2, s. 45, 1890. Wagner, Archiv. f. Heilk., 1866, s. 518. Colberg, Deutsches Archiv. f. klin. Med., Bd. 5, s. 565. I am inclined to think that the following case was also one of temporary stenosis, caused by extracardiac pressure, relieved by evacuation of an abscess. Otherwise I have none in my post-mortem records. Case XXV. Probable Stenosis of the Pulnioncj-y Artery. — A groom, age twenty-eight years, was admitted to hospital in July, 1883, with an abdominal tumor continuous with the liver and extend- ing into the epigastric and right hyperchondriac regions. Palpable pulsation over the pulmonary area, extending up to and under the clavicle and attended with a soft systolic bruit. No other signs of cardiac disease. In the following month two incisions were made into the tumor and three ounces of pus removed at each opera- tion. The man survived the operation, but died of progressive emaciation and sepsis. At the autopsy the liver was found to be greatly enlarged, weighing eighty-eight ounces. It apparently had Pulmonary Valve Affections ^) •compressed the lung-s, both of which were unusually dry, the left ■especially, and by pressure had caused the same kind of temporary stenosis of the pulmonary artery that is sometimes seen when aneurisms of the aorta by pressure alter the calibre of the vessel from a circular to a crescentic form. In congenital disease the cause must be laid to lack of develop- ment. In the acquired form, infection, according to my tables, plays a most important role, the order of frequency being rheumatism, aneurism, syphilis, gonorrhoea. Doubtless further researches into the etiology of this subject will enlarge the number of causes, affect- ing the ratio here given. Pitt, in his fourteen cases, found rheuma- tism a causal factor in eight, or 57 per cent. Males and females ap- pear to be about equally affected. In symptomatology there is a wide difference between the congenital and the acquired forms. In the former there is usually general cyanosis, though not always, as in the instance I have here given. There is ordinarily a lack of physical and mental developm.ent. The patient complains of headache and is somnolent, or has hebetude ; is undersized, and has a bulging chest and a protruding abdomen. There is defective development of the genitals, with clubbed fingers and toes. The eyes may be prominent. The physical signs are not very distinctive. The right ventricle is enlarged in complicated cases ; both are en- larged when the left ventricle is called on for extra work. The murmur is systolic and usually, if there are vegetations, loud, it may be heard all over the praecordial area, but its intensity is apt to be greatest over the pulmonary area, i. e., the second left inter- costal space, close to the sternum. In addition it is continued up towards and sometimes under the clavicle. Exceptionally it may be best heard lower down. In one case* (Hun's) it was best heard at the fifth left sterno-costal junction. In acquired obstruction we should look for an antecedent infec- tion, and especially for venereal disease or rheumatism. As distinguished from the congenital form, there is less often cyano- sis in the acquired ; and there are none of the characteristics of arrested mental and physical development. But if there is cyano- sis it is increased by coughing, and dyspncea is present. The mur- mur is more definitely located than in the congenital form, because the force of the stream, is undiminished by defects in the walls of the heart. It should be loud and rasping in the endocarditis forms. If the patient hold his breath it should be somewhat fainter. The * Albany Med. Annals, pp. 57-66, 1897. 90 Pulmonary Valve Affections apex beat is apt to be forcible and tlittuse. and there may be a thrill. Tlie second pulmonary sound should be faint, but there may be insufficiency and a double nuu-iuur. The imirniur is apt to be propagated from the base of the heart up toward the left shoul- der, as far as the clavicle. The jioint of g^reatest intensity is usu- ally in the secontl left interspace. l'suall\- there is an attend- ant pulmonary or bronchial disease, of a purulent character. When, as in the case 1 have given, the pulmonar}- stenosis is single, hyi)ertn)])hy sliould be conhned to the right heart. If for an\- reason the left heart has been called on for extra work it will naturally hypertrophy. There is nothing characteristic about the pulse. Some oedema, even anasarca and albuminuria, may be ex- pected toward the end. The diagnosis is never easy. Even in the congenital forms pul- monary stenosis is, as a rule, as I have said, only one of many anomalies ; two at least of them, viz. : the patency of the foramen ovale and of the interventricular septum, capable of producing in the one a diastolic, and the other a systolic murmur. In infants it is hard to distinguish between the two ; but as all heart anomalies afe apt to center about ])ulmonary stenosis, a bold guess will some- times be rewarded with success. In acquired cases, even when they have been most carefully studied as to every auscultatory detail,, the diagnosis has seldom been made. Paul and Mayer, however,. have each recorded a successful antemortem diagnosis. The prognosis is never good. Exceptionally, congenital caseS' have lived to forty ; usually they die before the fourth year of life,, and of tuberculosis. In the acquired form the prognosis is more favorable. One of Schwalbe's patients lived to be eighty-four, another to be sixty-eight, while Rindfleisch and Oberneier's died at sixty-five. Usually, however, they do not survive the third decade. It is well to remember that at the birth of infants having this malformation, after removing the mucus from the mouth and nostrils, the circulation should be stimulated by slapping the surface. Artificial respiration by Sylvester's method, the author's or others, should also be resorted to ; or the lungs may be inflated by the cathe- ter, introduced through the larynx. After the circulation has been es- tablished in this way, the infant should be kept in a warm, dry room. In general, patients with this congenital malformation should live an uneventful life, in a warm, equable climate. They should have systematic exercise and their diet should be carefully regulated. Pulmonary Valve Affections 91 Their methods of life should be such tliat they have no physical or mental strain. Matrimony should be sternly prohibited. In the acquired form infections and rheumatic tendencies should be combated ; and the cardiac symptoms should be met, as they arise, with appropriate treatment. Chapter VIII. TRICUSPID DISEASES.^ Serious affections of the tricuspid are comparatively rare and, with the exception of pulmonary valve diseases, are the most un- common. They are still more rarely single. Gibson, however, maintains that tricuspid insufficiency is the most common of valvu- lar diseases, while Sperling makes the incidence 26 in 100 of com- bined lesions, and three out of 200 of single lesions. In 44 cases of valve disease as shown by post-mortems I found the incidence 12, or 27 per cent., while I have observed no single cases. Tricuspid insufficiency is usually relative, and due to many causes, cardiac and extra-cardiac. Organic lesions of the tricuspid valve, due to endocarditis or atheroma, are usually consecutive to mitral or aortic diseases ; or to general arterio-sclerosis. Insufficiency and stenosis are the two forms recognized. Tricuspid insufficiency is the most common, and the number of recorded instances must easily run up into the thousands, for in Guy's Hospital alone 405 have been recorded. These figures are in striking contrast to the published cases of tricuspid stenosis, which in 1897, according to Herrick,- had only reached 154; so that although tricuspid insufficiency is comparatively rare, it is as com- mon, as compared with stenosis, as the latter is rare. Tricuspid insufficiency may be congenital or acquired; organic or relative. Ordinarily we see the relative (acquired) form, which is due to stretching of the valves, from dilatation of the right ven- tricle consecutive to chronic affections of the lungs, or enlargement of the heart, whether from fatty changes or some other form of hy- pertrophy ; perhaps from adherent pericardium. There are also other causes. In one of my cases the tricuspid was apparently di- lated from pressure on the right auricle b}- an aneurism of the as- cending arch, and the insufficiency was discovered during life. Tri- cuspid insufficiency is furthermore a legitimate sequel to organic diseases of the left heart, and it may occur in the last stages of all these diseases. The preponderance of the relative variety over the organic is well shown in the records of the 405 Guy's Hospital cases ' Originally published in the Med. News, Sept. 6, 1902. ' Boston Med. and Surg. Jour., March, 1897, No. i. Tricuspid Diseases 93 already referred to, where 394, or about 97 per cent., were classed as relative. My tables make it about 90 per cent. The question of insufficiency, however, has been disputed, even at the post-mortem table, some holding that perfect competency is uncommon, because in applying the water test there will often be a little oozing through the valve. As a matter of fact, such fine distinc- tions have little practical value, because a slight oozing is not recog- nizable during life by any ordinary symptoms, and at any rate may be a temporary afifair and of slight importance. For this minor degree of insufficiency may be due to faulty technic on the part of the op- erator, who fails to hold the organ squarely in his hand while apply- ing the test. Practically, unless a good-sized stream of water can be passed through the valve when the organ is held properly in position, it should be regarded as competent. Besides, the ring of the valve is well supplied with smooth muscle fibres, and the some- what relaxed condition sometimes found at autopsies may be due to general muscular relaxation which has occurred in the last hours of life, or even after death. Organic insufficiency is almost always due to endocarditis, and is a late manifestation of the general impli- cation of the valves, which by preference first attacks the mitral and then the aortic. Relative insufUciency is simply the result of physiological laws. When from any cause there is obstruction, or stasis, or slowing in the pulmonary veins, due either to chronic pulmonary disease or to disease of the left heart or pericardium, causing engorgement of the lungs with venous blood, the current of blood passing through the pulmonary artery finds an obstacle ahead of it. Consequently the right heart dilates, and then hypertrophies, in order to force the blood into the lungs. This dilatation has the effect of stretching the soft muscular substance of the tricuspid ring, causing insuffi- ciency; and yet this relaxation may, after a time, be overcome by the general hypertrophy. Later, however, Avhen the right ventricle begins to tire and contract irregularly from weariness or degenera- tion of its fibres, the muscular tissue of the ring will also participate in the degeneration and again become incompetent. This is one of the common incidents of heart failure, in the last stages of valvu- lar disease. In other enlargements of the heart, as in fat deposition and in chronic fibrous nephritis, a certain amount of enlargement of the elements of the valve may take place and even keep pace with the enlargement of the heart walls ; for it is known that in valvular dis- 94 Tricuspid Diseases ea^es even tlie leartets soinclimes enlarge, in order to close the ori- fice which ihey are intended ti> protect. If. however, there has been any deposit in the substance vi the valve of a librous nature, con- traction, rather than expansion, must take place. As soon as tricusi)id insufficiency has become established a col- umn of blood is forceil throui;h the tricuspid vah'e into the right auricle which also dilates and later nia\ hypertrophy ; but the s_\stolic action of the right ventricle, acting on the blood contained in the right auricle, communicates its impact to the systemic veins, dilating them, provided the dilatation reaches such a tlegree that the venous valves are no longer competent. And so the blood in the veins pulsates. This jjhenomenon of z'ciioiis f>u!satio)i is always best seen in the veins of the right side, because thc\ are in the direct line of the blood current as propelled through the insufficient tricuspid. As venous pulsation is specially well seen in the jugulars, it is called jugular pulsation. For the superior vena cava and the innom- inate veins have no valves, so that no bar to the backward wave is felt until they have been passed ; while at the right sternoclavicular articulation there is a valve in the jugular vein, which resists the wave, and in fact produces a dilatation below the valve, which is called the jugular bulb, where the vein is expanded into a rounded body that may be seen or felt. In many instances of tricuspid insufficiency the backward wave does not progress beyond this point ; the veins are simpl}- filled. But if the valve gives way, the wave is propagated onward into the external jugulars and sub- clavians, and may mount into the face. Distinct pulsation in these cervical veins is, therefore, an import- ant sign ; and yet it is not pathognomonic. Further, one must always distinguish between a true venous pulsation and a mere undula- tion of the current in the veins which occurs apart from tricuspid disease — the false venous pulse. True jugular pulsation is best determined by pressing down the column of blood in the cervical veins, when the impulse will be found before it. not behind it. Compression of the carotids cannot be accomplished without using considerable force, so that we are not likely to confound one with the other. To bring the bulb of the jugular vein into view, the patient should be made to cough, when it becomes distinct. A sign that has been given by Pasteur" is distention of the veins •f the neck with or without pulsation, when the liver is compressed Lancet, 1885, p. 524. Tricuspid Diseases 95 .by the two hands, 'i'liis actio)) slows the blood i)) the i)iferior vena •cava and causes increased tension in the superior vena cava, and so in the cervical veins. In my cases, however, the venous pulse was not noted as a prominent symptom. Stasis in the pulmonary veins of the lungs prrxluces c}-anosis and •dyspnoea ; in the systemic veins oedema and albuminuria. The degree of stretching possible in a case of relative insuffi- ciency was well shown in one of my cases, where the tricuspid ad- mitted seven fingers, while ordinarily it admits only two. In aver- age cases of insufficiency it will admit three to four fingers. In the comparatively rare form of insufficiency, the organic, the valves and their rings and supporting structures become infiltrated, thickened, distorted, and perhaps contracted ; for stenosis presup- poses insufficiency. Yet if the stenosis is only in the ring, narrow- ing may occur without insufficiency, as happened in one of my cases of aortic stenosis. Practically then, in organic tricuspid insuffi- ciency, there may or may not be dilatation of the outlet. Atheroma rarely attacks the tricuspid valve. One of the first symptoms is cyanosis. This is at first slight, but may become extreme. Associated with it is more or less dysp- noea, depending chiefly on the grade of venous stagnation in the lungs. Oedema of the hings is also more or less common, and for .a like reason there is oedema of the lower extremities, first seen in the feet and then slowly rising towards the trunk. When the liver and kidneys become indurated we may expect ascites and albumin- uria. One of the jiiost prominent and early s}mptoms is the venous pulse which has been described. Another sign is epigastric pulsation, btit it is appreciable only when the cardiac s}stole is forcible. The radial pulse is usually small, soft and ij'regular, and is apt to be frequent. A thrill is of rare occurrence. When it is felt it is probably due to an associated mitral or aortic disease. The most characteristic sign of tricuspid insufficiency is the sys- tolic murmur over the tricuspid area. It should be heard with greatest intensity over the lower half of the sternum, at the root of or over the ensiform cartilage (the nearest point to the tricuspid), to the right of the median line : occasionally as far as the right axilla •or to the left of the sternum at the left fifth costosternal junction (Cabot) or just above it. It should not. however, be propagated any considerable distance to the left. The murmur is usually soft .and faint. Exceptionally it is rough and harsh. 96 Tricuspid Diseases The second pulmonary sound, so far as has been noted, is weak^ because a comparatively small amount of blood is propelled into the pulmonary artery. Doubtless in a very large number of these cases there has at some time been an accentuation of the second sound, owing to the accompanying mitral disease ; but on the failure of the tricuspid this symptom disappears, and the weakness of the second pulmonary sound is theretore, at this period, an important sign as in- dicating an advance in the general valvular disease. This symp- tom, however, is one to which but little attention has been paid. Undoubtedly tricuspid insufficiency produces at first dilatation. and then hypertrophy of the right auricle, and this is noticeable in some cases, chietly at the level of the right auricle. The heart in its totality is not enlarged, however, when the insufficiency has been of short duration. In the heart failure which is so frequent an event in tricuspid insufficiency one often sees the facial discoloration, the wild expres- sion, the projecting eyes. The patient leans forward, as this position is the most favorable for respiration, and gasps for breath, owing to the stagnation of blood in the lungs. The veins stand out in the neck. Often he can hardly speak, and only in monosyllables. The radial pulse is weak and intermittent. The heart s action is tumultuous. Yet tricuspid insufficiency is seldom recognized during life, even under favorable circumstances. In 29 cases proved by autopsies at the Massachusetts General Hospital but five, or 17 per cent., were recognized during life. In ten cases from my post-mortem records the diagnosis was made in three, or 30 per cent. But by some the di- agnosis is regarded as a refinement of comparatively little importance, in the presence of other conditions more apparent, and even more immediately serious to the individual. The most distinctive sign, as I have said, is a systolic murmur over the lower half of the sternum and ensiform cartilage, the most common center of the greatest intensity being (according to my re- turns) the fourth left intercostal space close to the sternal margin. At times the greatest intensity is as low as the fifth left intercostal space, close to the sternum, and the corresponding area on the right side ; sometimes as much as an inch to the right of these points, so that on the whole this area is somewhat broader on the right side than on the left. Occasionally the murmur may be carried to the right axilla, but it is seldom carried much to the left of the sternum. As the tricuspid, however, is a large and rather Tricuspid Diseases 97 indeterminate areas as compared with the mitral, which overlaps it, it is essential for purposes of diagnosis that the two sounds or mur- murs in these two areas should be appreciably dififerent in character as to pitch, quality, duration or intensity ; and the propagation of the murmurs should be in different directions. Epigastric pulsation is the next important sign. It does not: occur in simple mitral or aortic disease ; but we should remember that tricuspid disease may be associated with organic mitral dis- ease in from 20 to 25 per cent. ; and with organic aortic disease in. from 15 to 17 per cent. It may, however, be absent. Faintness of the second pulmonary sound is also important, es- pecially if previously there has been accentuation of it. The jugular pulse, once thought to be pathognomonic, is not sO' regarded now. It is seen in other conditions. It occurred in one of my cases of aortic insufficiency, without tricuspid disease. Sim- ple fulness of the jugulars is, however, a noteworthy sign. Increase in the transverse dulness of the heart is not a reliable sign. It may occur or may not. It may not exist in wasting pulmonary diseases. The tricuspid murmur may be also mistaken for the murmur of aortic stenosis ; or the latter may mask the former, when it is propa- gated backwards, as it sometimes is, towards the apex. However^ the diagnosis of aortic stenosis should be established by the propa- gation of the murmur up the great vessels. Simple thickening of the tricuspid without roughness, like simple oozing, gives no sign. In general the prognosis is bad. There are cases, how^ever, in which heart stimulants will sustain the flagging heart and carry the patient into a region of comparative safety. In fact, successive attacks may be mastered in this way, but the danger is always near at hand. Still the prognosis is not so bad in the relative variety as in the organic, for the latter presupposes implication of other valves. When there is albuminuria and scanty urine the prognosis is worse. Case XXVI. Mitral Stenosis: Pulmonary, Aortic and Tri- cuspid Insufficiency. — A., twenty-six years old, single, was admit- ted to hospital September 18, 18S0. Twelve years before admission the patient had a severe attack of rheumatism, and for about a year had suffered from more or less of palpitation and dyspnoea. On phys- ical examination marked pulsation was noted in the epigastrium. Murmur with first sound at the apex, not heard behind or in the ax- illa. Want of synchronism between the two radials. H^•pertrophv of heart. Cyanosis, nausea and scanty urine. The dyspnoea contin- 98 Tricuspid Diseases lied, and with it marked pulsation in the vessels of the neck. About live weeks after admission a "purring: thrill" was noted in the fifth intercostal space, one and a half inches below the nipple, with some recession of the jsoft parts, more distinct during inspiration. Patient developed orthopntva and died in a uraMuic convulsion. The autopsy showed general anasarca. Heart weighed 16 oz. Mitral calcareous, only admitting index finger. .-Vortic slightly in- sufficient. Tulmonary insufficient. Tricuspid admits tips of four fingers. Right ventricle hypertrophietl. Walls of left ventricle thinned. Fibrous i^hthisis. ( )edcma of the lungs. Nutmeg liver. In this case the "purring thrill" of mitral stenosis had been noted, as this was the predominating lesion. Tricuspid obstniction or stenosis, for they both appear to be synonymous, is one of the most uncommon forms of valvular dis- ease. In 1881 h'enwick* had been able to collect only 40 cases; Pitt, of London, in Albutt's Syslcni (Vol. \TI, p. 25), only 87 cases during a period of 26 \ears, and Merrick, of Chicago,'"' 154 cases up to 1897. Since that date, however, some additional cases have been published, bringing the total, according to my reckoning, up to 162. These figures include two by Whyte;" one by Devic and Teyssier ;^ tliree from the records of the Path. Soc. of Phil., 1898, Vol. XVIII, pp. 132, 181 and 196, by Packard, Steele and McCarthy; one by Chadbourne,- and one by Sir George Dufifey." Total addition, 8 ; grand total, 162. Tricuspid obstruction must not. however, be considered as an independent disease. It is almost of necessity associated with tri- cuspid insufficiency, just as any valvular stenosis implies insuffi- ciency. In fact, so far as I know, there has never been a case of stenosis without insufficiency, unless it is one reported by Duroziez, the details of which I have not been able to obtain. And in only two cases (the one above alluded to and that of Devic and Teyssier) was there no accompanying mitral stenosis. Practically, therefore, we may say that mitral stenosis is a constant attendant ou tricuspid stenosis, and as the mitral disease is the older, the tricuspid may be regarded as a comjilication of the former. It is a very serious one. The former idea that tricusjiid stenosis was a congenital condi- * Path. Soc. of London. 1881, p. 46. 'Boston Med. and Sure;. Jour.. March, 1897, Vol. I. 'Scott. Med. Jour., 1890. p. 18. ^ Pror. Med. Lyons. 1900, XV., p. 61,^. * Ant. Jour, of the Med. Sciences, 1900, p. 306. 'Dublin Jour., 1901, p. 241. Tricuspid Diseases 99 lion has Ijccn largely abandoned, certain]}- in post-fcetal cases, be- cause the evidences at post-nif^rteni of its being- last in a chain of circumstances are pretty positive, -while the date of the first of the events (which, so far as the valves are concerned, is mitral dis- ease) can be proved with considerable accuracy. The exceptions to this rule are so rare that ])ractically they can be excluded. There is, of course, such a thing as congenital stenosis, which occurs usually, if not always, in association with other congenital malformations of the heart. In these cases, however, life is rarely much prolonged after birth, so that, as in aortic stenosis, these ex- ceptional forms are almost never seen. A feature of great diagnostic importance in tricuspid stenosis is that the great majority of the sufferers are females. In Leudet's loi cases published in his These de Paris, 1888^^ (as quoted by Whit- taker), 80 were women, so that the proportion of women to men v/as about four to one. In Fenwick's 46 cases, of which 41 were women, the ratio of women to men was about nine to one. In 12 cases that I have collected 10 were women, or five to i. The pre- ponderance in favor of women, therefore, is well showai, though the reason is not clear ; but whatever arguments tend to show that mitral disease is by preference a feminine lesion should apply here. Fenwick found that the average age at death was between thirty- one and thirty-six. In my collected cases the average fell in the thirties. Very few survive the forties, and a less number the fifties. It is generally accepted that rheumatism is the most frequent causative factor. Fenwick found it in 50 per cent. : my figures, in 10 cases, accord with this ratio. In half of them we have to look for the cause in influences that govern mitral diseases. The heart is always moderately enlarged, but there does not ap- ])ear to be much enlargement of the right ventricle ; indeed, it has sometimes been described as small. The right auricle is usually dilated and hypertrophied, its walls showing manifest thickening. In tricuspid stenosis, coming as it does as the last link in the chain of valve events, the marked organic changes seen in mitral stenosis, are not apt to be met with. \\> usually find merely an agglutination of the segments, causing a funnel-shaped opening. Ordinarily it should admit two or three fingers, but in stenosis it may admit only one, or the tip of a finger. The substance of the heart must bv this time have degenerated also, and we find induration of the lungs, snleen and kidnevs, with the nutmeg liver. Of the 12 cases of pure tricuspid stenosis 11 were reported by Leudet. loo Tricuspid Diseases There are syniptO))is in abundance, but they are rarely sufficiently distinctive to warrant a diagnosis. This disease, like all other valvular diseases, advances insidiously. The patient will complain of palpitation. In one-half of the cases there is cyanosis (Pitt), and it is apt to be extreme, while either a fulness or pulsation in the jugular veins may be observable. With it there will necessarily be dyspnoea, and perhaps orthopnoea, each of tliem severe. In 75 per cent, of the cases, according to Colbeck, there is albuminuria or dropsy. On palpitation there may be a pre- systolic thrill, anil yet the tlirill can be due to a mitral stenosis. In the epigastrium there will be pulsation, at times, from an enlarged liver '50 per cent., says Colbeck), and the force of tlic heart's impulse will be marked. The presystolic or diastolic murmur in the tricus- pid area (which, according to English ideas, means "over the fourth and fifth spaces to the left of the sternum") should be heard and was heard in five out of seven of Colbeck's cases, though at irregular intervals. Some locate the murmur over the fifth or sixth right cartilage or over the ensiform ; others, again, over the lower half of the sternum and as much as an inch to the left of it ; still others,, at the root of the ensiform cartilage or to the right of it. That there is some kind of a bruit was noted in the tricuspid area in 20 only of Fenwick's 32 cases. It should dififer in pitch, quality and duration and perhaps intensity, from the associated mitral murmur, and this was noted in Shattuck's case where the diagnosis was made intrO' vitam}'^ In about one-quarter of the cases no bruit has been de- tected. In about one-quarter of the cases, also, there has been aortic stenosis. Mental confusion or hebetude have been noticed. Thus far the diagnosis appears to have been made only in six instances (those of Colbeck and vShattuck) out of the 162 which I have alluded to. Of the greater number it may be said, in the first place, that many were not examined thoroughly, because there was no opportunity to do so; and second, in the face of the manifest mitral, and perhaps aortic, lesions, no special interest was taken in. those of the tricuspid. (3wing, also, to the inconstant character of the murmur and usually its entire absence, it is not so strange that the diagnosis has been seldom made. Indeed, for all time this lesion will be apt to escape notice, if we are to depend on specific ausculta- tory symptoms. More constant than these are: (i) A coexisting mitral stenosis r (2) an enlarged and dilated right auricle; (3) palpitation, cyanosis,. Boston Med. and Surg. Jour.. Vol. 124. i8gi. Tricuspid Diseases lOl 'dyspnoea and oedema; (4) the e])igastric pulse, and (5; a previous (history of rheumatism. If, then, a woman under forty has these symptoms and in the tricuspid area a diastolic murmur, the pitch, quality or other char- acters of which distinguish it from the mitral murmur, it will be safe to make the diagnosis of tricuspid stenosis. The prognosis is worse than in any other form of valvular dis- vease. In congenital cases patients seldom live more than a few days. In acquired cases much depends on the condition of life. A tri- icuspid lesion that would prove rapidly fatal in a working man may be maintained a fairly long time by a person in easy circumstances. Pregnancy is a dangerous epoch for women. In general, the louder the murmur the less the danger. With considerable stenosis there is apt to be a mild bruit. Though pa- tients rarely attain the age of forty years, in the case that follows •seventy was reached : Case XXVII. Mitral and Tricuspid Obstruction with InsuM- £iency: Pulmonary Embolism: Pleurisy, with Effusion. — L., sev- enty years old, was admitted to hospital January 3, 1881. On ad- mission the patient stated that up to a week before admission he regarded himself as well. Then he suddenly developed dyspnoea. Slight cough and oedema of legs. On physical examination an occasional squeak was heard in the right parasternal hne in the third interspace. Patient's sputum streaked with blood. Jugulars enlarged, almost pulsating. Heart sounds at first indistinct. Cardiac dilatation. Impulse diffuse. Systolic murmur loudest over ensiform cartilage. Tubular breath- ing. Pleuritic effusion. Retraction of soft parts at third left inter- space with inspiration. At the autopsy the right pleural cavity was found full of serum and the left nearly full. Infarctions of lung. Heart dilated and weiging 23 oz. Aortic and pulmonary normal. Right cusp of mi- tral thickened and bound down, orifice admitting seven fingers. Valves of tricuspid thickened and restricted (stenosis). ClIArTER IX. MYOCARDIAL AFFECTIONS. Bcrtin. in his little book on Heart Diseases, piiblislied in 1821, made this quaint remark: "General inflammation of the substance of the lieart is one of the maladies about which there is the most melancholv obsc u ri t y . " ' Bertin. however, did not distini^uish between inflammatory and other diseases of the heart walls, for at that early i)eriod such distinctions were impossible. His successors, even down to the present day, have not wholly relieved us of this obscurity, larj^ely because conflicting theories have been advocated as to the nature of these diseases. For example, Rokitansky' and others ])ut the seat of parietal diseases in the muscle tissue. Hristowe- in the inter- stitial, while lluchard-' as late as 1893 claimed that the cardiac ves- sels were to blame. Besides, the relations between muscle degen- erations or metamorphoses and inflammations have always been hazy, while the clinical ]:)henomena at our disposal have never been equal in amount or quality to the pathological data. Again, impor- tant discoveries have been overlooked. Hayem, as early as 1869, called attention to the fatty changes in the heart muscle of typhoid.* Germain See'' in 1883 confirmed these views, Avhile Romberg" in 1891, extending his investigations into the condition of the heart muscle in scarlatina and diphtheria, found a granular and fatty change, together with a small-celled infiltration of the connective tissue and multiplication of muscle nuclei. Hayem's work has lately been confirmed by Dehio" and Bollinger.'^ Now that the discoveries of Hayem and Romberg have been rec- ognized, the whole subject of fatty degeneration of the heart is comprehensible, and can be placed on a sound basis — the patho- logical. 'Rokitansky, Patli. Auat.. London. Vol. IV.. p. IQI. 'Rristowe. Pract. of Med., London, 1876. p. 516. ' Huchard, Maladies du Cneur. Paris. 1893. p. 196. * Hayem. Arch, de Phys. Norm, et Path.. i8(V), IL p. 699. 'Germain See. Maladies du Cueur, Paris. 1883. p. 199. 'Romberp. Deiitsch. Arch. f. Klin. Med.. Rd. 48 & 49. 1891-2. 'Dehio. Deutsch. Arch. f. Klin. .Med., 189S. I. s, i. 62. 'Bollinger. Path. Anat., L, p 74, New "^'ork, 1898. Myocardial Affections 103 I'Jut there are other matters which arc still obscure, and I know nothing more confusing in cardiac j^athology than the use made in text books and journal articles of the term "myocarditis." For no sufficient reason, I feel sure, Sobernheinr' in 1837 introduced it, intending that it should be used to include all diseases of the heart walls, in lieu of Corvisart's'" "carditis," proposed about twenty years earlier. Corvisart was an exceedingly acute physician, indeed, a man who made very important contributions to cardiac pathology, and there was no good reason for allowing his word "carditis," which included diseases of the heart muscle, interstitial tissue and vessels, to be supplanted by "myocarditis," which, while it was intended to cover all these affections, actually referred only to muscle inflammation. Clinically, also, it has led to misunderstandings, because with some it has meant simply fatty degeneration of the heart ; with others disease of the coronary arteries. Of course, it is not to be denied that inflammation of the heart muscles plays an important role in parietal changes, and Rokitansky's contention was correct, in so far as he maintained that there was a myocarditis, or muscle inflammation ; but he was wrong in holding that it had a preponderating influence. Bristowe's and Huchard's theories are equally correct, but neither one of these authorities ap- pears to have realized that most of the changes in the myocardium are not inflammatory at all ; some being physiological, like the hyper- trophy of the heart in pregnancy, or the changes of senility ; while others are nutritive, that is, dependent on disordered nutrition or innervation, and so forth. When pathologists differed as to fundamentals, it was quite natural that clinicians should abandon the pathological classification and adopt a symptomatic one. It is in this way that Ebstein's^^ insuMcientia myocardii, debilitas cordis and myasthenia cordis, and the "iveakened heart" came into use. But while these terms attract us by their simplicit}', and relieve us from the necessity of espousing this or that pathological theory, they are essentially unsatisfactory, because they leave us in doubt as to what the matter reallv is. They are also unnecessary, if it can be shown, as I believe is quite possible, that a pathological classification is practicable. And if this is pos- sible, it is the proper one, as all should admit. Abandoning, then, the words "myocarditis," "carditis" or "pancarditis," which latter ^ Sobernheim, Diagiwsfik d. i. Krankheiten. Berlin, 1837, s. 118. "" Corvisart, Lcs Maladies dii Cwiir. Paris. 1818. p. 64. " Ebstein & Schwalbe's Handbuch, Vol. I. s. 729. ►Involuntary. 104 Myocardial Affections has been suggested, I purpcise to show that the conditions mentioned are to be placed under the simple heading"Myocardial Affections," of which there are the following varieties, viz. : 1. Fatty changes \f pegenerations. ( I'. Depositions. 2. Simple hypertrophies as caused by a. Severe exercise Voluntary. /'. Pregnancy. c. Vascular obstruction, including aneurisms and atheroma. d. Unusually small vessels ■} • • j ' ■' ( Acquired. c. The emotional or neurotic heart. j f. The heart in mechanical injury. 3. Simple dilatations as caused by a. Infections.* b. Anaemia, etc. 4. Atrophies of the heart. * Tubercles are occasionally seen in the heart substance. HYPERTROPHIES OF THE HEART. The normal adult male heart averages from 10 to 12 ounces; the adult female heart from 8 to 10; the size of the organ in health varying somewhat with the dimensions and development of the body, and the work that it is called upon to do. \\'hether in animals or men, however, if the organ is called on for extra work, it will enlarge in order to accomplish it. Familiar exam- ples reminding us of this truism are well known. A horse or dog that is continually forced to work at a high rate of speed will sooner or later develop hypertrophy of the heart, and may die of it suddenly, at some time or other. Such instances are probably known to all of us. Again, among the athletic youth of the present day, it is a regular event for those who train hard, to have some hypertrophy of the heart walls ; so that it is to be expected in professional boat- ing or baseball men, and even in tennis experts. I have recently had under my care a case of hypertrophy, due, undoubtedly, to the strain of tennis tournaments. We also have all the' evidence that is required, to show that professional mountain climbers, and miners who have to climb long and steep ladders will very frequently con- tract hypertrophy of the heart ; though, doubtless, in these particular instances there are other contributing factors, the mountain climb- ers being compelled to breathe a highly rarificd air and the miners one vitiated by coal-dust or smoke. So, in many other instances, two or more causes of hypertrophy coexist. At first, the normal heart dilates under the strain, but it contracts Myocardial Affections 105 again when the strain is over, and is usually no worse for it. If the strain is prolonged, however, the heart contracts less readily, and if the strain becomes continuous, the walls of the heart gradually thicken by the enlargement of the muscle bundles — perhaps by an increase in the muscle cells — until the organ is so re-enforced by additional muscle-tissue that it is competent to do the work it has before it. This new development of muscular tissue in the heart, fitting it for larger work, superinduces a condition of so-called "compensation." But the demands made upon the heart, whether m the normal or compensated condition, may be too great, and some fibres will overstretch or even break. Hence "heart strain." The strain may occur in the substance of the walls, in the pap- illary muscles, or in the chordae tending, the heart dilating suddenly and having no pov^er to contract, and the patient dying then and there with cardiac paralysis. Such an accident occurred in Case XXVIII. Or, the patient may have a season of arrythymia and then recover wholly or in part, in which case he will have a permanently strained heart, "the irritable heart" which Da Costa^- saw so fre- quently among soldiers. In the pregnant woman there is a physiological hypertrophy of the heart that develops pari passu, I believe (though it has been denied), with the increase of the blood required for the nourish- ment of the uterus, its contents and the breasts ; but as soon as parturition has been accomplished, there begins at once a gradual diminution in the size of the heart, to correspond with the dimin- ished volume of blood needed by the parturient woman.^^ Reasoning by analogy, therefore, we have a right to assume that as the heart develops in pregnancy and then retrogrades, a similar process may take place in the athletic heart; and this is probably true, the en- larged hearts that remain, as permanent fixtures, in these men, being instances of strain from which they have not altogether recovered. Another physiological increase in the heart may presumably occur in gluttons or drinkers who habitually consume more than is required by the wants of nature, so that they create a surplus of blood in the system, requiring an enlargement of the heart to propel the increased volume of blood. There are many - varieties of pathological hypertrophy, using these terms to mean hypertrophy following lesions of the organ. I have in my records many examples of hypertrophied hearts, "Da Costa, Medical Diagnosis, Phila., 1895, p. 457. " An enlargement of the heart due to renal disease in pregnancy has also been described. lo6 Myocardial Affections the majority of thcni hypcrtroiihics of tho left ventricle, due to defects in the aortic or mitral valves. It is quite common in these cases for the heart to weigh 15 to Jo ounces; and not very uncommon to find it 20 or 30 ounces ; while it may have a much greater weight. Two of these cases were due to artcrio-sclcrosis. and arc worthy of brief notice. Case XXriH. Hypertrophy of the Heart. Arterio-selerosis. — One of these patients, a i)rinter, 44 years of age, entered the his- pital with extreme dyspncea and palpitation. Aortic and mi- tral organic murmurs were noted, with pulsation of jugulars. Pulse varied from 36 to 84. He died after being under observation about three months, having developed general anasarca. At the autopsy large atheromatous |)]atcs were found in the aorta, and the mitral \\as diseased. The heart was enormously enlarged, chiefly in the left ventricle, and the hypertrophy (the heart weighed t^i ounces) was ascribed to general arterio-selerosis. Rupture of chordae tendi- n.T was the immediate cause of death. Case XXIX. Cor. Boi'iv.uui: Arteriosclerosis. — In anc^ther case a laborer, 67 years of age, of full habit and robust, but syphilitic, was admitted to the hospital January 21, 1887, suffering from chronic diffuse nephritis and uraemia. He lived but a few days. At the post-mortem examination many signs of constitutional syphilis were noted, such as syphilitic meningitis and cirrhosis, in addition to the evidences of skin syphilis. On the heart were several milk patches, but the valves were free and sufficient, though slightly marked by fatty changes. The hypertrophy was thought to be due to the arterio-selerosis. The heart weighed 58 ounces, free of its mem- branes. This cor hovinum is the largest I have known, and one ounce heavier than the famous heart, weighing 57 ounces, that was placed in the Museum of the College of Physicians and Surgeons of this city by the late Prof. Alonzo Clarke. There is also a form of large heart seen in hysteria and various nervous affections, so that it might be called the neurotic heart. It is apt to be complicated with valvular difficulties, but occasionally we find one in which no valve lesions are recognizable. I have seen such a case in Graves's disease when there was no valvular disease, but a moderate swelling of the thyroid associated with tremor, paroxysmal tachycardia, acute dyspnoea, anginoid at- tacks, epigastric pulsation, and obesity. The heart was very large, and the apex beat was 5^ inches from the median line to the left. Myocardial Affections 107 (Case LXXV.) This form of liypertrojjliy was ]jrobably compli- cated with fat deposition. The tobacco heart is also apt to be enlarged. Enlargements of the right ventricle are less common than those of the left, but they will occur, whenever there is obstruction to the pulmonary circula- tion. At various times a form of enlarged heart due to a congen- itally small aorta, or small arteries, has been described. Morgagni'* wrote of it, and several writers have since then called attention to it; I fancy it is of rare occurrence. However, FrantzeP"' has given the record of a case associated with congenital stenosis of the aorta. Perhaps these cases are merely anatomical curiosities. Sometimes when there is a general hypertrophy, the hyper- trophy of the right ventricle will be most marked. This occurred in a case which I saw with Dr. W. N. Hubbard of this city. Case XXX. Hypertrophy and Dilatation of Heart ; Scoliosis. — The patient, an unmarried woman of middle age, with scoliosis of marked type was taken down with an acute attack of nephritis, in association with chronic endocarditis and anasarca. At the post- mortem examination the heart was found to weigh 14^ ounces. It was hypertrophied and dilated and the right ventricle especially was thickened. Mitral and aortic valves were slightly afifected. Hydropericardium and hydrothorax. Nutmeg liver. In this case the special thickening of the right ventricle, when one should ex- pect the left to be most thickened, was probably due to the obstruc- tion of the pulmonary circulation, due to the deformed and con- tracted thorax. It is usually easy to determine if a heart is enlarged. Bulging of the pericardimn, with or without pericardial adhesions, is com- mon in large hearts. On palpation, the impulse at the apex is diffuse and heaving; it may be in the 5th, 6th. 7th or 8th interspace; in the line of the nipple, or up to three inches beyond it. In medium grades it is in the 6th space, and line of the nipple. Percussion reveals an increased area of dulness. Beginning in the 2d inter- space or over the 3d rib, it may extend from one-half inch to three inches beyond the left mammillary line, and perhaps an inch and a half beyond the right border of the sternum. This dull area is more ovoid than in health. There should be little difficulty in determining by percussion whether the heart is enlarged, though it is impossible to distinguish between simple hypertrophy and simple dilatation " Morga.eni, De Sedibus cf Causis. Episf.. XVTIL. Art. 2 et 4. "Frgentzel. Krankhciten dcs Hcrzcn, Berlin, 1S88, s. 151. loS Myocardial Affections by percussion alone. If such a differential diagnosis is necessary, ra- tional signs nnist be utilized to settle the cjuestion. In making- a diagnosis we nuist carefully dift'erentiate from the lieaving- im[)ulse of i)alpitation. Then the increased area of dulness may. it nuist be remembered, occur in pericarditis with effusion, aneurism, mediastinal tumors, and localized pleurisy. In this regard, assistance will be furnished by calling to mind that there are titreg stages of hypertrophy. In the first there is the period of dilating compensation, where there is an irregular heart action, increase in .strength of pulse, and a tendency to accentuation of the second pul- monar\- sound. When the hypertrophy has reached the stage of full compensation, normal action in heart and pulse has been estab- lished {second stage). In failing compensation (the third stage) we have increased dilatation, as shown by a feeble impulse at the apex, soft and irregular pulse, and cardiac distress. To a certain extent, hypertrophy is a benign process, designed by nature to relieve another abnormal condition ; and so long as the bodily health is maintained, and the work of the heart is not exces- sive, but proportioned to the strength of the individual, there is no need for alarm. But if the primary disease, be it valvular, pericardial or vascular, so increases, that the heart is strained in maintaining its equilibrium ; or the patient has insufficient nourishment, or is over- worked, the heart will dilate (failure of compensation) and collapse will ensue. In directing the proper course of treatment these facts must always be borne in mind. At this point it may be well to make a brief statement about the vexed subject of dilatation and hypertrophy, and their relation to one another. The facts, I take it, are these : There is a close relation between the conditions, and they often coexist (eccentric hypertrophy), but not always. In hypertrophy there may or may not be dilatation. For example, in the early stages of arterio- sclerosis, where there is no increase of the blood, but more force must be applied, there will be hypertrophy without dilatation (con- centric hypertrophy). In the enlarged heart of the beer drinker, who has created new blood, there is dilatation of the heart cham- bers, to accommodate the increased amount of blood to be driven and the heart hypertrophies in order that it may be able to drive it. In dilatation, too, there may or may not be hypertrophy. For example, m the breaking down of compensation in the hypertrophic heart there will be dilatation, but in the dilated heart of accidental strain Myocardial Affections 109 to a healthy heart there will be no hypertrophy. A similar dila- tation without hypertrophy will occur in the stage of softening of the heart which attends and follows the toxaemias, such as typhoid, etc. Acute dilatation often occurs probably after prolonged strain, as in bicycle riding, "running, etc, At post-mortem examinations this condition may be deceptive, and the apparent encroachment on the chambers in concentric hyper- trophy may be due to the fact that the patient died while the heart was in extreme systole. So, on the other hand, appearances may be equally deceptive as to dilatation of the heart, which may be be- cause the patient died when the cavities were dilated in diastole, or because of changes in the substance of the cardiac muscles, due to post-mortem relaxation. Owing to these circumstances, the rela- tion of dilatation to hypertrophy is often a difficult matter to decide, even at a post-mortem examination. Atrophy of the heart is less common than hypertrophy. It may be a family peculiarit}^ or it may be due to arrest of development, or it may be acquired ; or the result of the physiological changes of senility. Church has recorded the case of an adult, aged 47, where the heart weighed only 3 oz., i dr., while Bramwell saw one weighing only 2 oz., 12 dr., ii grains in a woman, the mother of several chil- dren {BramzveU's Dis. of the Heart, N. Y., 1884, p. 631). There may be total or partial atrophy. When people die of starvation or of extreme old age the heart is apt to be atrophied, but atrophy may result from arteriosclerosis, phthisis, cancer, diabetes, or in fact, any wasting disease. In many of these cases, especially in death from starvation or wasting diseases, the heart is apt to have a brown color. (Brozvn atrophy.) There is also a special variety of the small heart described by Virchow as associated with the small vessels of anaemia. He called it hypoplasia cordis. But a heart may be atrophied as to its muscle elements, and still be large, for the affection may be associated with a fat deposit. In some instances of atrophy of the heart the organ is so shrunken that the tortuous vessels stand out in relief on the surface, while the whole surface is thrown into folds. This variety has been called the "zvithered apple heart." Bramwell has a good plate of it. On microscopic examination the muscle elements are found to be shriv- elled, and yellow granules or pigment are disponed around the nuclei and drawn out in a line with the fibres. While there are the usual signs of cardiac disease in the atrophied heart, there are none which no Myocardial Affections are distinctive, except that the heart may sometimes have a smaller area of duhiess than usual, with the impulse nearer the median line and higher up than normal. The other symptoms common to atrophy and other forms of cariliae diser.se are turns of fainting-, spots he- fore the eyes, singing in the ears, irregular pulse, palpitation. i)re- cardial distress, confusion ol mind. Tlie ti>lli'\ving ease is an exam- ple taken from my records: Case XXXI. .Ifrof^liy of the Heart: Carcinoma. — A working man of 59. anaemic and cachectic in apjjcarance, entered the hospital in 1884. and after a stay of about nine months, died of progressive emaciation ( and in part starvation ) . due to primary carcinoma of the omentum, and secondary implication of the mesenteric glands, liver and kidneys. The heart was found small, soft and fatty. It weighed only 8 oz. Case XXXII. — Another case on my records occurred in the practice of Dr. R. E. \'an Giesen of Greenpoint, and illustrates the atrophy that sometimes is found in sarcoma. The pleura and medi- astinum were involved in a sarcomatous growth. The pericardium varied from 3^ inch to 1 ^4 inches in thickness, and the inner sur- face was hairy. The heart weighed not more than 5 oz. The I)atient was 22 years of age and well developed, and the body was well nourished. Arteriosclerosis is well seen in the gouty kidney and in the physiological changes incidental to old age. There is a degeneration of the cell elements of the capillaries and smaller vessels, the proto- plasm undergoing what is know^n as hyaline, then fatty, and later, atheromatous change. lUit as I have intimated, the hard pulse of old age may be regarded as physiological. The causes, as far as we know, are syphilis, alcoholism. IJright's disease, hard work, dia- betes, gout, lead poisoning and emotional conditions. The changes produced in the w^alls of the vessels are caused by the toxins carried by the blood vessels. Xature, however, comes to the assistance of the individual whose vessels are so thickened by disease, and the left heart h}pertrophies in order to compensate for the increased work it has to do in driving the requisite amount of blood through the thickened and tortuous vessels. The old theory that the arteries are thickened by the blood forced against the walls of the vessels is now maintained by few pathologists. When arteriosclerosis attacks the coronary vessels of the heart we encounter a special phase of the malady. The coronary arteries are terminal, like those of the brain and kidneys ; that is, they do not Myocardial Affections 1 1 1 anastomose with their fellows, so that any occlusion of a coronary artery, whatever its degree, diminishes proportionately the vascular supply within the area of its distribution, while the nutrition of the heart wall is correspondingly afifected. When such an area has been deprived of its blood the jjarl un- dergoes what has been called "ancemic necrosis," a condition that was formerly known as inyoiiialacia cordis. This starved area has been called a zvliite infarct. Whatever the result of the process, the heart wall is left, of course, unsound. The result of a healed white infarct is a fibroid area, due to the deposit of fibrin as a substi- tute for the dead tissue. Such a heart would also be called sclerotic. Sclerosis may lead to cardiac aneurism, the sclerotic or fibroid tissue yielding under the contractions of the organ so that the heart w^alls bag out. It is claimed that embolism, or even thrombosis, in a coro- nary artery will produce sudden death. I have never seen such an instance, however; and it would be very difiicult, I fancy, if not im- possible, to prove it. Abscesses of the heart occur, but are extremely rare. In misplaced hearts, the statements of Bouvier,^^ Adams^' and Bradford^** that heart affections are superinduced by deformities of the vertebrae have found support in the experiments of Neidert,^'' who, in 31 cases of Pott's disease and lateral curvature, found that most of the bad cases died earty of heart failure. Spinal deformities cause mechanical embarrassment to the circulation, leading at first to hypertrophy, possibly to distortion of the valves, and eventually to heart failure.-" ^^ Bouvier, Legons C Uniques, Paris, 1858. p. 145. "Adams, Curvature of the Spine, London, 1882. ^* Bradford, Orthopccdic Surgery. 1890. p. 14.. " Neidert, Inaug. Diss., Munich; 1883, V. & H.., Jahrb, 1886, s. 371. ^Displacements of the Heart in Lateral Curvature, A^ V. Med. Jour., Sept. 30, 1899. Chapter X. THE FAT HEART. Corpulence and the fat heart are so closely related that a con- sideration of one involves the other. Chambers found that in thirty- six corpulent people twelve had the fat heart, while Quain's obser- vations were that patients with fat hearts were invariably corpulent. \\c may infer, therefore, that corpulence disposes to fat heart. Prob- ably the one is essential to the other. The term fat heart means nierel\- that the heart is burdened by an excessive deposit of fat ; not that it has undergone fatty degeneration. The fat heart is said to be in a condition of infiltration, pathologically speaking. Fatty degeneration of the heart is a more dangerous affection, but it may be a sequel to fat infiltration. If they coexist, which sometimes happens, the prognosis is vastly w'orse. Corpitloicc or obesity consists in an excessive deposit of adipose tissue in parts of the body which are comparatively free from fat in health. It is caused essentially by nutritive disturbances ; or to put it in another way, it is the result of a loss of the equilibrium be- tween assimilation and disassimilation. Obesity is a serious matter in many ways. First of all, it is a positive discomfort to the patient, for locomotion is made difficult, digestion is disturbed, and the faculties are often dulled. Obese people, too, have a constant tendency to constitutional disorders, such as gout, rheumatism and diabetes. There is also the ever- present danger of some serious illness, accident, or surgical opera- tion, which they may not be able to survive ; as corpulent people are deficient in vital power. Fat infants and children, in my experience, seldom reach adult life, w^hile in advancing years the obese may be totally unable to go about. I\Iiles Darden, whose height was seven feet six inches, and who weighed over a thousand pounds, had to be transported in a wagon during the last four years of his life. Corpulence may be a disturbing factor in social life. It is said that in Albania, corpulence, in the male, is a proper ground for divorce. Excessive weight has been treated successfully from very early times, the Greeks employing trained men to reduce their athletes, but corpulence, as a disease, was not plainly shown until the present century, when English physicians, such as Wadd (in 1825), Cham- The Fat Heart J 13 bers (in 1850), R liarvcy (in 1864J, and (Juain (in 1880-1885), wrote up tlie subject. Harvey was the physician of IJanting, and his method, known as the I Wanting system, Ijecame widely known and was extensively practiced. Adipose tissue is chiefly stored in the subcutaneous connective tissue beneath the serous membranes or in the inter-muscular septa. The largest deposits are beneath the skin of the abdomen, in the mesentcr}-, in the buttocks and thighs, and in the back of the neck. In women the excess of fat is usually in the thighs and buttocks. ,\ certain amount of fat is normally contained in the connective tissue corpuscles, in the form of minute specks. According to Michael Foster, these specks coalesce mto droplets, these again into drops, until, as the protoplasm of the corpuscles diminishes and the oil globules vmite, the original connective tissue corpuscle is con- verted into a fat cell. The remnant of the protoplasm is then gathered about the nucleus. To a moderate extent, fat tissue is natural, as it is a normal constituent of the system ; and within physiological lines ordinary fat tissue may be increased so as to sub- serve a useful purpose, constituting a reserve store upon which the body may draw for nutriment in periods of prolonged vital strain. But obesity has a progressive tendency, for as the bodily weight increases, and with it the dyspnoea and palpitation which necessarily follow exertion, there is a further hindrance to the oxidation of the blood, which is still more increased, when the heart becomes involved in the fatty process. Corpulence also begets plethora, and it in turn hemorrhoids, varicose veins, haemorrhages, vertigo, headache, disturbances of sight and hearing, dulness of the intellect and dys- pepsia ; all of which may be attributable to passive congestions. It must not be supposed, however, that all corpulent people are so afifected. Sam Johnson, the author of Rasselas, and David Hume, the historian, were corpulent, but led, for the most part, in- tensely active, intellectual lives, notwithstanding this malady. Obesity may occur at all ages. I have seen it in infants under one year. In a number of cases I have ascribed it to a surfeit from artificial feeding with food containing too much cream, or a super- abundance of starchy material. In two instances (see Cases XXXIII and XXXIV) the deficient oxidation of the tissues is shown by dim- inution in their normal percentage of urea. Both of these patients were lithgemic. as the diminution in the excretions of urea would mdicate. Lack of active exercise, too much sleep, and a secluded life also tend to corpulence. The obesity of some women of the 114 The Fat Heart East is explained by Charles Robin c)n the groiuul that the_\- take little exercise, eat all day long-, and sleep a great deal. Obesity is also hereditary, while races living in a low. cool and moist climate are especially prone to it. Drinking any liqnid in excess also in- duces corpulence. Fermented li(|nors and the alcoholics are special causes. Overeating may likewise cause it. Most persons eat more than is good for them. Persons who drink water in excessive quantities are usually corpulent, especially if the\- drink much at their meals ; perhaps Ix'cause the increased amount of water inter- feres with digestion and assimilation. IJesides, if the gastric juice is (.Hinted, the blood is made more li(|uid. and the red corpuscles are in a measure dissolved. Fat tissue ai^pears to be chiefly formed both from the carbo-hy- drates, and also from the sur])lus carbon of the proteids or albu- minoids ; from i)ure fat taken as food : and from water or other liquids. Some authors hold, however, that fat taken as food does not make fat tissue. Ebstein, of Goettingen, maintains this view. The truth ap])cars to be that when fat (or an albuminoid) is eaten in small quantity, no fat is stored up ; but when the fatty food or allju- ininoids are increased to a point where the carbon is no longer l:)urned. it is retained in the system as fat. W'e are not very fully informed as to the pathological findings in the corpulent after death. I, myself, never gave the matter much attention, although I liave made a good many post-mortems on cor- pulent people. P.ut after death, the tissues of the cor]>ulent are apt to be soft and flaccid, and decomposition rapidly ensues. In a case of fat heart occurring in my pathological service in St. Luke's Hospi- tal, where death was sudden in a man only thirty-three years of age, the left ventricle was found hypertrophied ; there was oedema of the lungs ; the spleen was large and soft ; the liver fatty ; while the liver, kidneys, and portions of the stomach were congested. The diagnosis of corpulence is simple, but it is generally ad- mitted that the presence of a fat heart cannot be positively deter- mined by physical signs. It is a matter of inference. But most agree with Quain, that where the pulse is small and weak, the first sound of the heart feeble, the impulse weak and the heart's area enlarged in a patient who is corpulent, it may be pretty certain that there is a fat heart. Henry Kennedy, of Dublin, in opposition to Quain, based his diagnosis on a large, full pulse, not increased in frequency, an enlarged area of heart dulness. and possibly a soft systolic mur- nuir over the aorta, with the first sound. In my experience a fat The Fat Heart 115 heart is often accompanied by valvular lesions, and 1 think that my experience will be found borne out by a study of rejjorted cases. Hence it is that Kennedy may, in his cases, have found a full pulse which was due to valvular lesions. In this connection, however, I ■ong-ht to say that during- the treatment for fat heart previous mur- murs will sometimes disappear, a fact indicating' to my minrl that these ])articular murmurs were probably due to a relaxed con- dition of the heart chambers or ostia, and not to an organic valvular ■disease. Obesity is a disease that can be successfully treated in most cases, if the patient has a fair amount of vitality ; and even in the feeble, the dangers attendant on a scientific course of treatment are small as compared with the risks in neglecting it. According to Maccary, as quoted by Worthington in his excellent These de Paris (1875). the methods of the ancients comprised venesection, the use ■of purgatives, exercises, friction, diet, and stimulation of the several emunctories of the system. These methods, however, were prob- ably not applied to the very young, the very old or the feeble. It seems hardly worth while to discuss the topic of venesection. Drugs, however, are still very extensively used. Liquor pofassae was rec- ommended by Chambers in 1850. The dose was from one-half drachm to one and one-half drachms. The theory of the action of this drug is, that "it increases the vital power of metamorphosis by saponifying, in part, the fat contained in the blood, enabling it to be burned ofif as carbonic acid.^ It is no longer used. Probablv no stomach could stand its administration for any length of time. Its ■effect, if any, was to prevent digestion. In other words, it was one of the many "starvation cures." Fowler s solution, in five minim doses three times a day. has been used. I have known it to be tried, but never with success. It is imcertain in action, and may increase the weight. Fnciis vesicidosus, or bladder w^rack. a species of seaweed found in the Atlantic Ocean, w^as at one time used, on account of the iodine and bromine it contains. It was given in a decoction of two to four drachms to the ounce. The taste is very offensive and the stomach is greatly irritated, so that gastric catarrh may be produced. The kidneys, however, are urged to great activity. Some have simplified this latter method by giving tincture of iodine in doses ■of two to four drops in a wineglass with lemon juice ; but this treat- ment also seems to produce catarrh of the stomach. ' U. S. Dispensatory. 1880, p. 862. ii6 The Fat Heart Bromide of aiiiiinniiiiiii in doses of five to thirty grains per day lias been roconunciidcd. It is unpleasant to the taste and irri- tating to the system in many ways. In line with this is the treat- ment b}- vmegar. It reduces the tiesh, but produces nervous dis- turbances. According to llrillat-Savarin ( W'orthington ) . it caused the death of a }e)uiig girl of eighteen who in>isted on taking a wine- glassful every tlay. The Banting method was at one time widely employed, lianting had trietl the waters of Leamington, Llieltenham and Harrogate; had taken plenty of outdoor exercise of a vigorous kind ; had tried Turkish and vapor baths, and had used liquor potassae as reconi- meiuled by Chambers, but with no eliect. Mis physician. Dr. F. ] larvey. then ])ut him on a regular diet that consisted of four meals a day. lie took eleven to fourteen ounces of meat. game, poultry or hsh (pork ami salmon excepted), tea without sugar, rusks and toast in small quantity all vegetables except potato ; four to seven glasses of claret and two to three ounces of fruit. Hot drinks of "grog" at night. lie is said, how'ever. to have also been ordered a mysterious black draught on rising, the ingredients of which I have not been able to discover. On this system, kept up for some- thing over a year, he fell off from 202 to 156 pounds, losing 46, or at the rate of 3 to 4 per month. The case, as described by the patient, is somewhat lacking in details from a medical point of view. The loss of weight ])er month was rather small — and the dietary, especially as to alcoholics, was, to say the least, liberal. The permanganate of potassium in doses of one-fourth to one grain before meals has been recommended by Bartholow. It is said, at any rate, to relieve the acute gaseous dyspepsia of the corpulent. CJiambers' system consisted in a diet of two meals each day, active exercises, rubbing, salt baths, alkalies such as liquor po- tassae in doses of one-half drachm to one and a half drachms, purga- tives, and even bleeding. The treatment at the baths of Marienbad, Taras]) and Carlsbad is due to the use of Glauber's salt, which reduces bv caus- ing watery discharges : but it is apt to be so violent in its action, owing to the very short time allowed for the treatment given, that it may cause flebility. palpitation, and even chronic diarrhoea. According to Worthington, Trousseau's plan was to allow his patient lean meat, fresh vegetables and fruit in their seasons, but to forbid him fat meat, butter, oil and milk. The amount of bread and milk taken daily was to be diminished to a point as low as his vitality permitted. The patient was to be weighed every two weeks. The Fat Heart . iij and he was expected to lose at the rate of one and onc-lialf to three pounds per week. Exercises in the open air on foot or on horse- back were ordered. In addition, he prescribed baths containing five to six otmces of the bicarl^cjnate of soda. The same drug was given internally to the extent of thirty grains per day. The pkui pursued by Ebstein, of Goettingen, is about as follows, the rules being modified somewhat according to the case : 1. Breakfast — ^:30 A. M. in summer and 7:30 in winter. Large cup of black tea without milk or sugar. Two ounces of white or brown bread. Plenty of butter. 2. Dinner. — 2 P. M. Soup ; four to six ounces of meat, with fat gravy ; plenty of vegetables of all kinds excepting beets, carrots, turnips and potatoes. A little sweet fruit after dinner. Salad or stewed fruit. No sugar. Two or three glasses of light white wine. After dinner a large cup of black tea. No milk or sugar. 3. Supper. — 7 P. M. A cup of tea. One Qgg, ham fat — in fact, any fat meat ; sausage, smoked or fresh fish. Two ounces of white bread ; plenty of butter. Perhaps a little cheese ; a little fresh fruit. This diet to be kept up indefinitely. Ebstein, as I have already stated, holds to an idea, opposed by most, that the eating of fat does not produce fat. Ocrtel, of Munich, had a somewdiat similar plan, but prescribed a peculiar course of exercises, and sometimes resorted to violent diaphoretics. Pie restricted the amount of liquids and solids, limited carbohydrates and fats, ordered prolonged walks, increasing the distances daily, making his patient ascend greater and greater heights {Terrain cur). In the winter, or wdienever his Terrain cur was impracticable, he used injections of the hy- drochlorate of pilo-carpine in doses of one-third to one-fourth grains twice a week. His dietary was as follows : Morning — Tea or coffee, four ounces with milk and sugar. Bread, two ounces (roll). Mid-day — Beef, ten to twelve ounces ; an egg. Vegetables, two to three ounces. Farinaceous food, one to five ounces. Fruit, three to four ounces. Salad, two ounces. Austrian red wine, three to four ounces. Afternoon — CofTee, four ounces, with milk and sugar. Evening — One to two boiled eggs, five ounces of meat or six ounces of game or fowl ; one to two ounces of bread ; salad : two to ten ounces of wine ; Moselle preferred. ^ Among the newer remedies that have been used in this countrv ii8 The Fat Heart is pli\toliiu\ the active principle of the i)h}tohicca ilecaiulra or poke- berry, wliich if taken in ten-drop doses before and after meals, is said to rechice without dieting, and at the rate of five to twenty pounds per month. The drug apparently acts on the subcutaneous fat, causing its absorption. Tlwroid extract is also extensively used. It produces ema- ciation, but is often poorly borne by the stomach, and is apt to be depressing. In one of my cases with hereditary ataxia it greatly aggravatetl the ataxic symptoms. The i^rapc cure is another means of reducing tlesh. The patient is restricted to unfermented grape juice for several weeks. At tirst he takes it in excessive quan- tities, then the amount is gradually reduced to the least amount comi)atible with vitality. Then it is slowly increased until enough is taken to fairly sustain the bodily activities. It is merely a sort of "starvation cure." The teas which are now widely ad- vertised, but whose ingredients are not generally known to the jniblic. are chieHy composed of senna leaves, with a varying quantity of chelonia. couch grass and coriander seed. To be effective the dose should be sufficient to produce two or more very watery move- ments daily. Dancel. the French surgeon, who with Trousseau wrote a treatise on obesity, used the hydrogogue scammony (the activity of scam- mony is due to its resin), of which the dose is five to ten grains. At the same time he reduced the quantity of food and drink. There are many baths in Europe that are resorted to for the cure of corpulence. First in order of repute are the cold Glauber's salt waters of Alarienbad, in Austria, and Tarasp in the Engadine. But if patients have cardiac difficulty, asthma or diarrhoea, the hot Glauber's salt waters of Carlsbad are better : or the hot alkaline mu- riatic waters of Ems ; the bicarbonate of soda waters of Vichy, in France : or the alkaline-saline of Brides in France, on the Italian frontier. Tn mild cases patients are usuall\- sent to take the saline waters of Kissingen or Homburg. but even these latter may prove to be too strong. Some years ago I had a patient weighing 220 pounds under my charge, who lost fifty pounds' weight at Kissingen, but his nervous system was so deranged that he told me he had felt "as if he would lose his mind.'' In fact, any effort to reduce the weight too rapidly, as is often done at the Continental spas, is apt to be harmful. It is not desir- able to lose flesh in this way ; nor is it always well to reduce the weight to the standard shown by our American tables. It is true The Fat Heart 119 thai professional trainers can do it, Init they usually have little weic^ht to take off, and the suhjects are men of exceptional vif< inches. Takes no breakfast. In place of it a glass of hot water. 'J'akes Apenta water at l)reakfast time, sometimes followed by hot water. After two months' treatment the patient reported of himself as fol- lows: ''Two months' treatment shows a loss of nineteen pounds in weight, and a reduction of ten inches in measure about the waist, with marked increase of strength and a greater freedom in breath- ing." May 2d — Resistance exercises, thirty to thirty-five minutes. Car- bonated baths have been gradually increased to their full strength, but are now suspended. May 7th — Has gained three pounds, but lost nothing in girth. Ordered baths again with one-half per cent, carbonic acid. May 14th — Weight, 332^ pounds. Lost six and one-half pounds in seven days. Bath now every other night. May 26th — Gained two pounds last week. Rubber bandages now removed. Patient walks easily. Ordered to take only one meal per day for one day, and two meals on the alternate da}'. June 4th — Weight, 327^/2 pounds. June nth — Patient going to the country is directed to take special resistance exercises daily. To take hot or cold water, one or two goblets with orange juice, before breakfast. Then to take a hearty breakfast and a light supper. To eat only twelve ounces of meat, fish or fowl daily, avoiding starchy and sugary food. To eat spar- ingly of small fruits ; to avoid fat in every form, including butter, milk and gravies. In January of 1899 the patient reported that under this treatment his weight had fallen during the summer to 317 pounds — a loss of forty pounds. During all this time he had attended to his daily pro- fessional routine of business, while in the city ; and made long trips out of town in consultation cases, where he was obliged of necessity to walk long distances in going to and from his train. Among the noteworthy features of this case is that, under the treatment, the eczema and oedema of the legs disappeared, and that he graduallv gained in strength, so that he was able to do more professional work, during the treatment, than he had done for a long time previously. Case XXXIV. Obesity: Fat Heart; Temporarx Diabetes. — A lady of about sixty-five came to me on October 4, 1898. She weighed 181 pounds, was nervous and anjemic. Skin bathed in 122 The Fat Heart j)erspu-alion. Color dusky. Tulsc lOO to 104. Weak impulse. Heart enlarged. Xo organic nuninurs. Urine examination (by E. E. Smith. I'li.O. ) : Sp. gr.. 1027. Faint trace of sugar by sev- eral tests ; no albumin. L'rea, 1.75 per cent., 7.95 grains to the fluid ounce. A little pus. A few uric acid crystals. Moilcrately large quantity of hyaline casts. October 2()th — Second examination. I'rinc. 60 oz. Sp. gr.. 1018. Alkaline : no albumin. Sugar absent. Urea, 2.28 per cent., 10.40 grains to the fluid ounce. I'us absent. Moderate number of hyaline casts. November 2d — C)rdered anti-litli:emic diet. Resistance exercises. November 14th — Resistance exercises and massage. One-half per cent, carbonic acid bath, at 97°, five minutes. Average pulse be- fore exercises and hath, 90; after, 81. November 22d — Weight, 178 November 28th — Weight. 177. December 21st — Weight, 171. The treatment was now stopped by an attack of influenza, the pa- tient leaving town subsequently for a short trip to the country. From a health resort, where she had been in the habit of going, she reported on January 24th : "The doctors here think me much im- proved." Loss of weight, about five pounds a month. Cose XXXV. Obesity; Fat Heart; Dyspepsia.— A gentle- man weighing 237 pounds, height 5 feet 6 inches, came under my care in December of 1898. Pulse 100, no intermissions. Apex beat feeble, difficult to locate; heart enlarged. Patient a smoker and lith?emic. Xo organic murmurs. Pain at apex, giddiness of head, acute gaseous dyspepsia, and d\'Spnoea. Apex four and three- fourths inches from the median line, and three-fourths of an inch below the intermammillary line. December 28th. — Dyspepsia and regurgitation. Under subgallate of bismuth, Carlsbad salts, anti-lith?emic diet, and abstention from smoking, these disappeared. Januarv 27th. — Patient took the modified X^auheim course of resistance exercises and baths. Apex now about four inches from the median line, and three-fourths of an inch below the intermam- millary line. Takes no medicine. Weight, 217 pounds stripped. Had lost about ten pounds in a month. Pulse of better quality; dvspnoea gone, and the patient able to walk fifty-five blocks in a single day. By methods such as are given here it is possible to reduce the The Fat Heart 123 weiglit, witliont detriment to tlic j:^eneral health; and we have a right to assume that the deposit of fat in the heart is, measurably at least, diminished with the loss of the visible adipose tissue. Ciiapti:r XI. FATTY DEGEXERATiOX Ul- THE HEART.' I'atty degeneration of the heart was first correctly differentiated from tlie fat heart of obesity by Laennec-, and a httle later by An- dral'', who called it niinollisscDiciit dii cociir. The source of this degeneration appears to have been discovered by Hayem,'', at least so far as typhoid fever is concerned. In 1883 Germain See' confirmed this view, while in 1891 Romberg," after an elaborate study of the heart substance in typhoid, scarlatina and diphtheria, discovered in all of them a granular and fatty degenera- tion of the heart-muscle, together with a small-celled infiltration of the adjacent connective tissue. In 1898 Bollinger" adopted this view and described three degrees of fatty degeneration, though he did not intimate that they might be three stages in the one process. In the same year Dehio"* confirmed Hayem 's views, so that w^e may now regard the matter of fatty degeneration of the heart as fairly under- stood, pathologicall}". It remains for us to attach, if possible, clin- ical phenomena to the successive stages of its development. It is very important to put this matter on a sound clinical basis, for how often sudden death, from heart failure, strikes down a person who, up to the time of the attack, appeared to have excellent health. In fact his physician, after examining his heart and, finding no signs of valvular disease, may have been content with the diagnosis of a "weak heart," and yet the heart substance may have been so pro- foundly diseased that it only needed a sudden, violent, or even pro- longed, "strain" to cause hyperdilatation and cardiac paralysis. I described such an instance at a meeting of the N^ew York Pathological Society some years ago :'^ Case XXXVI. — A gentleman, seventy-three years of age, who had led an active life up to a year before his death, was suddenly taken with dyspnoea, after some hill-climbing in California. Up to this time he had never had heart-symptoms. He recovered promptly, 'Originally published in the Med. News, Feb. 2, 1901. ^Laennec, Dis. of the Heart and Lungs, London, 1846, p. 607. ' Andral, Path, intern.. Paris, Vol. I., p. ,^24. * Hayem, Arch, de fihys. norm, et path., 1869, Vol. II., i, p. 699. 'Germain See, Maladies du cocur.. Paris. 1883, p. 199. "Romberg, Dcittseh. Archiv. f. klin. Med., Bd. 4S u. 49, 1891-92. 'Bollinger. Path. Anat.. New York. 1898, Vol. I., p. 74. -Dchio, Deutsch. Archiv. f. klin. Med.. 1898. LXII,, s. 1-62. ' Satterthwaite, Trans of N. Y. Path. Soc., Oct. 22, 1879. Fatty Degeneration of the Heart 125 however, from this attack. Later he took a 25-iTiile sleigh-ride and had anotlier attack, hut was restored by stimulants. Five weeks be- fore his death he lost consciousness in a street-car, and was taken home with some difficulty. Stimulants, however, again revived him. An examination by the family physician showed that he was anaemic and weak ; the pulse could not be felt, and the apex beat was barely apprecial)le. He did not rally. At the post-mortem examination, which 1 made, there was a marked blanching of the surface of the body. The lungs were oedematous and the kidneys pale and fatty. The heart was not enlarged, but it was pale and flabby. Microscopic examination of the cardiac muscular tissue showed that along the inner wall of the left ventricle the striations w-ere quite gone, though they were fairly well marked at the periphery of this ventricle. There was no valvular disease. In this patient the initial "strain" to the degenerate heart-muscle seemed to be directly traceable to the hill-climbing in California. Tliere was apparently no other lesion to cause death. The weak heart of fatty degeneration is common enough at all periods of life. In infants and children it occurs during and after the eruptive fevers and diphtheria, acute rheumatism, pneumonia, influenza, or. in fact, any acute febrile attack of toxaemia. In senil- ity, at whatever age this may happen, whether early or late in life, it is a phenomenon to be expected. In fact, w'henever there is a pro- longed fever, toxaemia, dyscrasia or mechanical injury, fatty degen- eration of the heart may occur. Very often the so-called "weak heart" is in reality the heart of fatty degeneration. And yet, to judge from individual experience, as derived from intercourse with physicians, and from our current literature, the matter is not so understood by the profession at large. In consequence fatty degen- eration may be recognized too late for treatment, as in the case just cited. The early, or preliminary stage is the one in which the prognosis is the most favorable for complete recovery ; in the second, or inter- mediate stage we should be able to hold the disease in check ; in the third, or tina/, stage palliative treatment alone is possible. If. however, we are to grasp the matter intelligently, we must first of all look to the minute structure of the heart-muscle. Though involuntary, it is made up, as we all kno\\-, of muscle-cells marked by longitudinal and cross striations. The body of each cell is cylin- drical and contains one or two nuclei. The nucleus is vesicular and oval, and is placed near the centre of the cell-bodv. The cells are 126 Fatty Degeneration of the Heart not onlv ioiiiecl at their ends with ciuilii;iunis cells; hut, throug-h hranchos. with other cells, niakini^' up a reticular uetwork. The ap- ]KXsition of the cells is effected hv a cement suhstance, that is not seen under ordinary conditions ; and the network holds in its meshes ves- sels, nerves and fat. In inflammation of this nniscle the cells become opaque, owing- to their intiltratit)n with i^ranular matter, or at least with something presenting that appearance (cloudy swellino), and the particles have been termed alhumiuoid, because they disappear to some extent un- der the action of weak acids or alkalies. One theory that has been proposed is that this albuDi'uioid material is formed from the cyto- plasm of the cells. Another theory supposes that the granules rep- resent the toxic elements of the disease : another that they are effete matters being eliminated; an(nher that they are micro-organisms; another that they are fatty particles in a stage of minute deposition. It is certain, however, that some of them are pigmentary, and also that in poisoning by phosphorus, arsenic and in typhoid fever, many are either fattv or of some closely allied substance. So much for the first stage. In the second, or intermediate stage, the muscle cells are clearly seen to be studded with oil globules, which appear to occupy the same position as the "albuminoid" and fatty particles of the first stage. In the final, or third stage, the fatty globules reach a higher degree of development, while occasionally the muscle-cells are pulled apart {sedimentation), or broken into fragments (fra,^inenfati'oii), as the result of hyperdilatation of the heart chambers. In this stage there is an engorgement of the blood-vessels of the internal viscera, limiting their functional activity and causing hyper?emia. oedema, thrombosis or embolism. Renaut^" has gone so far as to classify segmentation as a variety of chronic myocarditis, which he has called myocardife segmentaire chronique. At first, this view met with opposition from Zieglcr and Recklinghausen, who regarded seg- mentation as an agonal manifestation. Hektoen.''^ of Chicago, how- ever, after examining eighty hearts to test the matter, came to the following conclusions: Se^mevtation and fra^me^itat'ww do occur in heart-muscle durluf:^ life in consequence of irregular contractions or injuries, usually associated with disease of the heart-walls. If the segmentation or fragmentation is limited in area, it is not immedi- atelv fatal. Consequently we are forced to believe that both seg- mentation and fragmentation are real events in heart-strain, con- '"Renant. Cue. Med. dc Paris. lOQO. o. too. "Hektoen, Trans of Path. Snr. nf Phila.. tPqS. p. 267. Fatty Degeneration of the Heart 127 tribnting-, of ccnirse, to the fatal issue, though they hardly seem to lie worthy of a separate classification. Reverting for a moment to the subject of the so-called albu- minoid change, a theory has been advanced that in exhausting dis- eases associated with prolonged fever in which the cardiac muscle is actually starving from lack of nourishment it makes a demand, in its hunger, on the store it has already accumulated, viz., the meta- ])lasm of the muscle-cell ; but if this is exhausted and more is needed, it is compelled to consume its own substance. Now the reserve stock in the meshes of the muscle-cells is made up of carbohydrates, and there is no harm done to the cell by their consumption. When, however, the living tissue of the cell has to be sacrificed, there is a loss of the proteids or albuminoid substances of the cell, and the damage done is directly proportionate to the amount consumed ; and yet the combustion is incomplete, a granular debris being left behind in the cells. But consumption may proceed a step further, so that both the fatty matters and the fluids of the protoplasm are burned, though the combustion is still incomplete, and a further residue of oil is left behind in the cells. Still, even now, a restoration of the cells is possible, provided only the nucleus has been left unim- paired. Death of the nucleus, however, means death to the cell. Quite a different view has been given by Huchard.^- It is that the first stage of fatty degeneration is due to the irritation of a micro-organism or toxin, which, if sufficiently virulent, causes in- flammation and perhaps, ultimately, necrobiosis of the cell. This last theory is plausible, but it does not apply to the fatty degenera- tion seen in retrograde changes, such as occur in the parturient or athletic heart and in adherent pericardium, where the fatty de- generation of certain portions of the cardiac walls appears to be due directly to lack of use ; for when certain fibres are no longer needed thev are pretty sure to degenerate and eventually disappear. So much for the theories of the production of fatty degeneration. Accepting the dicta of Hayem. Romberg and Huchard, the acute stage is essentially a fatty one ; that is, so far as the acute softening in typhoid, scarlatina and diphtheria is concerned. Fat deposition or accumulation, in the heart, the fat heart of obesity, is quite another condition etiologically and pathologically. Fat accumulates in the connective or interstitial tissues lying be- tween the muscle-bundles. It is the result of overfeeding either with fattv food, or anv food material that is in excess of bodilv re- " Huchard, Ph.iJa. Med. Times, March 24, igoo. 128 Fatty Degeneration of the Heart qiiircmonts : but clinically the two processes are to some extent al- lied, for the muscle-tissue may sutier atrophy in the fat heart from pressure of tlie fat tissues ; or the fibres may be so separated or over- stretched that their intes;rity is impairetl, and thev will degenerate in consequence. . i-'at ileposition antl fatty degeneration may, there- fore, coexist in the same heart ; and yet while fat deposition is apt to cause fatty degeneration, fatty degeneration never causes fat depo- sition. To the naked e_\e there is little difhculty in recognizing fatty degeneration in the heart-muscle b\- its pale yellow color, well shown beneath the lining membrane of the left ventricle or papillary mus- cles, in nearly every heart in which there is chronic valvular dis- ease; but the eye will often fail to recognize it in the softened heart of typhoid fever or diphtheria, for the tissue will not be yellow, but of a muddy, brown color ; or, if there is a fibroid element, the color may be violet-brown or violet. It occurs in localized areas present- ing a mottled appearance ; or is difi;use and the special area of soft- ening "mushy." so that in handling the heart the fingers sink into it. The left ventricle is chiefiy afi'ected, at first. Fatt\- degeneration taken in the broad sense that I have indicated nmst be ((uite frequent. Roemer, of Tubingen, between 1870 and 1890, saw at his clinic 291 cases of valve lesions, in which 230 show'ed symptoms of disturbed compensation, while at the same time there were 2t,^ cases that he called myopathic heart-failure, with- out an\- lesions of the valves. Now, as most of these 234 cases were probably instances of fatty degeneration, heart-failure without valve lesions was about as common as heart-failure with valve lesions.'" Chronic fatt_\- degeneration of the heart is usually asso- ciated with cardiac hypertrophy, atrophy, fibroid disease, fatty depo- sition, chronic endo- and pericarditis, and some other cardiac or arterial disease. For example, Ouain found hardening or calcifi- cation of the coronary arteries in 13 out of t,t, cases of fatty degen- eration ; ]\larkham in one out of 12 (Whittaker) ; so that arterio- sclerosis may be regarded as one of the causes of fatty degeneration. It is an unfortunate idea prevailing in some quarters that coronary disease has a preponderating etiological connection with fatty de- generation. This is not true, though it is not at all uncommon for me to have a case of fatt\- degeneration turned over to me with the label "coronarv disease." With some physicians, I might also add, "Whittaker. Tivcnficth Crnlitry Practice. Vol. TV. p. 340. Fatty Degeneration of the Heart 129 the term "myocarditis" means fatty degeneration, though tliey are obviously two (Hstinct processes. We usually meet with the chronic variety of fatty degeneration in middle life, though it may of course occur at earlier periods. In 88 cases published by Hayden,^* fatty degeneration was found most commonly between sixty and seventy, less often between forty and fifty years of age. It is extremely important for us to recognize the early or prcnif^ni- tory stage, as bearing both on prophylaxis and treatment. Unfor- tunately this is not always possible. In mild cases the physical signs^ may be absent, for there may not be any appreciable dilatation, andl the physical signs depend on this circumstance. Hence the import- ance of outlining the heart by percussion ; for variations in outline from the standard will, in some degree, indicate whether the right or left ventricle is dilated ; and the position of the apex will aid greatly in determining whether the heart is enlarged. Besides, the impulse at the apex will be more or less feeble, and the pulse will be intermittent and rapid. The sounds of the heart will also be weak. There may not be any murmurs, or, in the absence of valvular disease, there may be systolic murmurs due to muscular insufficiency. If there is hypertrophy of the right ventricle, following dilatation of the left ventricle, there will be an accentuation of the second pulmonary sound. There may also be prrecordial pain or distress and spells of dizzi- ness or fainting. This stage may last a few days, weeks, or months ; or longer, after diphtheria and influenza. A few cases taken from my pathological records while pathologist to the St. Luke's and Presbyterian Hospitals illustrate the subject of fatty degeneration: Ca.se XXXVII. Acute Pericarditis; Empyema; Fatty Degenera- tion of the Heart. — A drinking man, thirty-eight years of age, en- tered the hospital with an empyema, the abscess discharging in the mammary region. Pulse 100; respiration 31 to 36; temperature 102° F. ; dyspnoea, prsecordial pain, cough, mucous expectoration and night-sweats. After battling with the attack for three months the patient died of cardiac failure. At the post-mortem examina- tion, the opposing surfaces of the pericardium were found to be acutely inflamed and "hairy." The pericardial sac contained three ounces of clear serum. The heart was dilated and in a condition of acute softening. Fifteen ounces of purulent fluid were taken from the pleural cavities. This was an example of fatty degeneration Hayden. Dis. of the Heart. Dublin, 1875, p. 66. 130 Fatty Degeneration of the Heart of the heart in the first stage, thie to a conihination of two causes, acute pericarditis and enipyenia. The cardiac syniptnms were not clear, beinq^ obscured by those of the empyema. Case XXXJ'IIJ. y'cllow fczrr; Fatty Degeneration of the Heart. — This ease also" ilhistrates fatty degeneration of the first stage, in a marked manner. M. C. thirt\-t\vo years of age, widow, stewardess, was admitted to the hospital July 25. 1870. with yellow fever. Her illness dated back only five days, when she was taken with frontal headache and general "soreness"" of back and legs. The initial chill was followed l:)y nausea, diarrhoea and fever. Pulse 108. and •weak: temperature 105'^ F. On the ninth (la\- slie vomited dark matter, became delirious and had albumin (50 per cent. b\- volume) ; scanty water. .\.t the post-mortem examination the heart was found to weigh, ten ounces and was soft, flabby and fatty. The valves, however, were free and normal. This fatty condition of the heart liad previously been noted by Dr. H. D. Schmidt, of Xew Orleans, as a characteristic of yellow fever, with at the same time fatty de- generation of other internal organs, including the brain. This case r regard as another instance of fatty degeneration in the first stage. I made the microscopic examination of the heart. In the seco)id stage the signs of a dilated heart are more pro- nounced. The left ventricle may reach to the left nipple or extend Ijeyond it; the right ventricle an inch or more bexond the right bor- '<^ler of the sternum. The apex may be in the fifth, sixth or seventh space. The pulse will usuallv be soft, intermittent and infrequent. There may be. and often is. a lack of harmony lietwecn the heart and pulse-beats. These manifestations are apt to be seen (though not always), in i)ersons who liave ]iassed middle life, and are in- clined to l)e stout, Init are aucemic in ai)i)earance. I'he ape.x beat will be difficult or impossible to locate by pal])ation. There will be dyspnrea and some precardial oppression, with occasional attacks of diz/.iness. Abdominal sxmptoms will always be in evi- dence ; occasionally gastric crises alternating with anginoid attacks. Cyanosis will occur at times. Such ]:)atients will usually be irri- table or whimsical, or nervous about trifles, and always concerned about their health. There will be a disinclination to undertake any- thing new, even to walk, and the gait will be uncertain. Occasion- ally there will be hemorrhages. usuall\ in the form of epistaxes. Lo- cal oedema of face, hands and feet will occur at times. The urine will contain a little albumin, and often a little sugar. This stage ma\' last frrmi two or three, to ten or fifteen or even twentv years. Fatty Degeneration of the Heart 131 depending- largely on the degree of the degeneration and the earc the patient takes of himself. The third stage is ushered in by symptoms that indicate secondary implication of other organs. There may now be pseudo-apoplectic attacks, due to cerebral embolism or thrombosis referable to imper- fect heart-action. Attacks of heart-failure are nu^re frefjuent and more alarming. Albuminuria is more in evidence and less ame- nable to treatment. In fact, sym])toms referable to chronic nephritis are the rule. Gastric disturbances become so pronounced that the patient is afraid to eat for fear of the distress it occasions. Local cedema passes over into general. Thrombosis may be a noteworthy feature. In one of my cases thrombi distending the right external jugular vein were distinctly felt. A low form of meningitis from efifusion at the base may be one of the final events. The mind will be disturbed and there may be, at times, Cheyne-Stokes breathing, though this is not necessarily a sign of immediate dissolution. Un- til stasis occurs in internal organs, however, we should not despair ; but where this takes place, and this condition characterizes the third or final stage, the end cannot be far off. With great care life may be prolonged a few months. Death may occasionally occur, how- ever, not from any of the above causes, but from rupt^irc of the heart. Ouain has seen it in 28 out of 83 cases. This stage is illustrated by the following three cases : Case XXXIX. Syphilis; Chronic Nephritis; Fatty Degeneration of the Heart. — A man, forty-six years of age, entered the hospital with the signs of general syphilis. Fie had cough, jaundice, dyspnoea and swollen feet. A soft systolic murmur was heard at the apex. The patient died fifteen days after admission, of chronic nephritis. At the post-mortem examination the pericardial sac was found to con- tain ten ounces of clear serum, and there were several milk patches on the heart. It weighed eighteen ounces. There were no valve lesions. The liver was large and fatty. ' The kidneys were the seats of chronic nephritis. At the autopsy, the murmur was held to be muscular, and due to fatty degeneration of the heart. Syphilis was pretty certainly the remote cause of the fatty degeneration. Case XL. Arteriosclerosis; Cerebral HccniorrJiagc : Fatty De- generation of the Heart. — The following is another of my cases : A woman, thirty-eight years of age. who said she had suffered from "malaria," was admitted to the hospital with oedema of the lower extremities. She complained of attacks of palpitation, with prse- mrdial pain, tonic spasms and dvspncea. The pulse was intermit- 132 Fatty Degeneration of the Heart tent, and the aortic second sound acceniualed. The patient died of cerebral lictniorrhage. The autopsy disclosed general arterioscle- rosis with chronic diffuse nepliritis. The heart was dilated and soft, but the valves were free and sufficient. The cause of the fatty de- generation in this case with aricrinsclerosis, and the death by cere- bral haMUorrhage illustrates one of the several wa}s in which the end comes at last. Case XLl. .-idiicroit Pcriainiiuni : Fatty Degeneration of Heart. — A woman. sixt}-three years of age, with a history of artic- ular rheumatism, was admitted to the hospital suffering from cough, hemoptysis, dyspnoea and chronic nephritis. She also had a systolic nnirmur over the apex, and over the aortic and pulmonary areas, with accentuation of the second pulmonary sound. She died of cardiac paralysis and chronic nephritis. At the autoi)sy the heart was ft)und to weigh twelve ounces. The valves were free and sufift- cient ; but the cardiac walls were soft and Habb)-, and the cavities of the heart dilated. 1lie heart and pericardium were united by an old adhesive pericarditis. The liver was large and fatty. In this instance we see the fatty degeneration of the heart always found in adherent pericardium, though the toxins of rheumatism may be assumed to have been early factors in causing degeneration, inde- pendently of the pericarditis, which operated, in a purely mechanical manner, to produce the fatty change. This case is another instance of fatty degeneration in the third stage. If, then, we realize that this affection of the cardiac walls is in- cidental to infective diseases, continued fevers, septic or suppurative processes, toxaemias, dyscrasias, hypertrophies and atrophies, we should be on our guard to protect the patient against the inherent damage to the heart resulting from these several conditions. We should thus hope either to prevent a break-down of the cardiac walls, or certainly to postpone it. In infants or young children con- valescing from eruptive or continued fevers we should watch care- fully their "weak hearts." With them rest in bed and minute doses of iron and strychnine, perhaps in conjimction with some malt prep- aration and cod-liver oil or quinine, will usually be sufficient, in uncomplicated cases, provided the diet is carefully regulated, and hurried movements, or any form of muscular strain or nervous ex- citement are avoided. In young people, such as are anremic or tuberculous, gymnastic exercises are appropriate for the intermediate stage, provided they are given under suitable medical direction and are not carried to Fatty Degeneration of the Heart 133 the extreme that is common at the present clay, in gymnasiums and outdoor games. There are plenty of schools for physical instruc- tion, under medical supervision, where those convalescing from ill- ness with weak heart-action can be greatly improved. On the other hand, I cannot too strongly condemn the class exercises of the day, if the patient has heart-weakness or in fact any form of heart-dis- ease. Class work calls for uniform movements, usually rapid, which give few intermissions for breathing; so that it is only suited for those whose hearts are sound. In fact, every case of weak heart should be treated by itself, whether in the young or old, and the exercises should never be car- ried to the point of increasing the rapidity of the heart's action be» yond its normal range, which of course differs with each individual ; for although we have adopted an artificial standard for the rapid- ity of the pulse, one man's normal pulse may be 60 or less, and an- other's 80 perhaps, or more. Systematic exercise of a specially '^ve- scribed variety should be insisted on, because habits of indolence tend to a fatty heart, and will increase the difficulty. In fact, oily matter of any kind should be consumed by muscle work. At the same time, patients should be put on a specially restricted diet. It prevents gaseous distention of the stomach and intestines, which provokes cardiac irregularity. When young or old people have not the strength for ordinary gymnastics they should have resistance exercises, with or without massage. These exercises- are more thorough than massage, and tend to rid the muscle-cells of their granular contents, whether they are toxic or otherwise. But with delicate patients massage and exercises may be too severe a tax on the strength, producing too profound a reaction. The treatment should always have the effect of toning up rather than relaxing the individual. Carbonated baths, of course, are to be used in conjunction with resistance exer- cises, in the intermediate stage of the disease; but baths and exer- cises are of little or no use in the third stage. And yet while they may not do any good, they may not do any harm. Massage, how- ever, is often very grateful. Roemer, quoted by Whittaker,^^' reports that in 234 cases of heart- weakness without valve lesions, where 81 of thern were treated by the mechanico-dietetic improved Nauheim plan, 46 recovered and 17 were improved. But neither exercises nor baths should be instituted, until a careful physical examination of the patient has "Whittaker, Loc cit. 134 Fatty Degeneration of the Heart boon made. If. for oxaniplc. lie is snfieriny from a violent attack of palpitation, rest in bed in a tjuiet room, and a restricted diet, sliouUl be ordered. Milk is excellent if it agrees with the patient. In ordinary cases of fatty dei^eneration the ])atient. if anaemic, should he ])ut on iron: if tul)erculous. on malt preparations and creosote or cod-liver oil: if arteriosclerosis, on the iodides: if rheumatic, on antilithiemic diet aild remedies, in conjunction with the hot-air treat- ment. In the third stage, when all hope of cure by any of the above measures is at an end. and it is merely a question (~>f prolon_t;inf;^ life and alleviating;- sutterinp;, dii^italis is ap])roi)riate, if there is an efTu- t^ion referable to the failing; action of the heart, through inaction of the kidneys. Merck's digitaline (m i/ioo grain doses every few hours). 1 have ft)und excellent: but digitalis should not be continued for more than a week or so at a time, and strichnine should follow it to maintain its effects. Other remedies that are useful in this stage are nitroglycerine, cafifeine, strophanthine and sparteine. Attacks of difficult breathing, if not severe, are relieved by oxygen gas. while sudden attacks of true or false angina are best treated by the nitrites. And yet in the third stage it must be remembered that the degenerate heart has a remark- able capacity for recovery, even without the so-called heart stimu- lants. If given, their action should be constantly watched and they should only be used for the briefest possible period. These remarks are especially applicable to digitalis, strophanthus, scoparius and nux vomica. The prognosis of fatty degeneration varies with the stage, the individual, his environment, and the influence of the disease which has produced it ; for fatty degeneration is not strictly a disease siii generis, but a degenerative process superinduced by a number of diseases. For example, the fatty changes attendant on infective dis- eases of toxixmias should disappear entirely, provided the heart has had rest during the stage of convalescence. On the other hand, if during convalescence the patient has been called upon to do an im- proper amount of physical work, dilatation may ensue and fatty de- generation be produced. In infants and young children fatty changes in the heart incidental to infective diseases, or as sequels of them, are quite common. On the other hand, a moderate amount of fatty degeneration is not inconsistent with an average life ; in fact, there is a certain amount of fatty degeneration in most adult hearts otherwise sound, reflecting probably the methods of life in what Fatly Degeneration of the Heart 135 we call civilized cfjmnmiiitics, where the intellectual rather than the physical parts of our system are most in use. 'Ihis is well shown in the hearts of athletes; for when hypertrophy has been caused by severe training, there seems to be always a certain amount of fatty degeneration coincident with the gradual return of the heart towards its normal size, which retrograde ])rocess takes place when ath- letics are given u]) for the ordinary routine of a business or pro- fessional life. In such cases, however, when the enlarged heart fails to contract to the normal size, we may infer that the delay is owing to some other organic heart affection, such as valvular dis- ease or mechanical injury or an old strain. In the middle period of life, when degenerative changes are the rule, a weak heart may be toned up and restored to a fair degree of soundness by appropriate treatment ; though it is one thing to make an organ sound physiologically and quite another to have it sound pathologically. And yet it is always a triumph of medical art to restore the functions of any organ. In the tinal stage when anasarca supervenes and the kidneys, from hypersemia or structural changes, secrete a lessened amount of urine, containing albumin and granular casts ; and there is transu- dation of fluids into the bronchi, lungs, or chlylopoetic tract, inter- fering with the functions of these organs, the prognosis cannot be favorable. The fatal issue is certainly near at hand and, though the heart may be sustained and the kidneys forced to do better work, it is a struggle in which Nature will eventually triumph most likely by thrombosis or embolism ; perhaps by apoplexy, meningitis or ura?mia. ; Chapter XII. SYPHILIS OF THE HEART. Before Ricord's^ time cardiac syphilis had been recognized, but he was the first to describe it clearly. Shortly afterwards Virchow- confirmed Ricord's statements. A few years later Lancereaux' classified it under four types. But grave doubts were still enter- tained of its existence, and they are only now being successfully overcome, though a great deal has been written on the subject since Ricord's time.'' The instances, however, that are conclusive, from a pathological point of view, have been comparatively rare. The naked-eye appearances in syphilis show nothing that is positively distinctive, if we except gummy tumors, and they arc seldom de- tected. Indeed, so keen an observer as Fagge^' had failed to rec- ognize more than four cases up to 1886, notwithstanding his long pathological service at Guy's Hospital. Only one of them was classed as a gummy tumor, three being fibroid infiltrations of the heart walls. In ni}- own pathological records I have only three cases put down to cardiac syphilis, and am still in some doubt as to their true character. And yet I believe many syphilitic manifestations are overlooked at post-mortem examinations, simply because the naked eye evidences are inconclusive. However, the researches oi Mracek^' and Kundrat, of \"ienna, should set at rest forever the question of the existence of this cardiac lesion, for in 1893 ^^^ published a series of 102 cases in which the evidences were established b}- autopsies. His table indicates the different ways in which he found that s}philis may affect the heart. As taken from the literature, including ten cases of his own, it is as follows: Myocarditis, gummatous l 10 fibrous 9 " gummatous and fibrous 8 Endocarditis 2 Pericarditis i Diseases of vessels 3 ' Ricord, Lettres sur la Syphilis, Paris. 1856, p. 349. ^ Virchow, La Syphilis Constitutionelle, Paris, i860, p. 117. ' Lancereaux, La Syphilis, Paris, 1866, p. 384. * More than a hundred contributions are tn be found in the literature. ' Fagge, Principles and Prac. of Med., 1886, Vol. II, p. 34. * Mracek, Arch. f. Derm. u. Syph. (Ergaenzungshefte), s. 279 u. 237- ; Syphilis of the Heart 137 Myocarditis with or without endocarflitis 15 Peri- and endocarditis i Diseases of myocardial vessels and myocarditis i Diseases of g-ang-lia, etc 11 61 It will be observed that he found gummas in 30, or about 50 per -cent., and as many or most of the other forms may be logically at- tributed to gummas, it follows that the lesion is the one par excel- lence of the disease. This preponderance of gummas points out an- other interesting fact, viz., that the disease is usually a manifestation of late syphilis, indeed, of the third stage. In fact, it may be ex- pected as a late event, perhaps as much as eight to ten years, or even more, after the initial lesion. In rare cases, however, it may occur in childhood and early youth, and is sometimes congenital. In 150 autopsies on infants with he- reditary syphilis Mracek found cardiac syphilis in four. Fischer'^ has also reported a case ; but they are extremely rare. WoUstein, Pathologist of the Babies' Hospital of this city, in her large experi- ence has never seen a single one. As one might suppose, it is more common in the male sex, and is usually seen between the ages of 20 and 40. The gumma varies in size. It is usually found in the ventricles, but may also occur in the auricles, septa or papillary muscles ; or in fact anywdiere in the heart. It is usually multiple, and the nodules, as we commonly recognize them, are from the size of a pea upwards. It may dissolve or break dov/n and discharge into the cavities of the heart or outside ■of it, causing a cardiac aneurism. If cicatrization follows a gum- ma, there will be atrophy of muscle fibres in the adjacent territory; and if there is a general sclerosis extending from the thickened vessels, there will be general atrophy of the muscle. If the gumma is near the periphery of the organ, the sclerosis will extend toward the surface, and may leave a point of thickening (milk patch) there. In the same way valvular deformities may be produced by the deposit of a gumma in the valve. Its dissolution, with subsequent pucker- ing, from loss of substance in the vafve, or a defect due to a gumma in a tendinous chord or papillary muscle, may cause distortion of the valve and incompetence or obstruction, or both. The gumma at first is of a pearly gray color, and enclosed in a pretty firm fibrous capsule. If haemorrhage ensues, it becomes red ^Fischer, Mucnchner Med. JVoch.. 1904, 51, s. 652. 138 Syphilis of the Heart or yellowisli. proxidoJ it iinderg'oes change or lircaks down and di>char>jcs. Indcr these circumstances, the central material is fatty or sticky, the latter when it undergoes a mucoid rather than a fatty cliaiige. It is this nuicoid suhstance which sticks to the fingers and gives its name to the gummy tumor. V'VA whatever the change is. that is. whether it undergoes absorp- iion or discharges its contents, the ca])sule contracts, hardens, and a.^sumes a wliitish color; and it" the material has l)een discharged fiom the center, it leaves a depression, looking like a depressed cica- trix, from which bands of fibrous tissue radiate outwards ; while the center is apt to be stained of a yellow color. j'li general these jieculiar changes depend on larger or smaller gummv tumors, originating in the walls of the vessels and spread- mg thioiighout the organ, along the line of the vascular network. The process appears to be originally an arteritis, wdiich begins in the substance of the vessel or its periphery. It is an axiom that syphilis loves arteries, so that, in general, to them, rather than else- where, we must look for the original focus of the syphilitic mani- festation. It follows from all this, that gummv tumors and even aneurisms are apt to be multiple ; but, as already saitl, the difficulty of recog- ni/ing any of these conditions, except the gummy tumor or the fibroid infiltration immediately connected with it, is very great, so th.it endocarditis, pericarditis or myocarditis occurring in syphilis, and aj- seen at autopsies, is likely to be attributed to anything but the constitutional disease. In fact, the problem of determining whether any fibroid infil- tiation, unless connected with a gummy tumor, is really syphilitic is to my mind ])ractically unsolved at the present time. Another reason for failure in recognizing cardiac syphilis, clinically, is that it is ovc of the latest phenomena of syphilis, occurring many years after all external manifestations of the disease have disappeared. Neitlier physician nor patient may have any suspicion of it. In fact. Weber's^ cases go to prove that the cardiac lesion may occur so long after every external sign has gone that nothing except specific treatment w-ill reveal its true nature. In many cases of heart syph- ilis we naturally expect t(j find sclerosis of the coronary arteries or their branches, for we know that syphilis is a common cause of ar- teriosclerosis, and the most frequent one of aneurism. We must be careful, however, not to impute all coronary diseases to syphilis. It is true that these affections are often associated with syphilis. Weber, Post-Craduaic, Nov., 1903. Syphilis of the Heart 139 Thefe are, of course, other causes of sclerosis. Syphilis may also affect the nerves and ganglia of the heart, as microscopic examina- tions have shown. The diagnosis, in any instance, is mainly based on a previous his- tory of syphilis, usually in a patient who has been treated according to the regulation methods with both iodides and mercurials, until the manifestations have disappeared, so that there are no visible or palpable signs of the disease remaining. In fact, it may have lain dormant ten, twenty, thirty or more years, according to Weber's experience. Some of the signs are as follows : Arteriosclerosis, a weak, intermittent and perhaps frequent pulse, dilated heart or an- gina, disease of the aorta, possibly aneurism, occasionally a valvular disease. If, in such instances, a course of iodides and mercurials greatly ameliorates or relieves the symptoms, and other possible causes of cardiac affections are excluded, the diagnosis is practically made. The late Dr. Whittaker.-' in an excellent article on this subject, tells us how he made a diagnosis under these circumstances and ciired his patient. The following is an illustrative case from my records : Case XLII. Syphilis; Tubercular Phthisis; Locomotor Ataxia; Mitral Disease. — Mr. A., married and about 35 years of age, con- sulted me first in February, 1897. He had contracted syphilis about seven or eight years earlier. I found him weak, emaciated and ataxic, walking with great difficulty and hardly able to get up or down stairs. Pulse hard and frequent, 125 — 130. Respiration 20. Temperature rising daily to 101° F., and more. Cough and abundant muco-purulent expectoration ; occasional bacillus of phthisis in spu- tum. Physical examination showed cavities in both lungs and a dilated heart. Apex in 6th space, and outside of nipple. Mitral regurgitant murmur carried to axilla. Patient had been taking digitalis daily, under medical advice, but it was stopped at once. Un- der treatment by iodides and hydriodic acid he improved so much that a modified series of baths and exercises were given him (Xau- heim plan), with electricity. Later he was kept on mercurials and iodides for a period of two years, during which he had no heart stimulants. Under this treatment the lightning pains disappeared, and he gained in health and strength to such an extent that in the autumn of 1897 he was able to resume his business, continuing at it, with only occasional interruptions, up to the date of his last illness in March of 1899. At that time he was taken down with an * Whittaker, Tzveniieth Century Med., Vol. IV.. p. 369. I40 Syphilis of the Heart attack of acute gastritis, to which he succunibed after a few days' iUness. The attack was superinduced by causes tliat were appar- ently in no way related to the specific disease or cardiac manifesta- tions. Whether in this instance the endocarditis was syphilitic or not I do not know. So far as my records go, it was, except for tuberculosis, the only predisposing cause of which I was aware. Without the anti-sypliilitic treatment the patient was unable to attend to his business, but under the alternate use of both iodides and mercurials, more especially the latter, he led a fairly active life. In this connection it is interesting to know that Schuster/" of Nau- heim, and others have noticed the connection between tabes dor- salis and heart syphilis. I have now under m\' care two gentlemen, one a physician, who have both had tertiary s^piiilis and have been treated for it, one by a well-known practitioner. In neither case did the Xauheim method give the usual relief until the patients were put on specific treatment, when the improvement was comparatively rapid. We are told by Huchard^^ that aiigi)ia pectoris is a most im- portant sign of cardiac syphilis. In no cases collected by him, 32 had a syphilitic history. If it is true that angina is essentially a dis- ease of the coronary arteries, judging b}- analogy, syphilis, which predisposes to coronary disease, should be an important cause of an- gina. The therapeutic inference is obvious. Case XLIII. Syphilis; Cirrhosis; Fatty Degeneration of the Heart. — The following is one of my hospital cases of general syph- ilis, with fatty degeneration of the heart, in which syphilis figures as the only predisposing cause : A man of 46 entered the hospital with swollen feet, cough, jaundice and dyspnoea. A soft systolic bruit was heard at the apex. The heart was found to be enlarged. At the post-mortem examination the pericardial .sac was seen to contain ID ounces of clear serum, and there were several milk patches on the heart. There were no valvular lesions. The liver was cirrhotic and there was chronic diflFuse nephritis. At the autopsy the murmur was attributed to the fatty degeneration of the heart. It is in cases like these where the cardiac lesions are possibly due to syphilis, that we still lack conclusive proof. It is to be hoped that we may soon have some method, chemical or biological, by which syphilis can be recognized at any stage. It is not unlikely that the milk patches in this instance were continuous with syphilitic sclerosis of the heart walls. The occurrence of syphilis as a factor in heart disease is probably "' Schuster, Deutsch. Med., Woch.. Oct. 8, 1903. V ' " Loc. Cit., p. 798. Syphilis of the Heart 141 not only more frequent tlian has been sujjposed, but the actual cause of death in many instances. Runeberg's^' statistics, which have been widely read, indicate this : He found in the experience of a single life insurance company that out of 734 deaths, at least 84, or about 11 per cent., were of persons who had contracted syphilis. Twenty- two of these deaths were attributed to progressive paralysis, and 33 to disease of the central circulatory system (that is, of the heart and aorta ) , 24 of the latter dying of syncope ; so that the danger of death from a syphilitic heart or aorta was greater than from syphilitic' disease of the central nerve system, and sudden death was tlie rule. In looking over my private cardiac cases I find that syphilis was positively present in about 5 per cent., and probably in another 5 per cent. : the inference being that in cardiac disease we should sus- pect that syphilis is a factor in at least 10 per cent. The prognosis is bad, but not altogether so. If the diagnosis can be made early and the proper treatment instituted, some success may be expected. Even in advanced cases where, for example, there is tabes dorsalis, improvement can sometimes be effected, as is shown in Case No. XLII. Yet, notwithstanding that we may be able to remove the deposits by medicine, a something will remain, so that if the part resumes its physiological activity it still may not be sound pathologically. We are obliged to conclude, therefore, that cardiac syphilis is more common that has been supposed. Like syphilis of the lungs, it exists, and the physician who fails to appreciate either of them falls short of his duties as a practitioner of medicine. In fact, neither heart nor lungs should be examined without always holding in view the possibility of syphilis, as the cause of the disease. Where it may not be possible to make a positive diagnosis, a probable one can often be reached. Appropriate treatment will confirm it. Car- diac syphilis is an insidious disease, and its manifestations are neither pronounced nor distinctive. For this very reason physicians in making inquiries and in physical examinations should pay partic- ular attention to the subject of syphilis. A cure may be possible, while relief is probable.. Iodides and mercurials are the proper remedies, but mercury is the sheet anchor. Sometimes both of them must be given for months and even years, with brief interruptions of a few weeks or so. If in such cases the physician fails to rec- ognize the existence of syphilis, he should not be surprised if his pa- tient is carried off. without warning, from sudden heart failure. Rnneberg, Dcutscb. Med. JVoch.. i 11. 2, 1903. CiiArrtK XIII. nisiM.ACi-:Mi-:\'rs oi- Tin- iii:.\irr. DisplaccnieiUs eit ihc heart arc indicated in a general way by the position of the apex beat. This, in the well developed adult (in the standing- position, with respiration suspended) is about 3"^ inches from the median line and in the 5th left intercostal space. More accu- rately, however, under similar conditions antl in the male it lies mid- way between the nijiple and the tip of the xiphoid ai)pendix, and the distance of lyS to 2 inches inside the nipple line. In persons of slight build the apex may he sical and subjective phenomena, and yet the one or the other, or both, may be absent. This statement may help to explain why my experience tells me that in thoracic and abdominal aneurisms the diagnosis is made only in a little more than 25 per cent, of the cases. In the diagnosis of a thoracic or abdominal aneurism we first think of a pulsating tumor. If the orifice leading into the sac were large, the walls thin, and the contents only liquid blood, we should more often feel the abnormal pulsation. The opening, however, mav be small and the contents largely composed of clotted or laminated blood. Perhaps the sac is so deep down in the tissues as not be reached by any kind of palpation. In such instances, we recognize neither pulsation nor heaving impulse. If, however, the sac, in a thoracic aneurism, for example, reaches the level of the intercostal cartilages, the episternal notch or the ribs, pulsation may be felt. When the sac is large, it may be mapped out by percussion. or bv the X-ray. I successfully accomplished this by the latter method in a thoracic aneurism brought to my notice by Dr. Katzen- bach of this city as early as 1897. In this instance the aneurism was probablv filled with more or less laminated fibrin, which gave the shadow. Aneurisms are most frequently found in the arch of the aorta, and I think it best to consider this class together, whether they pro- ceed from the ascending, transverse or descending portion, because it is practically impossible infra vitam to distinguish just where they originated. The symptoms, being due to pressure, can not be True Aneurisms 253 referred to the vessel, but to the sac, and the latter may assume any position in the thorax, that is, it may project to the right or left, upwards or downwards, forwards or backwards. Still it is true, taking the sum total of signs in a number of these aneurisms, in the several divisions of the arch, there will be certain symptoms more apt to be specially connected with each division, as will be shown. In general, if the sac compress the superior vena cava, there will be enlargement of the veins of the head and neck ; if the inferior vena cava, oedema of the lower extremities. If the sac press on the trachea, it may produce cough and dyspnoea, and even suffocation, as in Case No. LXXXV ; if on the right pulmonary artery, embolism may follow. If the recurrent laryngeal is pressed on, there may be hoarseness or difficulty in phonation. Compression of the oesoph- agus will cause dysphagia ; pressure on the vertebra, erosion of the spine. Rupture may take place into the oesophagus, peritoneum, pericardium, superior vena cava, trachea or bronchi, etc. Very oc- casionally an aneurism bursts externally. If there is a large thoracic tumor, there will generally be displacement of the heart. A small aneurism may give rise to a diastolic or systolic murmur, or both, and yet, at times, it may be impossible to distinguish these murmurs from the valvular. However, the murmurs are usually louder than the latter. The sternum may, in advanced cases, be eroded and pushed forward, making a tender and painful tumor. The hand pressed on it may detect a thrill, or perhaps a pulsation. Separation of the fingers placed over the pulsating area may show its expansile character. Usually the pulsation is to the right of the sternum. If the sac has solid or semi-solid contents, there will, of course, be no expansion. The sac may also press on the thoracic duct. The in- nominate or left carotid, or sub-clavian, ma}^ be involved in the tumor. There may be pain from pressure on the cardiac plexus, on the nerves of the pleura, pericardium or skin. Pressure on the branches of the sympathetic causes inequality of the pupils, as seen in Case No. LXXXIII, pressure on the pneumo-gastric, spasm of the oesophagus and vomiting. If there is pressure on a bronchus there may be catarrh of the mucous membranes, with retention of the secretions and broncho-pneumonia that will cause death. Pressure on the innominate or sub-clavian artery \vill necessarily produce some effect on the pulse of the affected side, and this is a valuable sign. Pressure on the innominate vein may produce venous congestion of the side of the head. There may be compression, ob- struction and obliteration of the pulmonary artery. An important 254 True Aneurisms sign of aneurism in this kication is thought by some to be "tracheal fugging. This is produced in the following way: let the patient stand and raise his chin to the farthest extent, then seize the cricoid cartilage between finger and thumb and raise it gently ; if there is an aneurism of the arch, the pulsation of the aorta may possibly be transmitted through the trachea to the fingers.^ This should be an early sign, but it does not appear to be very reliable. Grimshaw found it in i6 per cent, of persons who had no aneurism. There may be or may not be cardiac hypertrophy. A laryngeal examina- tion is important, as it may reveal paresis of a vocal chord. If there is any weakness of the chord, it will be indicated in uttering the exclamation "Ah." Paroxysmal attacks of dyspnoea are attributable to paresis of the pneumo-gastric. Bronchorrhoea and suppuration of the lungs ma}- also be due to paresis of this nerve. These signs may occur when there is even a small aneurism of the aorta, and such aneurisms are often fatal. The pain may be ver)- intense. Small aneurisms of the transverse portion, where the tumor is no larger than a hen's egg. are common, and the diagnosis may sometimes be made by an experienced clinician, from a due consideration of all the signs physical and rational, as Case LXXXIII. shows. When the tumor is the size of one's fist, percussion should indi- cate its locality, but I have known a thoracic aneurism ten inches in diameter to escape the notice of a careful practitioner. A loud murmur indicates a small opening, and vice versa. In one of my cases the sound resembled the strokes of a locomotive piston. In such cases we ma}' distinguish these murmurs from those of the heart. According to Douglas Powell, however, in about one-half the cases there is no murmur in thoracic aneurism. In seven of my cases murmurs occurred in but two. The bruit may perhaps be best heard by opening the mouth and introducing the stethoscope between the teeth. The heart is pretty sure to be hypertrophied and sometimes displaced, while valvular lesions will often be a complica- tion and the diagnosis difficult. The following cases are taken from my records during the period when I was pathologist to the St. Luke's and Presbyterian Hospitals of this city: Case LXXXII. Aortic Disease; Aneurism of the Ascending Portion of the Arch; Syphilis; Death from Heart Failure. Ten- dency to Spontaneous Cure. — M., 38, a painter, was admitted to hospital January 10, 1883, with a history of syphilis, and complain- ' Oliver. True Aneurisms 255 ing of soreness over the Unver ])art of his chest. On pliysical ex- amination an aortic regurgitant murmur was recognized. The patient died after a short stay in hospital, during a sudden attack of dyspncea lasting only 25 minutes. At the post-mortem examination there was found to be both aortic regurgitation and stenosis, and the cause of death was at- tributed to heart failure ; but there was also a sacculated aneurism about the size of a hen's egg above the aortic valves. The sac lay partly under the root of the right lung, where it had caused much irritation, leading to deposits of fibrin, which had prevented rupture. Gummy tumors were found in the liver. This case is a good illus- tration of the fact that a thoracic aneurism in this locality up to the size of a hen's egg is seldom diagnosticated, even by the best clini- cians. In aneurism of the transverse portion of the arch, there is a wide range of pressure symptoms, but, as a rule, they are not so marked as in aneurism of the ascending portion. Case LXXXIII. Broncho-Pnciunonia; Chronic Diffuse Ne- phritis; Aneurism of the Transverse Part of the Arch; Death Due to Pneumonia and Chronic Diffuse Nephritis. — R., 38, painter, was admitted to hospital September 28, 1885, with a previous history of gonorrhoea and alcoholism. He complained of pain beneath the sternum, cough and expectoration, dyspncea and vomiting. Pulse 120 and weak. On examination, signs of broncho-pneumonia were noted in both lungs, with enlargement of superficial veins over anterior portion of the chest. Stridor and orthopnoea supervened, with ursemia. Dilata- tion of left pupil. An aneurism of the arch was diagnosticated. The patient was put on the iodides, but succumbed in less than ten days, during an attack of dyspnoea. At the post-mortem examination a sacculated aneurism the size of a hen's egg was found projecting from the posterior portion of the transverse arch, just beneath the origin of the innominate, the opening into the sac being only three- eighths of an inch in diameter. The sac had pressed on the trachea, the right side more especially, eroding its rings. Both lungs had deposits that looked like gummas. The sac had not ruptured. The cause of death was ascribed to the broncho-pneumonia, which may have been due to retained bronchial secretion, to paresis of the pneumo-gastric, or to chronic diffuse nephritis, of which there was ample post-mortem evidence. This case is remarkable in that, with so few signs, this small aneurism was made out during life. The 256 True Aneurisms diagnosis was based on the tracheal ini]:)lication, broncho-pneumonia, and uneven dilation of pupils, backed by a syphilitic history. Case LXXXIV. Aneurism of the Transverse Portion of the Arch, Rupture of the Sac; Internal Hemorrhage. — J., 40, France, agent, was admitted to hospital July 31, 1883. with symptoms of dysphagia, dyspncea and difficulty in retaining food. Suspicious looking ulcer on legs. Pulse, 132. temp. 98. resp. 32. Patient died four days after admission in a suffocative attack, which lasted about an hour and a half. At the post-mortem examination it was found that an aneurismal sac had developed from the superior and posterior aspect of the transverse part of the arch, the innominate and left common carotid being involved. The sac had pressed on the trachea and oesophagus, and there was in it an orifice 1x3^ inches in diameter leading from the sac. The stomach contained about 40 ounces of blood with clots. In this instance no diagnosis was made during life. Death was due to internal hemorrhage. Case LXXXV. Ajiairism of the Descending Part of the Arch; Death by Strangulafioi from Pressure on the Trachea. — A male of 27, saddler by occupation, entered the hospital Nov. 2, 1882. He had a cough, dyspnoea, paroxysmal asthma, and tracheal ob- struction, with cyanosis. Respiration stridulous, rough and pro- longed. A prominent sternum complicated the diagnosis, and led to the suspicion of enlarged mediastinal glands. The only relief ob- tained was from the inhalation of oxygen. At the post-mortem examination there was found an aneurismal sac the size of a pullet's tg^, given off from the upper and posterior part of the descending aorta, the left common carotid and left sub- clavian being also involved. The lower margin of the sac had com- pressed the trachea, causing the embarrassed respiration. The aneurism was not recognized during life. Cause of death, strangu- lation. In aneurism of the descending arch, pain is a most prominent symptom. The pressure signs are less noteworthy. There is some- times a severe burning or aching pain near the spine in the entire scapular region. There may also be intercostal neuralgia. The sac mav press on the left bronchus, which may obliterate the pulse in the abdominal aorta, or delay pulsation in the arteries of the lower extremities. The sac mav erode and destroy portions of the ribs and eat away the bodies of several dorsal vertebrae. One of the most con- True Aneurisms 257 stant signs in disease of this part of the arch is severe pain, striking through from the third left interspace or fourth rib to the body of the scapula. Other signs are cough, paroxysmal asthma, dulness on percussion, evidences of pressure on the trachea, and possibly pain in the epigastrium. There is usually a fixed pain, occasionally a pul- sation in the scapular or epigastric region. The left chest wall may be expanded. CASE LXXXVI. Aneurism of the Descending Part of the Arch; Death due to Urccmia. — A laborer, 34, entered the hospital June 8, 1878, complaining of a pain in the back, that had lasted a year. He also had epigastric pain, tenderness in the lumbar region, tumidity of the abdomen, and mucous evacuations. He died of urjemia. At the post-mortem examination a large aneurismal sac five inches in greatest diameter, and extending upwards six inches, was found behind the descending arch. It was adherent to the body of the fourth dorsal vertebra, and had destroyed the bodies of the tenth and eleventh dorsals. The necks of the ninths tenth and eleventh ribs were eroded. No positive diagnosis appears to have been made during life. The aneurismal sac was pretty well filled with laminated fibrine and had not ruptured. Even in this case of a large aneurism the tendency to spontaneous cure was noteworthy. Case LXXXVII. Aneurism of the Descending Arch; Rupture into the Trachea; Death from Internal Hemorrhage. — A male of 46 was admitted to the hospital on September 19, 1872, with the following symptoms and physical signs : Cough, expectoration, pul- monary emphysema, flatness over left side down to fourth rib. Below fourth rib, resonance with loud blowing sound. Bronchial breathing. Heart hypertrophied and beating tumultuously. No valvular murmurs. No emaciation. These physical signs were attributed to phthisis. The patient died of internal hemorrhage and at the post-mortem examination the following facts were disclosed. The upper part of the left pleural cavity was occupied by an aneurismal sac the size of one's closed fist. It sprang from the inner and descending part of the arch and grew backwards. Rupture of the sac into the trachea had taken place. The left lung was crowded down by the sac. and that portion nearest the latter contained puriform liquid. Diagnosis not made. Sometimes aneurisms of the thoracic aorta may develop below 258 True Aneurisms tiic arch. They are apt to be of large size, and erode dorsal verte- brae, as the following case indicates. Case LXXXFIII. Aneurism of the Descending Thoracic Aorta; Death frvni Internal Hemorrhage. — A glass cutter, aged 41, was ad- mitted to the hospital Aiay i, 1879. He stated that a pain about his heart had kept him from work. There was also pain to the inside of the left scapula.. Insomnia. Patient unable to lie on left side. Lower part of chest expanded. On examination, a pulsation was seen and felt at the lower and inner margin of the left scapula. At this point there was a double murmur. The patient died of internal hemorrhage. At the post-mortem examination it was found that a large aneurismal sac had developed from the upper part of the descending aorta and had ruptured at the lower and posterior portion. It con- tained 90 ounces of serum and clots, and had eroded the bodies of the fifth, sixth, seventh and eighth dorsal vertebrae ; also the fifth, sixth and seventh ribs, cutting the latter in two. Aneurisms of the abdominal aorta are usually just below the diaphragm, near the coeliac axis, and above the superior mesenteric artery. The sac may project in any direction. If it push forward, pulsation may be felt below the ensiform cartilage, usually to the left of the median line. Palpation will detect it if there is any ex- pansile pulsation. In these aneurisms, however, such pulsation is not always present. Or if there is pulsation, it may come from a tumor beneath the vessel or above it. Besides, pulsation of the abdominal aorta is very common in nervous people with vaso-motor disturbances. If the tumor projects upwards it may attain considerable size without being detected. The chief symptoms are subjective. Pains of an annoying character referred to the spine may radiate into the chest or down through the abdomen, but they may be intermittent. The sac may displace the internal organs, such as the kidneys. It ma\- press on the common bile duct, or on the cseliac axis and its branches. Small aneurisms sometimes form on the branches of the abdominal aorta, the splenic, superior mesenteric and hepatic arteries. Sometimes the superior mesenteric is obstructed by embolism or thrombosis, and hemorrhage and infarction of the intestines may be the result. The chief symptom is pain or numbness. It may be referred to the back or front. Uusually there is a fixed pain in the epigastric region. Inspection shows a rounded tumor that may have an expansile True Aneurisms 259 pulsation and ilirill. Auscultation gives a diastolic or systolic mur- mur, or both. The femoral and radial pulses may be delayed. Pulsating tumors of the stomach, liver or pancreas are mobile, and the pulsation disappears to a considerable extent when the patient is put into the knee-elbow position. Case LXXXIX. Aneurism of the Abdominal Aorta; Rupture into the Retro-Peritoneal Region. — A male of 25, addicted to alcohol, with a probable history of syphilis, was admitted to hospital October 4, 1876, with the following symptoms : Dulness in the small of the back, a sense of heaviness on both sides. Flying pains about the body. Pain in the left thigh extending to ankle. Pulsation in left lumbar region, and in the middle of the abdominal cavity. Thrill and bruit below the ensiform cartilage, and over the lower dorsal spines. The diagnosis was correctly made. At the post-mortem examination it was found that the aneuris- mal sac extended from the last dorsal to the last lumbar vertebra. Its dimensions were 7x43^ inches, and it had an hour glass con- striction at the center. The opening from the aorta was just below the cteliac axis. The body of the last dorsal vertebra was eroded. The escaped blood formed a tumor the size of a child's head behind the peritoneum. Possibly a spiculum from the eroded vertebra tore open the sac. Case XC. Aneurism of Abdominal Aorta; Rupture into the Peritoneum. Death froifi Internal Hcemorrhage. — A male of 40 entered the hospital December i, 1882, complaining of pain in the epigastrium, right hyperchondrium, both groins and stomach, for which he was taking opiates. His urine and stools were dark colored. On examination, a pulsating tumor was found in the epigastrium. Death occurred from, rupture of the aneurismal sac into the peritoneum. The sac itself was only two inches in diameter. It sprang from the front of the aorta and involved the caeliac axis and superior mesenteric artery. The rupture took place just above the level of the pancreas. Four ounces of blood-clot, and four of bloody serum, were found in the peritoneal cavity. As the sac was small, the symptoms prior to rupture were not pronounced. Case XCI. Aneurism of the Abdominal Aorta. Death from Internal Hcemorrhage. — A male of 47, car driver, was admitted to hospital January 27, 1887, with a bubo and gonorrhoea. He de- scribed himself as a moderate drinker. Shooting pains down the thighs, legs and in the abdominal cavity were ascribed bv him to a severe cold bought on by exposure to cold and wet. The pain in 2C)0 True Aneurisms tlie lower extremities was found to be contincd to the left sciatic and crural nerves. The patient died of internal hemorrhage, and at the post-mortem it was found that a small sacculated aneurism, rising from the anterior surface of the abdominal aorta, just below the coeliac axis, had eroded the underlying vertebra and that a spicu- lum of bone had lacerated the sac. causing internal hemorrhage and death. Nodules resembling gummas were found in the lungs. There were also copper-colored scars on the legs. Aneurisms of the pulmonary artery are comparatively rare, and in half the cases, are probably associated with congenital disease. On the other hand, aneurism of the branches of the artery are com- mon, if we include under this name the minute aneurisms found in tuberculosis phthisis. Rupture of these aneurisms in phthisis often causes death from hemorrhage. The aneurism begins as a peri- arteritis and endarteritis. This matter does not interest us at present. Generally, dilatations of the pulmonary artery are due to obstruction of the branches of this vessel, or constriction at their orifices. This latter is very rare. The following is an example of the latent variety. Case XCII. Aiiciirisiii of the Puliiionary Artery. Death from Embolism. — C. A., widow of 50, entered the hospital August 4, 1881, with a history of rheumatism, anaemia and cyanosis. She was also found to have dyspnoea and oedema of the extremities. Pulse weak, irregular, intermitting every fourth beat. Heart enlarged. Loud blowing murmur at the base, and diffused over nearly all the precordial space, but most distinct between nipple and sternum. First sound rough. Ths patient died suddenly. At the post-mortem examination the pulmonary artery, witli its right and left branches, was found considerably dilated. On the right pulmonary was an aneurismal sac the size of a duck's tgg, with solid contents. On the left pulmonary, at a corresponding point, was another aneurism of about the same size. The cause of death was supposed to have been embolism in one of the pulmonary arteries, by w^hich the blood was rapidly dammed back on the heart. In thoracic and abdominal aneurisms I am disposed to think, from my experience, that surgery has been unsuccessful, and that, distal pressure, ligation, introduction of foreign bodies like wire, injection of fluids, as the perchloride of iron, application of electric- ity, or compresses, achieve but temporary, if any, improvement, while medical remedies offer far better hopes for the unfortunate patient. Of all considerations to my mind, the first is rest; the second is True Aneurisms 261 restriction in food and drink; the third, a cardiac sedative. Our ob- ject is to coagulate the blood, remembering that this is the remedy adopted by nature in curing aneurisms, which, as Case No. LXXV. shows, may be cured spontaneously if the tumors are small. First in importance is rest in the recumbent position. It causes relaxation of the sac, and favors slow coagulation, which may lead to solidifica- tion of the fibrine in layers. Second in importance is diet. The Tufnell method is perfectly legitimate. It is a modification of Val- salva's, who treated his patient by frequent bleedings, and of Bell- ingham's, whose was a mild starvation. Tufnell's method allows the patient, for breakfast, two ounces of milk or cream, and two ounces of wheat bread with butter. For dinner, three ounces of meat, three ounces of potatoes or bread, four ounces of water or claret. For supper, four ounces of bread and two ounces of milk or tea. In all, twelve ounces of solids and eight ounces of liquids are given. Tufnell reported ten cases successfully treated in this way. His ob- ject was to reduce the volume of blood, while the fibrine was in creased. If improvement is attained, it should appear in from four to six weeks. Iodide of potassium or sodium are drugs that may be used. Commence with five grains three times a day and increase to fifteen or twenty ; or iodine in other forms may be used. Stop only when there are symptoms of iodism. The treatment may be continued for months and years. When there is a visible tumor, cold may be applied by means of Letters tubes, part of the bag rest- ing on the aneurism. Apply at intervals, at first, and then continu- ously ; cold tends to relieve the pain and reduce the sac. After a thorough course of two months, the patient may gradually resume his work, if the symptoms warrant it. In the case of a cure, the tumor will remain, but it will shrink into a hard ball. Among the remedies that are useful is aconite in from one to two minims of the tincture, increased gradually to four or five minims every four hours. Digitalis is dangerous ; it may burst an aneurism. Broadbent has reported a case of aortic aneurism that lived ten years, and Hayden a case of abdominal aneurism that lived eleven years. There is, therefore, some encouragement in the medical treatment of aneurism, though aneurisms of large size do not afford us much ground for hope of a cure. The following is a summary of the important points to be re- membered : In the diagnosis of thoracic and abdominal aneurisms, no sisrns 262 True Aneurisms are pathognomonic, but botli subjective and objective phenomena arie to be considered. Success in the treatment of these aneurisms depends on their early recognition, as large aneurisms are pretty surely fatal, either from rupture or pressure. Syphilis, gout and alcoholism are causal factors, so that the importance of combating them cannot be overestimated. Unfortu- nately, physicians do not sufficiently recognize the agency of these conditions, and are apt to be especially unsuccessful in detecting syphilis. The larger aneurisms, whether thoracic or abdominal, have thus far baffled the best efforts of modern surgeons, while medical treat- ment has at least insured a longer lease of life and offers greater chances of cure, if treatment is undertaken early. ClIAl'TKR XXIII. AORTITIS. Most persons have aortic disease after middle life, and many at an earlier period. This much was probably known centuries ago ; for wherever post-mortem examinations were allowed and practised, aortic lesions must have been readily recognized by the naked eye. It is not improbable that they were known before the Christian era. Certainly Galen's presumed contemporary, Aretaeus,^ the Cappa- docian, alluded to them, and he is supposed to have flourished in the second century. Not to mention other medical writers, Mor- gagni- described some phases of them. But up to the time of Scarpa^ they were so little understood that the most characteristic type of chronic aortitis, the cylindrical or fusiform (false aneurism), had not been diiTerentiated from the sacculated or true aneurism. There are two principal division of aortitis, the acute and chronic (known also as the subacute), for there is no pathological or clinical line of distinction that can be profitably drawn between the latter two. So far as etiology and pathology are concerned, these matters are tolerably well understood, but the clinical features of aortitis have elicited sharp discussion since Portal's time (1803), and as regards the acute form, without making much progress. For many, in- deed most, clinicians do not believe that it can be recognized, in any locality, even under the most favorable circumstances intra vitam, independent of traumatism. On the other hand, in some instances, the chronic form, as seen in the ascending arch of the aorta in the variety known as Hodgson's Disease, can sometimes be differentiated with little difficulty, as is shown in Case XCVI. As simple dilata- tion of the aorta may not be inflammatory, it is considered separately. There are two varieties of acute aortitis, the acute primary, where it constitutes the sole inflammatory lesion, and the acute secondary,*" which is invariably associated with the chronic form, as exemplified by such chronic manifestations as fibroid deposits, fatty ^Aretaeus, On the Causes and Symptoms of Acute Disease, London, 1856, Book II, p. 445. (Trans.) ^ Morgagni, On the Seat and Causes of Disease, Vol. I, p. 389. (Trans.) ^ Scarpa, Reflections et Observations Anatomico-chirurg-icales, Paris, 1809, p. I. * Huchard. 264 Aortitis degeneration. artcrioscUrosis. atheroma, or a combination of them. On the other hand, the primary acute form includes infiltration of the walls of a vessel with serum, fibrin or lymphoid corpuscles ; or suppuration, ulceration, formation of granulation tissue, or even gangr'jne ; making it easy to separate it from the chronic form, on a purely pathological basis. The acute secondary form is found only in association with chronic processes, to which it bears the same relation as the acute manifestations of typical rheumatic gout bear to the chronic enlarge- ment of the joints, of which they are part ; for the two processes work together simultaneously within the affected area. Acute aortitis is also occasionally caused by tuberculosis or syphilis, both of which are known to have special affinities for ar- teries. It is also due to infections, such as malignant endocarditis and puerperal fever ; possibly to eruptive fevers, and probably to acute gout or other diatheses or intoxications. It may originate in the walls of the vessel, or be a metastatic deposit, or an extension from adjacent parts, as in pericarditis, possibly in pieuritis or pneumonia. Case XCIII appears from prima facie evidence to be an example of the latter character, though it is not altogether conclusive to my mind. I give it because out of 915 post-mortem examinations of which I have clinical notes, it is the only one I have found. Case XCIII. Articular Rhenmatisni ; Malignant Endocarditis; Ulcer of the Aorta. — R. 56, male, was admitted to hospital May 21, 188 1. Four weeks previously he had his first attack of articular rheumatism, which involved the large joints and left him feeble and scarcely able to stand. Convalescence began in three weeks, but d\ spepsia, headache, epigastric distress and irregular chills, followed by fever and sweating, supervened. There was never at any time oedema, but the urine was scanty and contained a trace of albumin. On examination a double mitral, and later a double aortic mur- mur were detected. Pulse irregular. Ten days after admission pne-r.iior'-' '•' n and caused deatli on the sann^ da; A diagnosis of probable ulcerative endocarditis had been made. At the autopsy, which unfortunately was for some reason delayed and was confined to but a few organs, blood was found in the peri- cardium. For an ulcer had eaten through the substance of the heart from the aortic to the mitral valves, and blood was extravasated beneath the endocardium. There was also an ulcer in the aorta. As old infarcts and puckerings were found in the spleen, it is probable that there had been a benign endocarditis at some time, and that the Aortitis 265 malignant or ulcerative character was a superadded manifestation. This case is obviously incomplete in many ways, but it appears none the less to fall into the category with Andral's single case'' and the four of Lebert/', Spengler/ Schutzenberger,^ and Leudet," respec- tively. In a case of aortic and mitral disease Spengler found a small .abscess, the size of a hazel nut. just above the semi-lunar valves. Schutzenberger also found in his case an abscess the size of a nut at the origin of the aorta, and between the middle and internal coats. There was an associated pericarditis. In Leudet's case, likewise, there was an abscess fthe size of a filbert) between the internal and middle coats, communicating by .an orifice the diameter of a small pea with the lumen of the aorta. In all these instances there were the clinical evidences of a purulent infection. In tuberculosis the aorta may also be the seat of acute or chronic tubercular deposits. A number of such instances have been de- scribed by Blumer.^" Syphilis of the aorta has also been recognized Iby n'jmerous clinicians. So far as the prognosis is concerned, there is always a bare probability that an acute attack may end in recovery. That such an event is possible is shown in Case XCIV, where more or less <:icatnzation was found in the aorta ; but inasmuch as the causes, so far as we know with certainty, are apt to be chronic affections like ■syphilis, tuberculosis and gout, the disease is most likely to assume the chronic form. Even if the acute variety is not purulent, but is represented by an infiltration with fresh plastic matter (the so-called gelatiniform plaques), degeneration will in time occur, ulcers may develop, or plates of atheroma of a bony hardness, so that the acute will pass by slow transition into the subacute or chronic form. Of course, in cases associated with malignant endocarditis, or a purulent infection, a fatal termination is to be expected. Acute aortitis was first brought prominently to the notice of the profession by PortaP^ in 1803, but. as already stated, widely divergent ideas as to its clinical aspects have prevailed about it since "his day. "Andral, Path. Anat., Vol. II, p. 243. " Lebert. Krankhcitcn der Artericn. J^ircho-iv's Path, and Thera., 1867, "Vol. II. s. 347. ' Spengler. Virchoxi-'s Archk:, IX, 1852. s. 166. ' Schutzenberg-er. Archives Generalcs. 1861, II, o. 581. ' Leudet. Archk: Gen. de Med.. Ser. 5. 18, p. 581. 266 Aortitis In 1824 Bertiii and Bouillaiul'- reported sixteen cases, but the changes seen at the autopsies were not typical, and apparently the reddened condition of the aortas, on which they laid so much stress, was due to post-mortem inhibition. Indeed Huchard,^-' a firm believer in acute aortitis as a disease capable of being recognized at the bedside, has accepted only one of these cases as conclusive. In 1837 Bizot^^ published three cases, claiming that the signs were anasarca, intense fever, prostration and delirium, while, as a matter of fact, oedema and delirium have no necessary connection with acute aortitis. His first case was probably one of pericarditis, and the last two of Bright's Disease, which was unknown at that time. These misconceptions, however, were in due time pointed out by Laennec.'^ who showed that inflammation of a vessel w^as to be distinguished from post-mortem inhibition, and that among its characteristics were swelling, thickening and a development of new vessels. In detail the pathological changes are as follows : The signs of inflammation arc, as a rule, seen first in the internal coat, which be- comes reddened, and later takes on a pellucid grayish or grayish- yellow color ; then the inflamed part swells and is raised up above the level of the surrounding tissue. These elevated plaques are soft and have a translucent appearance — whence they are known as gelatbuform plaques — and they may either remain of a gray or yellowish-gray tint or become rose colored. They are infiltrated with serum, fibrine or lymphoid corpuscles, perhaps an admixture of two or more of them ; which accounts for the variations in their color. After the plaques soften, they may fungate and leave ero- sions. The outer coat is eventually involved, the middle coat, which contains clastic plates and fibres and smooth muscle tissue, suffering least. Acute inflammation is in a measure produced bv injuries caus- ing hyperdistension, as in the arch of the aorta, where the full force of the systole is felt ; but even in acute aortitis, as it is seen in the arch, when intense pressure has been brought to bear on the walls of the vessel by violent physical exercise, there is apt to be, and '" Blumer, /int. Journal of the Med. Soc. 1899, n. s. cxvii, pp. 19-25. " Portal. Cours d'Anat. Medicale, Vol. Ill, 1803, p. 144. " Benin and Bouillaud, Treatice des Maladies du Coeiir, et dcs gros vais- seaux. 1824. p. 4. " Hiichard, Maladies du Canr, etc., 1893, p. 445, ct scq. " Bizot, Soc. Med. d'Observ., 1837, p. 332. Aortitis 267 perhaps alwa}'s is, some vice in the circulatory fluid which trans- forms a simple dilatation intfj an af>rtitis with dilatation. While, therefore, there is no doubt that aortitis occurs as a path- ological fact, clinicians have, as stated, been disposed to give it a wide berth. Even Jaccoud"^'' has differecl from many of his confreres of the French school, and stated that there are no symptoms by which the acute can be separated from the chronic form ; while Von Schroetter^" denies that it is an independent disease, with distinctive signs and typical course. Accordmg to Peter,^* the clinical diagnosis turns on palpitation, difficult breathing, local pain, a burning sensation under the sternum and active pulsation of the aorta, but he is unable to distinguish it from angina pectoris. Ouain^'' has made the signs acute substernal pain, with oppression, palpitation, quick and feeble pulse, elevation of temperature and a harsh systolic murmur at the seat of inflam- mation and transmitted up the vessel. Huchard^" says that if the patient has the characteristic dyspnoea, with a substernal sense of burning or tearing, one thinks of aortitis, and if, in addition, the heart is hypertrophied, without much valvular accentuation, and there is a double-bellows murmur, more or less rude in quality, the diag- nosis is easy. To him, however, the acute primary form has three special signs (i) labored breathing, (2) pain, and (3) syncopal at- tacks. Unfortunately, he gives no illustrative case that is satisfac- tory. Certainly in the vast majority of cases the acute stage does not reveal itself by any pathognomonic signs. ^° In the absence of proof, therefore, that acute aortitis is capable of demonstration dur- ing life, it is useless to discuss its treatment. Chronic aortitis is a peculiar affection, combining, as already stated, acute manifestations (the acute secondary of Huchard) and the chronic ; both of them progressing side by side. The causes are diatheses such as gout, or intoxications like lead and alcohol, while hypertension from over-work, perhaps from tobacco, together with senility, are contributing factors. The chronic ma\' supervene on the acute process, itself induced by infections like typhoid or the eruptive fevers. " Whatever causes the inflammation, the net result is that the vessel w^all gets to be thickened, less elastic and less vascularized. The process may involve the orifices of the branches, which are narrowed and stiffened, and if the disease extends become obliter- ated. This sometimes occurs to the orifices of the coronary arteries. The loss of elasticitv in the aorta, infiltration of its wall and narrow- 268 Aortitis ing of the calibre of its branches, inevitably lead to dilatation, unless it is checked by the calcifying process (atheroma). Joseph Hodgson, in his prize essay {Diseases of the Arteries and Veins, London, 1815), appears to have been the first to call attention to the chronic aortitis especially associated with the peculiar dilata- tion of the ascending portion of the arch of the aorta which goes by his name. It is also known as the cylindrical or fusiform aneurism. Hodgson's description of it holds good to-day. He says it is most frequently found in the ascending part of the aorta, the vessel forming a huge pouch, usually commencing just above the semi- lunar valves, but there is no loss of continuity in the vessel ; in fact, it may occupy only one side of the vessel. His subjective signs were dyspnoea, palpitation, syncopal attacks, and copious expectoration of mucus. As an objective sign was the small and intermittent pulse. There are, however, many others. Inasmuch as the disease begins with an endarteritis, there may be a bellows murmur, pain if there is pressure from dilatation, prolongation of systole, and cardiac dilatation. So soon as the aorta is dilated it is also elongated, and the right subclavian is pushed up. If the patient lies on the back and the shoulder is elevated, the dilatation can be felt. By percussion it may be found that the vessel is broadened ; it is normally iy'2. to 2 inches wide in adult males; i to i^^ inches in adult females. In dilatation the right margin of the vessel may be as much as 53^ inches from the median line. The following is an illustrative case : Case XCIV. Chronic Aortitis of the Ascending Aorta; {Hodg- son's Disease), Stenosis and Insufficiency of the Aortic Valves; Chronic Nephritis, and Meningitis. — W.. 64, male, was admitted to hospital July 8. 1882. with a previous history of alcoholism, rheu- matism and privation. He complained in particular of a sense of constriction beneath the sternum, and of cough. His extremities were oedematous. Urine was found to be scanty and albuminous, containing casts of various kinds. Chronic nephritis was a constant feature of the case. On auscultation a double murmur was heard at the base of the heart, which, from the post-mortem findings, may have been " Laennec, Dis. of the Chest, p. 743. 1838. ''Jaccond, Lecons de Clinique, 1884-5, s. 117. "von Schroctter, Nothnagcl's spec. Path. u. Ther., XV, Theil. II. " Peter. Mai. du Cocur, 1883, p. 776. " Quain, Diet, of Medicine, 1&S3. " According to Douglas Powell, in Pepper's System, Vol. Ill, p. 800. Aortitis 269 due to endocarditis of the semilunar valves. Apex in the fifth space and one-half inch outside of the nipple. Among other notevi^orthy symptoms during his illness, vi'hich lasted fourteen weeks, v^ere irregular pulse, syncopal attacks at night, dyspnoea, delirium alter- nating with hebetude, and at the last, coma. At the post-mortem examination there was found an adherent pericardium, and aortic stenosis with insufficiency due to aortic en- docarditis ; while the aorta represented a great variety of changes, from simple inflammation to fatty degeneration, or atheroma, or de- struction of tissue with some attempt at repair. The whole arch was notably dilated and constituted a true fusiform or cylindrical aneurism {Hodgson's Disease). Both kidneys were examples of chronic diffuse nephritis, one being much contracted. There was thought to be slight cirrhosis of the liver. Ascites, Chronic cere- bral meningitis. This case presented several features of interest from the point of view of the aortitis. It was of the chronic form, illustrating the acute manifestations often seen in that affection. The cicatrization also demonstrated that nature can and does effect some sort of cure. But there was no evidence that any of the signs, subjective or objec- tive, belonged to the aortitis, which contributed little if anything to the fatal result. This was due to uraemia, conjoined with meningitis, though the cardiac difficulty may have been a predisposing factor. Even the substernal constriction was relieved by stimulants. It should have increased, if the pain had been due to aortitis. It is not unlikely, however, that the diagnosis could have been made, if special attention had been directed to the matter. Per- cussion would in all probability have disclosed an increased area of dulnss over the aorta; it would have been found that the aortic direct murmur was carried more to the right than usual, while the aortic endocarditis and the elongated heart would have made the dilatation probable or possible in a man sixty-four years of age. Nowadays the X-ray would have shown the dilatation, as it did for me in the following case: Case XCV. Chronic Aortitis; Aortic Endocarditis ; Albu- minuria; Glycosuria; Infrequent Pulse. — R., a retired man of busi- ness, 64 years of age, was referred to me in May, 1899, by his physi- cian, on account of a troublesome epistaxis, ascribed to arterial disease. The subjective symptoms were shortness of breath, occa- sional fainting attacks ; at times pain over the heart, sometimes at the apex, sometimes in the neck or joints. Gouty deposits in the 270 Aortitis finger joints. P\ilse 80, intermittent. Respiration 16. Enlarge- ment of the superficial veins of the chest, especially on the right side. Facies arterio-sclerotica. Double bruit over the aorta. Loud systolic nuirmur with first sound, propagated up the great vessels and with second sound radiating to the right and also down the sternum. No mitral murmur. Heaving impulse. The apex was found just within the nipple and two inches below the intermammillary line. The loud murmur with the first sound at base about corresponded with an area 5 inches in diameter, ex- FiG. 40. tending 2/^2 inches to the right of the median line and 2 inches to the left of it. By fluoroscopy-^ this area threw a somewhat dark ^' Prof. Samuel Lloyd assisted me in making the X-ray picture, which I drew on the fluorescent screen, and on the same day, in sending a copy of my fluorograph to his physician, I wrote : "There appears to be above the heart a tolerably well-defined shadow which corresponds to the aorta, while at this point I find a double bruit. I therefore think there is a dilatation of the aorta, probably with extensive atheroma, and that this condition causes the aortic double sounds primarily." In the year following this condition was depicted by Cabot (Physical Diagnosis, N. Y., 1900, p. 172). Cabot believes that dilatation of the ascending portion of the arch occurs in almost every case of aortic regurgitation. Aortitis 271 shadow, and to my mind indicated a fusiform dilatation of the aorta (ascending portion of the arch), although (see Fig. 40) the shadow was not as dark as 1 have seen it in sacculated aneurism. Examination of the blood showed 95 per cent, of haemoglobin. Daily amount of urine, 24 ounces ; specific gravity, 1025 ; traces of albumin ; sugar, 2 per cent. ; hyaline casts ; urea, 6 grains per ounce. The patient took a course of baths and resistance exercises at Nauheim. On his return he was no longer short-winded, but had occasional shooting pains over the heart. Pulse "^2, one inter- mission instead of four per minute. Respiration 16. Superficial veins of chest not so prominent. Murmur the same, but cardiac enlargement diminished. As the patient contracted a rheumatic at- tack on his return voyage, he was put by me on the hot-air treat- ment and the iodides were given. On January 2, 1901, the examination of the urine was as follows: Specific gravity, 1015 ; amount, 33 ounces; no albumin; no sugar; traces of indican. On March 23, 1901, the patient expressed himself as free from all disagreeable symptoms, although the auscultatory signs were little changed. The X-ray examination was made for the purpose of determining between a true or sacculated aneurism and a dilated aorta. I did not elicit any increased dulness over the dilatation, probably because in percussing, I failed to place the patient in the position with the chest bent downwards. There were no mitral murmurs, but the evidences of aortic stenosis and insufficiency were recognized, as is seen by my notes, and they are confirmed by my colleague. Prof. S. S. Burt. A feature of the case, however, was paroxysms of the infrequent pulse, which varied from 48 to 58 during a great part of the three years and more he was under my care. In the summer of 1903 he passed from under my observation, and I have no subsequent notes of his case. He died in the December following. Percussion may be made directly on the sternum, and if the breadth is found to be greater than the normal we have dilatation. If there is pericarditis it may involve the pericardium, and we may have the signs of dry pericarditis. Pressure on the brachial plexus may also cause atrophy of the corresponding limb, or d3"sphagia may result from pressure on the oesophagus. Again, it is said, the pouch of the aorta may press forward and cause pulsation, seen and felt through the skin in the second right space. A most noteworthv sig-n is aortic insufficiencv, and with it the 2y2 Aortitis "long heart,"' two conditiotis that are very apt to be associated with chronic aortitis. Gueneau de Alussy-- thinks that an important sign is a second cardiac sound heard over the course of the vessels, and metallic or clanging in character, the "chant du crapaud" or "bruit tynipan- u]uc," so-called from its resemblance to the croaking of a frog or the clanging of a drum. According to Paul {Dis. of the Heart, N. Y., 1884) the signs of Hodgson's Disease are: Dyspnoea on etitort ; vertigo due to cerebral anjema ; hard radials ; sinuous arteries. As the aorta does not extend beyond the sternum in health, and is 15 to 20 centimeters below the episternal notch, if the dulness extends beyond these points we have dilatation. Bruit in aorta and large vessels, and over surrounding organs. Un- equal pulse due to obstructive changes in vessels. Dulness over upper part of the sternum and right lung. The bruit may be as much as 4 centimeters from the right border of the sternum. The aorta may be perceptible above the aortic notch. The bruit, which lasts through the entire ventricular systole, may be double when there is a sharp projecting plate, which gives a murmur both in systole and when the blood flows back to close the semilunar valves. As the roughness in the aorta increases, there , is more harshness in the murmurs. The heart now hypertrophies, and the apex may be in the sixth left space. There may be compres- sion of the trachea. Laboulbene {Anat. Path., Paris, 1879, p. 640) gives an additional sign of Hodgson's Disease, namely, the projection upwards of the subclavian as a means of determining the dilatation of the aorta. Sansom (Tzuentieth Century Med., Vol. IV.) gives the following signs : Difficulty of breathing with a sense of weight or constric- tion of the chest, the peculiar respiration being that of a long and painful inspiration with a short expiration. Orthopnoea. Pain of a severe character in the mid-sternum, or radiating to the neck and down the right arm. (Albutt^^ finds this pain may be absent, and he refers it to the root of the aorta.) Other signs given are insomnia, coldness of the extremities, vertigo, dyspepsia. Angina pectoris is apt to be associated. If there is decided prsecordial pain, the patient should rest in bed, while cold applications may be made to the chest. Chloralamid in 20 to 30-grain doses may be given to promote sleep, perhaps an '' Gueneau, de Mussy, Clinique Medicate, Vol. IV, p. 470 et seq. Albutt, Lancet, July 18, 1903. Aortitis 273 opiate for a similar reason, or to relieve pain. The treatment in general is that of arteriosclerosis. Simple dilatation of the aorta, independently of disease of the coats, may occur as a result of obstruction of the vessel in advance of the dilatation, or of violent cardiac action, and is common, accord- ing to Quincke, among men whose work consists of violent mus- cular effort, such as stokers and sledgers. It is due to the resistance offered to the systemic circulation by muscular contraction ; and also to the backward pressure in the distended veins. There is only one place where the dilatation of the aorta can be felt by the fingers, and that is in its abdominal portion, where it may also be seen. Such dilatations may be permanent, but more commonly are of a temporary character, and due to paresis or paralysis of the vaso- constrictors. Chapter XXI\' ARTERIOSCLEROSIS. The lucaniug of the word arteriosclerosis, originally applied to proliferative ami degenerative changes in the aorta and larger vessels, has been gradually expanded in accordance with our increas- ing knowledge, so that now. while it is strictly limited, ctyniologi- cally speaking, to changes in the arteries, it is intended to be de- scriptive of systemic processes that embrace not only arteries, capillaries, and veins, but lymphatics also. IMainly, then, Tlioma was correct in contending that arteriosclerosis is no longer adequate to express this condition of the vessels, which is more properlv an angiosclerosis, if we look at the subject from the broad point of view taken by pathologists. At the same time, there is no reason to abandon the word arteriosclerosis, because both from a pathological and clinical point of view, the changes in the arteries are the most conspicuous incidents of the affection. To be sure, it may not have been demonstrated that angiosclerosis can affect everv organ and tissue of the body, but it is certainly true of the capillaries and small arteries of the pia. retina, kidneys, heart, lungs, spleen, stomach, brain and spinal cord, so that it is probable that no organ, tissue or vessel escapes. In the capillaries and smaller vessels, where the disease appears to originate, the changes consist of infiltration, fatty, calcareous and hyaline changes, with pigmentation, followed by dila- tation, then contraction, perhaps embolism, thrombosis, or even rupture. These changes are less conspicuous in the veins, though they, too, undergo hypertrophy, atrophy and degenerative alteration, certainly in such systemic diseases as gout, syphilis and tuber- culosis ; and all vessels are in a measure similarly though not equally affected. In syphilis and gout, however, the arteries suffer most from the poison. So far as the larger arteries are concerned, the following anatomical facts should be borne in mind. A layer of flattened endothelium cells lines the vessels. External to them is the tunica intima, or true internal coat, composed of networks of elastic tissue arranged longitudinally. These two coats go to make up the internal coat of the older writers. More externally, the middle coat is made up of muscular fibres arranged transversely, together with elastic fibres. Still more external is the outer coat, made up of con- nective tissues. Arteriosclerosis 275 In arteriosclerosis, using the term in its restricted sense, as ap- plied to arteries only, and as the condition is seen by the naked eye, there are three stages into which it can be conveniently divided. Exposing the interior of the vessel, the inner surface is marked here and there, in a somewhat irregular way, by greyish-white or pellucid patches, which appear to be actually adherent to the lining membrane. As a matter of fact, they lie between the tunica intima and media. This is the first stage. The material of which the de- posit is made up is a firm but elastic substance, the result of inflam- mation, and developed from the deeper cells of the tunica intima. The condition is therefore an endarteritis, and Virchow's conten- tion, that it is developed from the tunica intmia, is correct. I>ut this newly formed tissue is not destined to produce healthy tissue in every instance. Like all the results of inflammatory action, it is deficient in vitality, and is soon apt to fall a prey to fatty change ; so that the original whitish or pellucid substance may become yellow, and its consistence pasty. In other words, we have atheroma — the second stage. Now, this atheromatous process once started may continue to extend. At first the endothelial coat resists, while the internal coat ofl^ers less resistance ; but in the end the former gives way, leaving the inner surface of the vessel rough and worm-eaten in appearance — the atheromatous ulcer. On the other hand, while the patch may disintegrate, it may not discharge its contents into the vessels, but may simply dry up and calcify. This is the third stage. The appearances are now dis- tinctive. If in the aorta, plates or spicula of bony hardness, possibly an inch or more in length, may project into the lumen of the vessel. In the larger arteries these plates may take the form of bands encir- cling the vessels. Arteriosclerosis in the second and third stages is quite common in the aorta. Indeed, after middle life there is usually more or less of atheroma or calcareous substance in it, and at this period each of the three stages can often be seen in the aorta of a single person ; the pearly deposits of the first and the bright yellow of the fatty and calcareous deposits of the second and third stages being outlined against the reddened tissue of the normal portion of the vessel. In syphilitics this process may be seen in young persons who have not undergone appropriate treatment. Sclerosis, however, is not evenly distributed in the arteries, so that the discovery of stifif radials does not imply a similar condition in every vessel of the body. There appears to be some determining cause that relegates the disease to a special part, and in point of 276 Arteriosclerosis frequency, so far as our present inforniation goes, we may safely say that the distribution is about in the order following : first, in the aorta, then in the cerebral vessels, coronaries. and rLiial vessels, and finally in arteries of the extremities. There are various dangers to which the arteriosclerotic individual is exposed. Owing to the retardation of the blood current by ob- struction, and the loss of elasticity in the vessels, there will be failure in the nutrition of the various parts. In the brain this may cause cerebral softening, independently of embolism or thrombosis. Where there is an atheromatous ulcer in a vessel, the blood may penetrate between the coats and cause a dissecting aneurism, or the yielding of the external coat may cause a saccular aneurism. Sometimes the vessel bursts ; this is liable to occur in cerebral vessels that have very thin walls. Occasionally a diseased coronary bursts ; or an artery may be more or less completely blocked by fibrine lodged on a cal- careous spicule or a roughened surface. This may cause senile gangrene, and it is observed in the extremities. Embolism in dis- tant parts is also another incident. Owing to the rigidity of the arteries, the left ventricle is forced to hypertrophy in order to do more work. Dropsical effusions are also common, not so much from the dilated arteries as from the dilated veins, capillaries and lymphatics. In the capillaries the disease appears to begin with some altera- tion in tlie contents of the endothelial cells about the nuclei ; the whole body of the cell being infiltrated, subsequently, so as to be- come turbid in appearance. In the arteries the several coats are successively invaded, until the walls of the vessels become infiltrated with a material that is at first fibroid, later fatty, and finally cal- careous, if the process proceeds sufficiently far. As for the veins, it is probable that the disease commences in the same way — from the endothelium of the inner coats. Those who maintain this theory believe that the special irritation causing the inflammation is due to poisonous bacteria, or their toxins, coursing in the blood ; or, as in lead poisoning, to the absorption of metallic substances. But others believe that the poisons are absorbed by the vaso-vasorum of the vessels, and penetrate from without inwards. This latter explana- tion w^ould hold good for arteries and veins only, and not for the capillaries, for they have no vaso-vasorum. On the whole, if we are to accept a single theory, the former harmonizes best with known facts. Arteriosclerosis is also a senile change, due, perhaps, to paralysis Arteriosclerosis zyj or atony of the muscular coats of the vessels. There are two forms of arteriosclerosis, the nodular and the ditlfuse. The nodular chiefly affects the larger vessels of the body and extremities and those at the base of the brain. In this form the process, microscopi- cally speaking, seems to be as follows : The deeper layers of the in- tima are thickened by the irritation of bacteria, or by the morbid con- stituents of the flowing blood. These poisons cause proliferation of the cells, which eventually develop into fibroid tissue. Later the muscle cells become swollen and undergo hyaline change. Eventu- ally the adventitia, or external coat, is so involved that, as already said, there gets to be general infiltration of the entire vessel. In the diffuse form the change is more uniformly distributed. Both intima and media undergo the same hyaline change, while the elastic coat disappears. When the smaller arteries are involved, their lumens are apt to become contracted ; though infiltration of a vessel may take place without appreciable narrowing of the lumen. However, in a certain number of cases the contraction may be so great as to lead to obstruction, partial or complete, and so to thrombosis and embolism. Occasionally an artery may be entirely obliterated by this process of infiltration and contraction — obliterating arteritis. A probable chain of events, so far as the heart and arteries are concerned, appears to be: first, an increased tension of the arteries, due to obstruction in the capillaries, followed by a loss of elasticity in the arteries and slowing of the blood stream, so that the vessels no longer aid in propelling the blood. Influenced by these condi- tions, the left ventricle becomes hypertrophied, and later dilated. Increased tension, however, leads to infiltration, and this in turn to degenerative changes, by which in the final stage the artery may be converted into a rigid tube. To a certain extent the infiltration of the walls of the vessels is a compensatory process, for by it the dilated vessels are strengthened ; but fortunately this new tissue is apt to suffer from innutrition, and degenerates in consequence, so that an aneurism will form, or even rupture may take place. In syphilis we see examples of the one, and in senile change, of the other. On the other hand, the new tissue may become tolerably well organized, and, contracting, aid in restoring a dilated vessel, more or less, to its former size. Unfortunately, the beneficial results of the cicatrical contractions are apt to be few, and the degenerative changes many, so that the vessel is unevenly distended. In some cases, the heart is not found hypertrophied ; it has then probably been at some time hypertrophied, but has afterwards con- 2/8 Arteriosclerosis r tracted. Tliis wuuUl explain, in i)art. why the senile heart in arterio- sclerosis is sometimes small. Another cause of contraction may lie in the shrinking of the heart walls from the fibroid changes. But the disease extends beyond the vessels, for in every organ affected the parenchyma is sure to suflfer, because its nutrition is affected. In the brain, as \vc have seen, there may be softening; in the kid- neys, contraction ; in the heart, atrophy or degeneration of the muscle fibres, with interstitial fibroid deposits originating in the siieaths of the vessels and penetrating between the muscle bundles. When the pulmonary or bronchial arteries are affected, the lung parenchyma also suffers. There are other conditions, nainely, acute aortitis and acute arteritis, which should be alluded to here, because they have a bearing on the chronic disease. There is no doubt that acute aorititis exists, and its occurrence has been associated with a sense of oppression or substernal pain, dyspnoea, some irregularity of the pulse, and fever. But we have not yet, I think, reached the point where it can be differentiated from acute endocarditis. Acute arteritis, however, oft'ers less difficulties. It may occur in acute or chronic infective diseases, such as typhoid and influenza, acute rheumatism and diphtheria. It appears to elect by preference the arteries of the lower limbs. In fact, the theory that inflammation of the smaller arteries plays an important role in the causation of the exanthems of eruptive fevers, due possibly to the toxins of the causative bacteria, is plausible. In diseases where the strain falls on the left heart, the left ventricle is more prone to this connective tissue infiltration and muscular degeneration ; but where the burden falls on the right heart, the right ventricle is most often affected, as in tubercular and syphilitic phthisis. The occurrence of haemor- rhage in arteriosclerosis is thus explained. The greatest pressure on the arterial wall is just in front of the thickened part. Here it begins to yield, little by little, becoming thinned and stretched and finally somewhat sacculated. When the sac gives way. hemorrhage takes place. In arteriosclerosis there is an increased tension in the vessels. The radial pulse is hard and firm ; in advanced cases, rigid. The heart is usually hypertrophied, though in senile cases it may be of normal size or even atrophied, owing to causes that have been described. The heart usually beats with vehemence. Stiffness and tortuosity of the radials is another important sign. In determining the character of the peripheral arteries, the pulse especially, three fingers are useful. If. when moderate pressure is made with the finger nearest the heart, you can Arteriosclerosis 279 still feci the pulse beat with the other fingers, there is a moderate amount of arteriosclerosis. If by moderate pressure you do not affect the pulse beat on the distal side, there is great arteriosclerosis. Other symptoms are vague tingling or numbness, especially in the left arm and fmgers when these parts are at rest, and coldness of the limbs and feet. The muscles are soft and there is a tendency to corpulency. The pulse is also apt to be less frequent than normal. Precordial pain is often developed by exercise or unusual exertion. After middle life a ringing second sound over the aorta is thought to indicate arteriosclerosis ; if coupled with high arterial tension it may be regarded as pretty good evidence of coronary sclerosis. Angina pectoris has been held to indicate implication of the coronaries ; but the connection is not constant. In fact, angina is rather rare in coronary sclerosis ; and yet coronary sclerosis is very common in angina. Among other prominent signs that have been thought worthy of note is the sallow, pale face ; its color, however, may be red from the abnormal development of the arterioles, the fades arteriosclero- tica. Sometimes pecular wreaths or festoons formed of dilated venous radicles are seen as a girdle about the lower part of the chest. I have several such cases under my observation now, but they are not pathognomonic of ordinary arteriosclerosis ; at least they are to be seen sometimes in the phthisis of young people. If the heart gives way, the pulse will become weak, intermittent or deficient ; attacks of gastralgia may occur with or without angina, with palpitation and cardiac asthma. Sometimes there will be verti- go, or the Adams-Stokes syndrome. There are various types of the disease. In the first place there is the cardiovascular, such as is seen in the gangrene of the extremi- ties in diabetics and in senility. The following case is illustrative : Case XCVI. Gangrene of Feet; Arteriosclerosis, Aortic and Mitral Endocarditis. — Some years ago I made a post-mortem exam- ination in the practice of one of our late surgeons. An abstract of the case is as follows : A gentleman, 49 years of age, was seen in consultation on August 15, 1877. Some 20 years previously there had been a rheumatic attack and subsequently others, attended with cardiac symptoms. In the previous spring the patient, while in bed, became suddenly unconscious and remained so for three hours. In the latter part of June he began to suft'er from pain in the lower extremities, chiefly in the calves, and particularly in that of the left 28o Arteriosclerosis leg. A week before, he first noticed a violet discoloration in the fourth toe of the left foot. When examined by the attending physi- cian, no pulsation was found in the femorals below Scarpa's space. Four days after the beginning of the gangrene in the left foot, a similar process, in a similar place, appeared on the right foot. No cardiac murmurs were detected. If present, it was thought they had been masked by the feeble action of the heart. The question of am- putation was entertained, but this procedure was not advised. The patient lingered several months, to die with symptoms of pneumonia. At the post-mortem examination the b.eart was found large, lioth ventricles were dilated, the left considerably hypertrophicd. Aortic orifice contracted and calcified, also the mitral (button liole open- ing.) In the upper lobe of the left lung there were hccmorrhagic infarctions of various sizes, with surrounding pneumonia. Kidneys also contained infarctions; surfaces granular; Spleen small, con- tracted and containing calcific deposits and cicatrices. Abdominal aorta marked by atheromatous patches throughout its whole extent. The right common iliac thickened by calcific deposits and at points ulcerated. Occlusion of the left femoral just below the point where the profunda was given off. From this point downward the vessel was filled with a firm plug. In the right femoral the plugging oc- curred in the lower part of the vessel, just above the popliteal. In another case (Case XCVII), occurring in the hospital prac- tice of the late Dr. Alfred C. Post, where gangrene had involved nearly all of the left hand, the patient was a man 58 years of age, who entered the hospital sufifering from great debility, emaciation, nausea and vomiting. At the post-mortem examination all the arteries of one extremity were found to be thickened and athero- matous, the radial being occluded by a thrombus. In these instances of arteriosclerosis in peripheral arteries, there are apt. of course, to be associated, as in Case XCVI, symptoms of vascular disease in other parts. But there may be also the purely gastrointestinal type, due to interference with the circulation and leading to congestion of internal viscera, as indicated by signs of acute or chronic dysj^epsia, marked gastralgia and flatulency, perhaps nausea and vomiting. On the other hand, these same symptoms may be due to interstitial thickening of the chylopoetic viscera. The glycosuria so common in aged arteriosclerotics, however, may be explained by the sclerotic condition of the pancreatic arteries. On the other hand, there may be localized ischsemia of the stomach, causing functional inadequacy. The theorv that many gastric or duodenal ulcers are due to cir- Arteriosclerosis 281 culatory disturbances is based on soiincl tbeoretical principles, in so far as such disturlmnces are competent to produce embolism, throm- bosis, or even ha^morrhag-e, anywhere in the body ; but as a matter of fact, it does not ajipear that the stomach or intestines suffer much from this cotuhtion of the circulation, probably on account •of their excellent collateral circulation. Still Berthold,' of lierlin, has reported that of two hundred and ninety-four cases of gastric ulcer, in one hundred and seventy (or 58 per cent.), there were disorders of circulation, chiefly endocarditis and atheroma, and Steiner- found an even larger percentage (71 out of no, or about 64 per cent.). The following is an illustrative instance of this type: Case XCVIII. Gastric Ulcer; Arteriosclerosis.— Mrs. D., 67, English, an alcoholic subject, was first seen by her physician Septem- ber I, 1883. She then complained of pain in the right side, loss of strength, sleeplessness and gastric distress, associated with acid eruc- tations and vomiting. Constipation and colicky pains, with move- ments that were at times dark, and even black and offensive. The patient had been dropsical for years and had suffered from asthma. Weight, about 200 lbs. On examination there was found a diffuse heart beat, no mur- murs, but sounds muffled. Heart's action irregular. Pulse 80-100. Small, rigid radials. Indications of pneumonia and cirrhosis. Gen- eral oedema. Urine scanty, high colored and albuminous. Patient peevish, with signs of hebetude, but no special brain symptoms. She ■died in coma. At the post-mortem examination the heart was found enlarged and the aorta dilated, but the valves were free. In the lower lobes of both lungs small areas of pneumonia. Kidney granu- lar. Liver cirrhotic. The stomach contained a small ulcer, but it was thought to be so insignificant, that it could have given no signs. Its cause, however, may have been the rupture of a minute artery in the organ. The following case of arteriosclerosis is interesting because the cause of death, while ascribed to some affection of the stomach or ■duodenum, is still obscure. Case XCIX. Hcemorrhage, Probably from Duodenal Ulcers Due to syphilitic arterisclcrosis. — A laborer, between 40 and 50. had been complaining of a pain in the cardiac end of the stomach for several weeks before admission to the hospital. While at his work, in which ^Berthold quoted by Welch, Amcr. System of Med.. Vol. TI. ^ Steiner, Pepper's System, Vol. II, p. 487. 282 Arteriosclerosis he was not exposed to special strain. Ik lK\L;an brin^in^- np blood by the mouth and later passed it per anuni. lie ilied a few hours after admission, with all the siij^ns of internal hemorrhaj^e. At the post-mortem examination there were found clearlv marked copper- colored spots on the left Ic"'. Left heart atro])hied. All valves free and sufficient. In the aorta, atheromatous patches and calcareous plates. Aortic arch dilated throu.^hout. At the junction of the first and second portions of the arch on the convex side, a small sacculated aneurism. Tn the remaining portions of the artery, en- darteritis. Colon and lower ])ortions of small intestines filled with blood. Tn the stomach, which contained blood, the rugae were prominent and deeply stained with blood. No ulceration of the stomach, but in the duodenum, just below the pylorus, were several suspicious-looking spots in the mucous membrane, with apparent loss of substance, possibly from the rupture of miliary aneurisms. The liver was larger than normal, but not cirrhotic. The evidences therefore pointed to death caused by minute ulcers of the duodenum, due to syphilitic arteriosclerosis. Tn chronic renal disease wath induration, there is an early dis- turbance of renal functions, though the urine at first shows nothing pathological. There are then no positive subjective symptoms. But w'hen there is a low specific gravity and an occasional trace of al- bumin with casts, renal sclerosis is at hand. In fact, a diagnosis based on these points is apt to be correct ; especially if there are hyaline casts with the granular, and the amount of urine is ab- normally large. Even here, however, there is often a general hyper- trophy of the cardio-vascular system more or less pronounced, from the one extremity to the other. The following is an illustrative case: Case C. Lead Poisoning ; General .h'teriosclerosis.—'K, a male, painter, aged 79, was treated by his physician before admission to the hospital for wrist-drop from chronic lead poisoning, and weak heart. Under the use of the iodide of potassium he partially re- covered the use of his hand. Shortly before admission, while at W'Ork. he had an attack of aphasia, became unconscious, developed mania, and later had a right hemiplegia, which lasted until death. . At the autopsy, February 6, 1885, the heart was found enlarged, but the valves were free. The aorta, however, was a mass of athero- matous patches. In the muscular tissue of the heart the striations were indistinct, and showed evidence of brown pigmentation. A diagnosis of brown atrophy was made. Arteriosclerosis 283 Kidneys small and contained cysts. Surfaces j^ranular. Liver an example of red atrophy. Dura mater thick and adherent. These changes may be taken to have implied vascular thickening. The following is a more marked instance: Case CI. Arteriocapillary Fibrosis of Kidney; Uraemia. — A patient of 67 was attacked with continuous nausea, vomiting and some dyspnoea. Varying quantities of a pale urine. Sp. gr. loio to 1018. Albumin 2 to 20 per cent. All kinds of casts present. Obstinate constipaition. Slight muscular twitchings, relieved by morphia. Pupils contracted. Patient died semi-comatose. At the post-mortem examination the heart was found hypertrophied, the liver fatty and pigmented. Aorta dilated and thinned. In lungs fibroid induration. Spleen hard and indurated. Chronic diffuse nephritis (the small contracted kidney). The left kidney weighed only three, and the right four ounces. Stomach small and con- tracted. Fibroid induration of the pylorus, and a constriction about a foot above the sigmoid flexure. In this case, where the clinical symptoms indicated an arterio-capillary fibrosis (Gull and Sutton), there was some fibroid induration of internal organs, while the aorta and peripheral arteries apparently showed no thickening. Then there is the cerebral type, associated with cerebral anaemia, haemorrhages, miliary aneurisms, and softening, as well exhibited in the retina and choroid, with many psychic disturbances, such as loss of memory, or senile dementia, vertigo, pain in head and neck, involuntary tremors, and diplopia, with specks or flashes before the eyes. Case CII. Cerebral Hemorrhage, Arteriosclerosis. — A man 84 years of age w^as found locked in a room and unconscious, with some right facial paralysis and right hemiplegia. Superficial re- flexes absent on both sides, and deep reflexes on the right side. Died of pulmonary oedema a few hours after admission to the hospital. At the post-mortem examination the heart was found but slightly hypertrophied; but the muscular substance w^as soft, pale and flabby. Valves free. In the aorta some fatty changes, but no atheroma. Oedema of both lungs. Kidneys small and granular. Chronic diffuse nephritis. Liver small and apparently cirrhotic. In the brain a clot the size of a hen's egg involved the anterior and ex- ternal portion of the lenticular nucleus and external capsule, en- croaching on the convolutions of the Island of Reil. About the clot the cerebral substance was soft. 284 Arteriosclerosis Liver and kidneys instances of arteriosclerosis ; also a cerebral hemorrhage, due. presumably, to the bursting of a miliary anciirisDi. In the spi)ijl t\pc, well exempHtied in the locomotor ataxia of syhpilis, we have a disease that presumably originates in the vessel of the cord, as does also, probably, the general paralysis of the insane. In the pnUnonary type evidences of endarteritis and periarteritis have frequently been found in the lungs and bronchi in cases of emphysema and spasmodic asthma, leading to the conclusion that these vascular changes may sometimes be due to gout. Similar changes are seen in pulmonary tuberculosis and syphilis. The following case is an example oi arteriosclerosis associated with .syphilitic phthisis. Case cm. Syphilitis and Tubercular Arteriosclerosis. Death from Puhiionary ITcouorrhage. — J., 30, stone cutter, of tubercular ancestry, had suffered from cough and pain in the right side of the chest for six months before admission to the hospital. During this time he had lost 15 pounds of flesh. For the last three months had suffered from dyspnoea, and for the last four weeks from night sweats. He died of pulmonary hemorrhage. At the post-mortem examination the heart was found enlarged, the left side more espe- cially. Valves free. At the apex of the left lung was a large cavity surounded by smaller cavities, but the whole lung was interspersed with fibroid tissue, separating the small lobules in a peculiar man- ner. There were also numerous nodules from the size of a pin's head to that of a pea. Most of them could be shelled out of the capsules, leaving cavities with a smooth lining. There were still other nodules that looked like miliary formations. The hemorrhage had taken place from one of the cavities lined by a smooth wall. The lung was thought to be the seat of both syphilis and tuberculosis, but a diligent search for the bacilli of tuberculosis both in the lung tissue and in the sputum, was unsuccessful. The right lung was in a similar condition. The kidneys were the seat of chronic parenchy- matous disease. While no special examination of the vessels was made, it is a known fact that the vessels in syphilis are usually, if not always, involved, so that in the absence of the bacillus tuberculosis after diligent search had been made for it, the conclusion seemed to be justified that the cause of death was internal hemorrhage due to the rupture of a syphilitic vessel. Though arteriosclerosis is emi- nently a disease of advanced life, it may occur earlier, especially in syphilis and in chronic nephritis. Inasmuch as the longer we delay treatment in these cases, the Arteriosclerosis 285 less are the chances of success, it behooves us to make an early diagnosis and immediately set about a regular plan of treatment. Of course, prophylaxis aside, we should endeavor as soon as possible to remove the cause of the disease, though this may not be alvi^ays possible. Age and heredity are and ever will be the bars to suc- cess ; and it may not be possible for a painter, for instance, to give up his profession. But over-indulgence in food and drink, and the "over-strenuous life," can be combated, while the danger of gout and syphilis can be minimized, for they are not altogether in- tractable. In fact, we may say that both of them, as well as tuber- culosis, can, in many instances, be held in check. Apart from these considerations, the patient should lead a quiet life, free from its turmoils. And with good fortune and little treatment, an arteriosclerotic may live to a good old age. All exercise should be moderate, but at the same time a certain amount of exercise is necessary. Baths and resistance exercises are as use- ful in the milder cases, as they are useless or dangerous in advanced cases. If hot baths cause excitement, as they are apt to do in these cases, or resistance exercises cause pain or any other untoward symptoms, they should be stopped and not resumed. If there are any suspicions of apoplexy, both baths and resistance exercises should be sternly interdicted. In arteriosclerosis the medicine that is indicated before all other is iodine. It should be used year in and year out, if we are to expect good results. Iodide of sodium, iodide of potassium and hydriodic acid may be followed by the /odides of arsenic, iron and strontium, or free iodine. Iodine ap- pears to lower the blood-pressure without diminishing the force of the cardiac contractions. Aconite is also useful, and camphor, but digitalis and convallaria are harmful. The nitrites, however, are always of service. Together with the iodides, they are at present our sheet anchors. Chapter XXV. slrgi-:rv of T11L-: heart. Jt has long been kr.own that wHnnuls of the heart may not be immediately fatal, but when Fischer' published his series of 452 cases in 1S67 he shewed that persons could live for several days with heart wounds, and that spontaneous recovery followed in from 7 to 10 i)er cent. There are three classes of cases. In die first the puncture is very small, such as might be made by a knitting-needle, and the muscular tissue about the wound closes it, so that little if any blood escapes into the pericardial cavity. In the second class, the wound does not reach any of the chambers of the heart, so that unless the foreign body happens to open a good-sized vessel, the only result is oozmg of a small amount of blood into the pericardium. In the third class the wound is "valvular," that is, a chamber of the heart is opened, but by so oblique an incision that it is closed by every cardiac contraction, and no very large quantity of blood escapes. It is only within the last ten years that operations on the heart have been successful. The experiment of heart suture on a dog by Del Veichio- in 1895 fi^st showed the possibility of a successful operation on the hu- man kind, which was accomplished by Rehn^ in 1897. Up to Oct. i, 1904. acording to the Lancet, there had been 60 cases of cardiac suture with a recovery of 22, or 38 per cent. Accordingly, a pre- ceding mortality of at least 90 per cent, has by skilful surgery been converted into a mortality of only 62 per cent. According to the Lancet: "The symptoms of wound of the heart varv. If the pleura is wounded and blood escapes into the pleural cavitv there are anremia and the signs of pneumo-haemothorax. A splashing sound indicates pneumo-haemopericardium ; in some cases a friction sound is heard. If there is external haemorrhage the stream may be continuous or in jets. If the blood is confined to the pericardium the pulse is very feeble and death may result from pres- sure on the heart. The diagnosis of wound of the heart may be difiicult or impossible. The position of the external wound is not 'Fischer, Arch. f. Klin. Chir., Band IX, 1867-8. ^Del Veichio, Reforma Med.. 1895, Vol. II, p. 38 et seq. 'Rehn, Verhand. d. Deutsche. Gesellschaft. f. Chir., Berlin. 1897, XXVI. * Lancet, Oct. i, 1904. Surgery of the Heart 287 a safe guide. The rule in (Kaibtful cases should be to enlarge the wound, to ascertain if it penetrates the chest wall, and if there be symptoms of hsemorrhage or of pressure on the heart to operate." In the history of a case of successful suture of the heart reported by Hill"' in a negro stabbed with a penknife, the results in 37 cases were reviewed and the following conclusions drawn : The operation for heart suture is entitled to a permanent place in surgery. Every heart wound should be operated on immediately. Even if there is only a suspicion of it, an exploratory incision should . be made. Chloroform is the preferable anaesthetic. The wound should not be probed. Rotter's" operation renders the access to the heart easy. Steady the heart before attempting to suture it, either by placing the hand under the organ, and lifting it up ; if the hole is large enough, introduce the little finger. Catgut sutures should be used, as wounds of the heart heal promptly. The sutures should not involve the endocardium, should be interrupted and tied during diastole. As few as possible should be used. The pericardium should be cleansed, but no fluid poured into the sac. The wound of the pericardium should be closed. If symptoms of compression enstie, reopen the wound and drain. In a bullet wound case recently reported to the Paris Society of Surgery (Tufifier, Bull, et Mem. de la Socicte de Chir, 29, 1903, p. 957), where the radiograph disclosed a foreign body in the left wall of the heart, and moving with that organ, a portion of the second left costal cartilage was removed. The finger passed under the border of the lung located the bullet. The overlying tissue was then laid bare and the ball extracted. The patient recovered. " Hill, Me.d Rec, Nov. 29, 1902. ° Rotter, Verhandl. d. Gesell. Deutsch. Natiirfor. lutd Aersfe, 1899. II, 541. APPENDIX. I. CONGENITAL HEART AFFECTIONS. Malformations of the heart are numerous. They may be serious or trivial. In either case they rarely attract much clinical interest, because radical treatment is impossible. At best it can only be palliative. Most of the defects are due to arrested development in the valves, septa, or large vessels. Of these the most common are either patency of the foramen ovale in the inter-auricular septum, or im- proper closure of the interventricular septum. Among other in- stances of arrested development is the heart with only one auricle and one ventricle, or two auricles and one ventricle, the bi-locular and tri-locular hearts respectively. Valvular anomalies are also comparatively common. The leaflets may be more or less than the usual number. In some cases ante- natal inflammation may have glued the segments together, as in inflammatory rheumatism of the mother during pregnancy. Among the anomalies of the larger vessels, the aorta and pulmonary may originate jointly ; or the aorta may be displaced to the right, or even arise from the right ventricle. Then the ductus anteriosus, or Bo- talli, which in foetal life unites the aorta with the pulmonary artery, may remain open after birth. But if there are defects in the pulmonary artery or aorta, this patency of the ductus arteriosus may be salutary. In fact, if there is a stricture of the pulmonary orifice, a supply of blood to the lungs through the ductus arteriosus may be the means of maintaining life. Without doubt, many of the minor anomalies are co-related to the major forms, one in one place compensating for one or more in others. In some instances, however, the malformations are not sufficiently compensated for, and the circulation is profoundly dis- turbed. Others are of little consequence. Minute orifices in the auricular septum or in the valves may evoke no symptoms ; in fact, the fora- men ovale may remain partly open, without deranging the circula- tion. Even in conspicuous malformations, life may be maintained for years. Of i8i cases collected by Peacock, 119 came in this category; 155 or 86 per cent, living beyond the 12th year. Appendix 289 As for symptoms, the chief is cyanosis, which appears within the first week of Hfe, and is seen in the fingers, toes, Hps and ears. The fingers and toes are usually clubbed. This condition is called morbus caruleus (blue disease), and is due to imperfect aeration of the blood. As additional symptoms there are dyspnoea and cough, and the patients are lethargic. There is another condition called cardiac hypoplasia, where the heart is small from birth, while the rest of the body develops in proper proportions. Virchow believed that this condition was closely related to chlorosis or haemophilia. The volume of the heart may be reduced one-third. The arteries of the aorta are also small. After a time the increased work of the heart may cause hypertrophy. In some instances there is a defective development of the front wall of the chest. Again, the pericardium may be absent. II. TUMORS OF THE HEART. Tumors of the heart are very rare and are usually secondary. The varieties "are sarcomas, myomas, myxomas, Uhromas, gummas, an- geiomas, lipomas, carcinomas, and cysts. Secondary carcinoma is the most frequent of all neoplasms, though still comparately rare. It has no preference as to site. Often it is merely an extension from a contiguous disease. Sarcomas are rarer than carcinomas. They occur, however, at any age, and are of several varieties. Myxomas have been found in 9 instances. (Whittaker.) Rarer still are myomas and the remaining four of the connective tissue group. Tuberculosis is not uncommon in the heart ; it is apt to involve the pericardium. III. ANEURISM OF THE HEART. This term is applied to a partial dilatation of the heart wall or septum. A weak spot develops in either, from some process of softening or rupture, and then the weakened tissue is "ballooned out." The clotted blood collected in the sac may then cause sudden death by discharging into the heart cavity, causing embolism ; or the sac may burst, causing death as the result of shock, from the sudden haemorrhage. Syphilis is probably the most frequent cause of cardiac aneurism, either by myocardial softening due to gummatous tumors or infil- trations ; or from the arteriosclerosis of a vessel in the substance of the heart. 290 Appendix There are no characteristic syniptoins. and it is not probable that a positive diagnosis has ever been made, even w here canHac aneurism has been suspected. The iirognosis is unfavorable, as the disease does not tend to self-limitation. The treatment is svmptomatic. In a case that came to m\ knowiediix. Iioucvcr, a man in attem])tini; to lift a heav\ weight was very suddenly taken with heart failure, as shown by his rapid and irregular pulse. A cure came w'ith rest. Possibly, and I think probably, in this instance some fibres in the wall of the heart ruptured an dthere was a temporary acute aneurism, from which he recovered when the ruptured fibres hatl healeil. I\-. PARASITES OF THE HEART. The C\sticercus and the Ecchinococcus may be found in the heart. They are comparative)} rare, and are usually met with in the walls of the heart, but occasionally involve the valves, rendering them incompetent, tlydatids vary in size from a pin's head to an orange. If the sac ruptures into a heart chamber, death may at once ensue. This accident has happened on several occasions. Deposits of actinomycosis have also been found in the walls of the heart. The diagnosis cannot be made wdth certainty, but it may be suspected, if deposits of the parasites have been found elsewhere in the body ; in such instances embohsms frequently occur. If a tumor can be located in the walls of the heart, aspiration may possi- bly reveal the parasitic character of the tumor ; or if a distal vessel is plugged, the embolism may be found to be parasitic. Surgical treatment offers the onl\ ground for hope of life. v. TREATMENT OF CJIROXIC HEART DISEASE AT FRAXZENSB.M). The success that has attended the management of heart diseases in Nauheim. Germany, has led to the introduction of the same line of treatment m other European Spas, notably in Franzensbad. which lies in the northwesterly comer of Austria, where it touches Saxony and Bavaria. Situated on a broad and well-cultivated plain, through which the beautiful river Eger and its tributaries flow, and at an elevation of more than 1,500 feet above the sea, it is w^alled about by moun- tains and forests that protect it from the cold winds and storms, while the air is necessarily cool, pure and light, even in the middle of summer. The town itself is attractive, quiet and restful. Shady walks are numerous. Picturesque drives extend in every direction. Good Appendix 291 hotels and apartments are numerous. Excellent music and a good theatre are other attractions. All the bath houses and springs are under the control of the municipality, whose officers are intelligent, progressive and efficient, Franzensbad, like Carlsbad and Marienbad, occupies a central position in Europe, and is conveniently reached by the best express, sleeping car, and de Luxe services from Dover, Paris, Berlin, Frank- fort and Vienna. The springs are a dozen in number, all charged with carbonic acid gas and other chemical ingredients, in which they onl\' differ as to relative proportions. According to published analyses, some of them are more strongly charged with carbonic acid gas than any other springs in Europe. The most prominent ingredients are the carbonate of iron, Glauber's salt, common salt, and the alkaline carbonates, together with the free carbonic acid. The waters contain but small percentage of the salts of lime, silicic acid and earthy matters. The springs in which iron predominates are used internally for improving the character of the blood. Those that contain alkalies and Glauber's salt constitute a feature of the treatment. Those having the largest amounts of carbonic acid and iron are used for the baths. The temperature of the waters varies from 50 to 55° F. Those used for bathing purposes are heated by different methods. By the Pfrieuis system, steam is turned into the tub, so as to bring the water up to the desired temperature. The water is by this system heated directly. This, in common parlance, is called the Mineral bath. The proportions of gas and iron are small. It is suited for weak, delicate or nervous persons. It is the initial bath for those who take the cure. Stronger baths are prepared by the Schzt'ars or Reiner^ systems, in which the tub has a double bottom, the inter- mediate space being fitted with steam coils, so that the water may be heated to the desired temperature without being diluted. Such a bath is called a Steel bath, also an arbitrary word, but meaning that the water is heated indirectly. These Steel baths are suited for robust men or women, or for patients who require a stronger bath than the Mineral. Lastly, there is the Flozving bath, where the carbonated water, which has been previously heated to the required temperature, flows through the tub in w^hich the patient is im- mersed. These last are taken at the close of a course in heart diseases. The appliances at the baths are such that any degree of strength 292 Appendix can be obtained, and brine, the chloride of calcium or other in- gredients may be added in any proportion that may be necessary. Each of the three kinds of baths, whether Mineral, Steel or Flowing, has three grades, the strength of the bath constantly in- creasing with each successive grade. In point of strength the order is as follows : Mineral, i Steel, i 2 The weakest. 2 The medium. 3 3 Flowing, A B The strongest. C In the regular heart disease course, the patient takes his carbonic acid gas treatment in these nine different grades of strength. The weakest baths contain no brine. If the duration of the bath is not too long, the effect is very stimulating, but if too long, irritability and fatigue will be the results. To prevent inhalation of the gas the water should not be allowed to reach more than to the middle of the chest, or the tub may be covered by a linen sheet. Inhalation of the gas will, of course, cause some headache, dyspnoea or palpitation ; but as a matter of fact such an occurrence is very rare, because the gas rises only a few inches above the level of the water. At the strong ■flowing baths, however, where the agitation of the water causes the gas to rise higher than in the other baths, there is always an at- tendant in the room. Usually the sensations after the bath are very agreeable ; the large and airy bathrooms, that are features of the Franzensbad bath-houses, obviating the likelihood of any possibly unpleasant effects from inspiring the gas. For further particulars, the reader is referred to the book entitled Franzensbad ; Its Mineral Waters and Baths, by Dr. L. Felhier, 1904. Fellner^ agrees with Winternitz of Halle that the carbonic acid gas is absorbed by the skin, and that it has a reflex action on the vaso-motor centers, causing dilatation of the arteries and capillaries, which produce a sensation of warmth. Through its influence on the pneumo-gastric it lessens the frequency of the pulse, and deepens inspiration. Dilatation of the vessels permits them, of course, to be ^ Fellner, Verhand. der Clir. Hcrzkrankheiten, T904. Appendix 293 better filled. Diminution in cardiac frequency favors diastole, so that the ventricles are also better filled, and discharj^inj:^ more blood, take up more blood and so relieve venous congestion. Deep breath- ing also increases the siphon-action of the heart. In these ways there is a tendency to restore the balance of circulation between the arterial and venous systems. The heart itself is likewise improved, for the coronary arteries are better filled, and the organ is supplied with more and better nourishment.^ According to Fellner, resistance exercises also lessen the fre- quency of the pulse and increase the blood pressure, because they contract the muscles, causing them to press on the delicate walls of the veins and lymphatics, facilitating the flow of their contents towards the heart. The organ, therefore, is better filled, and the left ventricle has more blood to distribute throughout the systemic circulation, and so the tendency to congestion of the veins and lym- phatics, so common in chronic heart disease, is overcome. VII. REGIMEN IN CHRONIC HEART DISEASE. Rules to Be Observed by the Patient. Liquids. Do not drink more than half a glass, to a glass (four to eight ounces of water), at meal time. Water may be taken freely two hours after eating ; on rising in the morning ; and at bed time. In case stimulants are necessary, pure Moselle wine can be taken at lunch or dinner with an equal quantity of water, preferably High- land water. Aerated water should be avoided. A small quantity (half an ounce) of good whiskey can be taken in place of the Moselle. Use no fermented liquor, and take alcoholics only as above directed. May take Zoolak or Vichy. Avoid coffee or tea, unless the latter is weak. Take Postum in place of cofifee. Use milk only if it agrees. Foods. Eat no white or rye bread. Use Graham, whole wheat bread, unsweetened Zwieback or toast. Fish. Avoid salmon and white fish. Eat broiled, baked, or boiled fish, but without dressings or sauces. May eat oysters and clams. Meats. May eat roast beef, mutton, lamb, veal, venison, sweet- bread, fowl or game. Avoid ducks and geese. Avoid, however, gravies, stuffed and breaded meats. May eat plain omelettes or scrambled eggs. Vegetables. May eat peas and Lima beans (in moderation), ' Many walks in Franzensbad are laid out with reference to the Terrain cur. As the distances are indicated by signboards, patients can follow the directions of the physician in walking the exact distance he prescribes. 294 Appendix string- beans, ovster i>lant, tomatoes ami spinacli. koli-rabi. young carrots and beets (stewed), egg plant, rice and hominy. Dessert. May eat plain rice and hominy, or custard, or apple pudding. Wine jellies, if not sweetened ; stewed fruits. May eat, occasionally, ripe peaches, pears, and grape fruit. May eat stewed cherries, pears, peaches, and apples. Avoid all forms of cheese. Tobacco. Avoid all forms of tobacco. Eat slowl\ and at regular hours; masticate tiioroughly. Do not partake of a great variety of dishes at any one time, nor eat large quantities of anything very hot or cold. Under-cooked vegetables, overdone meats, hard-boiled eggs, are to be avoided. A moderate quantity of food for adults should average daily about ten ounces of animal food, thirty ounces of vegetable food, and riftv to eight\' ounces i>f li(|ui(ls, princi]nilly water. VII. Ill-: .M(M)ll-IIil) RIVA ROCCI .Sl'lIVGMOMAXOMETliR. Fig. 41- This instrument is thus described by the makers: It is an ap- paratus for estimating artificial blood pressure or pulse force, modi- fied by Dr. Henry W'ireman Cook, of the Jolms ll()])kins Hospital, Baltimore, Md. The most valuable indication derived from palpation of the pulse Appendix 295 is the indication of arterial tension. The value of sucli estimates is in (Hrect proportion to their accuracy. A knowle(Ij:^e of actual, definitely determined pulse tension is of special value in the diagnosis of many morbid conditions where variations from the normal are characteristic, as, for example, in apoplexy, traumatic brain compression, surgical or traumatic shock, nephritis, cardiac diseases, aneurism, lead poisoning, haemorrhages, uraemia, etc. ; also in the treatment of conditions where correction of an existing pulse tension is aimed at, under which are included all the conditions just mentioned above, and in addition, the larger class of toxic cases in which depression of the vaso motor system is a prominent feature and calls for stimulation. In these cases it is specially important to be able to follow variations in pulse-force ac- curately, and to meet such variations with proper therapeutic measures. The apparatus consists of a system of closed tubes connected with a rubber bulb held by the operator, a hollow rubber band (placed around the arm or leg of the patient) , and a mercury mano- meter. By the law of the diffusion of gases, equal pressure is trans- mitted to every point throughout this closed air system. When the pressure is raised by the operator to such a point that the pulse of the patient distal to the constricting band is obliterated, the height of the mercury column in the manometer is held to be equivalent to the maximum arterial blood pressure. The arm-piece is placed around the patient's upper arm, midway between the elbow and shoulder, and adjusted to fit. The operator, with one hand, increases the pressure by squeezing the hand bulb, and. with the other hand, palpates the patient's radial at the waist. When the pressure just obliterates the pulse at the wrist, the height of the mercury column is noted, and it is then allowed to drop slowly until the pulse returns. This manoeuvre is repeated without letting the air out, and by merely squeezing and releasing the reservoir bulb. The point above which the pulse is obliterated and below which it returns is the reading of maximum arterial blood pressure. A determination within two or three millimeters should be con- sidered satisfactory. A reading of mean arterial blood pressure may be made with this instrument, as described by Prof. Gumprecht, by finding the point when the greatest excursion of the mercury column occurs during cardiac systole after clamping off the tube leading to the reservoir bulb. 296 Appendix The normal maxinuini blood pressure averages, when lying at rest: For children of 1 to 3 years 85 to 95 mm. For children over 3 years 95 to no mm. F""or adult females 115 to 125 mm. For adtilt males 125 to 135 mm. The mean arterial pressure is about three-quarters of the maxi- mum. Any one at all trained in pulse palpation can make an ac- curate reading at the first trial. An estimation takes from fifteen to thirty seconds. Sold by the Kny-Scheerer Co., 225 to 233 Fourth Ave., New York City, or Eimer & Amend, i8th St. and 3rd Ave., New York Citv. INDEX. Abscess of heart, in. Abnormal rhythm, 171. Accentuation of heart sounds, 19. Aconite in heart disease, 224. Adams-Stokes syndrome, 278, 186, 187. Adherent pericardium, 168. Adonis vernalis, 227. Afifections of the substance of the heart, 102. Allorrhythmia, 171. Anaemia, 25 ; murmurs in, 25. Anaemic necrosis, in. Aneurisms, 251; abdominal, 258; aortic, 254; Bellingham's treatment, 261; cardiac, 288 ; course, 252 ; defined by radiography, 252 ; diagnosis, 252 ; etiology, 251; expansile pulsation, 258; eye symptoms, 253; fusiform, 251; miliary, 282; percussion, 254; pressure signs, 253; of pulmonary, 260; sacculated, 251; sex in, 251; symptoms, 261; thoracic, 254; thrill, 259; tracheal tugging in, 254; treatment by diet, 261; rest, 261; sedatives, 261 ; Tufnell's plan, 261. Angina Pectoris, 38, 207; diagnosis, 213; etiology, 212; false, 208; history, 207; in chronic aortitis, 272 ; mild, 208 ; morbid anatomy, 212 ; motoria, 208 ; pathology, 219; primary, 208; prognosis, 216; pseudo, 208; reflex, 212; secondary, 2o8j sex, 214; severe, 208; sine dolore, 213; symptoms, 213; treatment, 214; true, 208. • Angiomas of the heart, 288. Angio-sclerosis, 273. Aorta, atheroma of the, 269. Aortic area, 23. Aortic diseases, 67. Aortic insufficiency, 67; angina in, 70; arteriosclerosis in, 68; cannon ball pulse, 71; Corrigan's, 71; diagnosis, 71; etiology, 68; murmurs in, 70; or- ganic form, 67; pistol-shot pulse, 71; relative form, 67; stages, 72; sud- den death in, 246; symptoms, 70; thrill, 70; triphammer pulse, 71 ; venous pulse, 71; water-hammer pulse, 71. Aortic obstruction, yj ; and aortic insufficiency combined, yj; diagnosis, 80; etiology, 79; frequency, yy \ physiology, 79; prognosis, 81; sex, 80; symptoms, 80; without insufficiency, 78. y'U/rtitis, 263 ; acute and chronic, 263, 277 ; acute primary, 263 ; acute secondary, 263; causes and modes of development, 264; diagnosis, 267; etiol- ogy, 264. Aortitis, chronic, 267; causes and modes of development, 268; morbid anat- omy, 268; symptoms, 268; treatment, 272. Aperients, 225. Apex beat, 14. Apocynum, 228. Apoplectiform seizures, 282. Araiocardia, 181. Argentum Crede, 221. Arrhythmia, 173; causes, 173; reflex, 173; toxic, 173. Arsenic in heart diseases, 223. Arterial tension, 294. Arteriosclerosis, 273 ; a senile change, 275 ; association of with other morbid processes, 274; asthma associated with, 283; cardio-vascular type, 278; cardiac hypertrophy, 276; cerebral type, 282. 2gS Index Arteriosclerosis, 274; clinical types of, 2yS; embolism in. 275; oiulartcritis in, 274, 276; gastro-intestinal types, 279; gouty, 2~ji,; granular kidney in. 2S2; hypertrophy of the heart associated with, 27b; kidney disease associated with, 2S1 ; lead poisoning in, 281 ; mechanical means of de- termining arterial resistance, 293; mental overstrain in tlie causation of, 284; of coronary vessels, 216, 219; pathology, 276; physical diagno- sis, 277; pulmonary type, 283; spinal type, 283; syphilitic, 283; stages of, 274; treatment of, 284. Arteries, calcareous infiltration of, 274. Arttrio-capillary fibrosis. 281. ^2. Arteritis, 277; acute, 275; in infective diseases, 277; obliterating, 276. Artery, pulmonary, 82; anomalies of the. 287; diseases of the, 260. (See Pulmonary arterj'.) A'-tificial bath, 238. Asthma, arteriosclerosis associated with, 283; dolorificum, 207 (see Angina pectoris) ; treatment of, 214. Atrophy of the heart, 104, 109. Atiieroma, 274. Auricle, left, 41, 58; dilatation. 41, 58; hypertrophy, 41, 58. Auricle, right, 41, 58; dilatation, 41, 58; hypertrophy, 41, 58. Auscultation in heart diseases, 37. Author's tables, ^,2. t,Ti. Bacteria in endocarditis, 28, 46. Banting system, 116. Basedow's disease (see Exophthalmic goitre), 194. Batht.. carlxinated, 290; how to prepare them, 290; and e.xcrci>es. 230. Baths in heart disease, 290. Belladonna, 224. Bradycardia, 181. Breast-pang (see Angina pectoris), 207. Bromide of Zinc, 224. Brown atrophy of the heart, no. Brown induration of lungs, 41. Brucine, 22;^. Bruit; pistol-shot, 71; du diable, 25; du scie, 36; du rape, 36; d'oboe. 36; de soiifHc. 36; diastolic, 55; auricular systolic, 55. Cactus grandiflorus, 223. Caffeine, 227. Calomel, 225. Camphor, 224. Capillary pulsation, 71. Carbonic acid gas treatment, the dry, 230; the wet, 230. Carcinoma of the heart, 288. Carditis. 103. Cardiospasm, 219. Cardiogram, 14, 15. Caton's method, 220. Cereus grandiflorus, 223. Chambers' method, 116. Cheyne-Stokes respiration, 11, 131, 249. Chorea and valvular diseases, 28. Clinical examination of the heart, 7. Climate, 223. Colloidal silver, 221. Compensation, 40, 41, 53, 222, 249. Congenital affections of the heart, 287. Convallaria, 227. Cor bilocular, 287. Cor bovinum, 106. Index 299 Cor trilocular, 287. Cor villosum, 160. Coronary arteries, 208, 209; angina pectoris in diseases of, 208, 209, 210, 212; atheroma of the, 209; associated with arteriosclerosis, 209; without an- gina pectoris, 210. Corpulence, 112. Corrigan"s disease, 67, 71. Cretsegus, 23. Cyanosis, 95; congenital heart lesions causing, 228; in pulmonary stenosis, 89; in valvular heart disease, 35, 89. Cysticercus of the heart, 289. Cysts of the heart, 288. Death, sudden, 39. 41, 141, 245, 246, 249; from bursting of aortic aneurism, 256, 257, 258; other causes, 254, 255, 260. Debilitas cordis (see Weak heart), 103. Degeneration, fatty, of the heart, 124; hyperdilatation in, 126. Delimitation of the heart, 15. Delirium cordis, 11, 199. Dermatographic pencil, 13. Diagnosis of heart diseases, 7. Diastolic sounds, 18. Diastolic murmurs, 249. Diet in heart diseases, 225, 292. Digestion, 12. Digestive troubles in valvular disease, 25 ; treatment,, 225. Digitalis, 226; in arteriosclerosis, 284; in valvular disease, 228; in the treat- ment of cardiac disease, 229; substitutes for, 227. Dilatation of the aorta, 272. Displacements of heart, 16, 142; in pleurisy, 1/^4; in other conditions, 145; intrinsic, 142; extrinsic, 142; prognosis, 142, 144, 158. Division of cardiac sounds, 21. Diuretics, 28. Dropsy; from fatty heart, 131; in heart disease, 40; treatment of, 228; the use of needles, 228. Dulness in percussing outlines of heart, 16. Durosies's sign, 72. Dwarf beats, 174. Ebstein's reduction method, 117. Echinococcus of the heart, 288. Effusions into pericardium, 162. Embolism, 39; of brain, 39; of lungs, 39; of liver, 39; of spleen, etc., 39. Endarteritis, 274. Endocardiopathies, 27; age, 28; angina in, 38; auscultation in, 2>7 \ classifi- cation, 27; compensation in, 40, 41; cyanosis in, 35; diagnosis, 39; etiol- ogy, 27 ; embolism and apoplexy in, 39 ; micro-organisms in, 28 ; organic and inorganic murmurs, 35; percussion in, 38; pathologj-, 28; pulse, 36; rhythm, 36; statistics, 31; S3aTiptoms, 28. Endocarditis, acute, 42 ; benign, 42 ; blood examination in the diagnosis of. 43 ; diagnosis, 43 ; diphtheritic, 43 ; etiology, 42 ; prognosis, 43 ; gonor- rheal, 46; infective. 45; in the exanthems, 42; malignant, 45; etiology, 46 ; mycotic, 45 ; septic or ulcerative, 45 ; treatment, 44. Epigastric pulsation, 63, 95, 97, 200. Epistaxis, 269, 275. Erlinger system, 242. Examination blank, 8. Exercises in heart disease, 229; passive, 232; resistance, 22,2; rationale of, 292; modus operandi, 238. Exocardial sounds, 26. 300 Index Exophthalmic goitre, 194 (see Graves' disease); acute, 194; course of, 202; chronic, 194; definition, 194; diagnosis, 194, 200; essentials, 194; eti- ology, 197; history, 195; neurotic disturbance in, 197; palpita- tion, 197; pathology, 197; pigmentation in, 199; primarj-, 194; sec- ondary, 194; treatment, 203; tremor, 196. Express wax crayon, 13. Fades artcrio-sclerotica, 278. Fatty degeneration of the heart, 124; diagnosis, 129; etiology, 128; pathology, 125; prognosis, 134; stages. 125; treatment, 133. Fat heart, the, 112; diagnosis, 114, 133; prognosis, 123; treatment, 115. Fibroma of the heart, 288. Fingers, clubbing of, 288. Flatness in its relation to the percussion area, 13. Flint murmur, 66. Fluorography, 12. Fluoroscopy in heart disease, 12. Foramen ovale, defective closure of, 287. Formes frustes in Graves' disease, 195. Fowler's solution, 115. Fragmentation of the heart muscle, 126. Fret)tisse»ieut cataire. 36. Frequent pulse, 173; chronic. 179; etiology, 173; paroxysmal, 175; permanent '^7S'- physiology, 174; prognosis, 177; temporary. 184; treatment. 176. Franzensbad, treatment of heart diseases in, 289. Friction sounds in pericardium, 161. Fucus vesculosus. 115. Functional cardiac diseases. 170. Functional murmurs, 21. Gallop-rhythm. 20. Gelatiniform plaques, 266. Gout, arteriosclerosis in, 273. Graefe's symptoms in exophthalmic goitre, 200. Graves' disease, 194; treatment by galvanic puncture, 285. Gummas of the heart, 288. Hairy heart, 160. Head symptoms in heart disease, 11. Haemic murmurs, 25. Haemopericardium, 166. Heart, affections of the heart substance, 10; aneurism of the, 288; anomalies in the chambers of the, 287; atrophy of the, no; anomalies in the valves of the, 287; bilocular, 287; bovine, 106; carcinoma of the, 288; contour of. 13; condition of, in exophthalmic goitre. 209; congenital anomalies, 287; displacements of the, 142; death from rupture, 105, 106; fatty de- generation of the, 124; fibroma of the, 288; functional disorders of the, 170; gummas of the, 136; head symptoms in disease. 11; hairy. 167; physiological action of the, 18; hypertrophy of the. 104; infrequent pulse in aflfections of the, 181; long, 41; trilocular, 288; hypertro- phy of; associated with the granular kidney. 106; concentric, ic^; ec- centric. 108; from muscular effort, 104; from pericarditis, 168; from plethora, 105; in aortic diseases, 70; in mitral stenosis. 58; in preg- nancy, 105; in pulmonary stenosis, 90; irritable, 105; location of the, 14; murmurs of the, 21 ; myxoma of the, 288; neurotic, 171 ; palpitation of the, 170; parasites of the, 289; percussion of the, 234; rapid action of the, 173; sarcoma of the. 288: Schott system, 230; sounds of the, 21 ; sounds, division of, 21 ; strain, 105 ; suture, 285 ; syphilis of the, 136; trilocular, 288. Heart, normal weight of, 104. Index 301 Hodgson's disease, 269. Hydatids of the heart, 289. Hydrogogues, 222. Hydropericardiiim, 163. Hyperhydrosis in exophthalmic goitre, 200. Hypertrophy of the heart, 104; concentric, 108; eccentric, 108; etiology, 104; physiological, 105; pathological, 105; stages, 108; symptoms, 107. Hypoplasia Cordis, no, 288. Hysteria complicating exophthalmic goitre, 200. Impulse, II. Infective endocarditis, 42. Infrequent pulse, 181; causation, 185; chronic, 184; diagnosis, 182; etiology, 184; following injuries of cervical vertebrae, 184; paroxysmal and chronic forms, 184; pathological, 183; physiological, 183; prognosis, 187; symptoms, 187; temporary, 175; treatment, 176. InsuMcientia myocardii, 103. Insufficiency of aortic, 70; mitral, 50; pulmonary, 82; tricuspid, 92. Iodides, employment of, in arterial and heart diseases, 225. Irritable heart, 105. Jugular veins, 94; distention of, 94; fulness of, 94; pulsation of, 94. Lateral curvature, displacements of the heart in, 145. Laxatives, 225. Leiter's tubes, 261. Lipomas of heart, 288. Liver, examination of, 12; cirrhosis of in valvular disease, 24; hob-nail, 24. Lungs, examination of, 12; embolism of in heart disease, 39; in aortic disease, •80; mitral obstruction, 63; oedema of the, 95. Management of heart diseases, 220. Massage, 238; general, 239; abdominal, 239. Measurement chart, 9. Micro-organisms in heart disease, 28. Milk-spots of the pericardium, 160. Misplaced heart, in. Missed beat, 11. Mitral area, 24. Mitral insufficiency, regurgitation or incompetence, 50; and mitral obstruction combined, 53; compensation in, 52; diagnosis, 54; etiology, 51 ; inorganic or relative, 53; organic, 51; physiology, 57; prognosis, 247; symptoms, 51; statistics, 31; temporary, 51; venous pulsation in, 52. Mitral murmurs in anaemia, 26. Mitral obstruction (stenosis), 55; age, 60; diagnosis, 57; diastolic murmur 61; embolism, 63; Flint murmur, 66; physiology, 58; physical signs, 60 presystolic murmur, 61; prognosis, 60; pulse, 60; stages, 59; sex, 60 statistics, 56; symptoms, 66; thrill, 66. Morbus coeruleus, 288. (See Congenital affections of the heart.) Motility of the heart. 16. Murmurs, 22; accidental, 21; anaemic, 26; musical, 35; valvular, 21. Myasthenia cordis, 103. Myocardial affections, 102. Myocarditis, 103. Myomalacia cordis, in. Myoma s, 288. Myxomas of the heart, 288. Nauheim methods, 230 ; Franzensbad methods, 289 ; the artificial bath, 238. Needles in dropsy, 228. Nervous_ system, symptoms referable to the, 207 ; in exophthalmic goitre, 197. Neuralgia cordis, 207 (see Angina pectoris). j02 Index Neuralgia (^Ic.vtis cariiiaci, 207 (see Angina pectoris). Neuroses of the heart, 170. Neurotic heart. 170. New growths in heart, 288. Nitrites, 224. Nitroglycerine, 224. Obesity, 112; etiology, 112; symptoms, 112; treatment, 112. Oertel's plan, 117. (.)ligocardia. 181. Opiates, 222. Organic murmurs, 21. Pain in heart disease, 11. Pain, cardiac pathology of, 11; in angina pectoris, 213; in aortic aneurism, -54- Palpitation, 11, 171; causes, 170; direct, 170; prognosis, 171; reflex. 170; symp- toms, 171; toxic, 170; treatment, 172. Pancarditis. 103. Paracentesis of the pericardium. 165. Paraldehyde, 225. Parasites of the heart. 289. Percussion, 38, 234. Pericardial diseases, 159. Pericarditis, 159; acute, 160; chronic, 168; course, 162; diagnosis, 160; eti- ology, 159; morbid anatomy, 160; physical signs, 161; primary, 159; prognosis, 163; secondary, 159; symptoms, 161; treatment, 162; tuber- cular, 167. Pericardium, adherent, 168; air in the, 168; blood in the, 166; dropsy of the, 166; effusion of serum, 162; paracentesis of the. 165; pus in the, 167. Physical examination of the heart, 13. Physiology' of heart's action, 18. Pilocarpine, 227. Pleural friction sounds, 26. Pneumopericardium. 168. Position of heart, 13. Praecordium. bulging of. 163. Pregnancy, cardiac hypertrophy in, 105; chronic valvular disease in, 243; prognosis, 243. Premature beats, 174. Presystolic murmurs, 66. Presystolic sounds, 18; bruit. 55. Prognosis in heart diseases, 244; age, 244; embolism, 245; in functional dis cases. 244; in valvular lesions, 245; myocardial, 244; order of gravity, 248; relation to compensation, 249; sex, 244. Pulmonary, aneurisms of the, 260; area, 23; congenital anomalies of the 288; obstruction or stenosis of the, 87; associated with congenital anom- alies, 85; diagnosis, 89; etiology, 85, 89; insufficiency of the, 82; hjemor- rhage, 41; physical signs, 90; prognosis, 86, 90; symptoms, 85; treat- ment, 86, 91. Pulse, 7; arrythmic. 11; alternating. 11; arteriosclerotic, 7; bigeminal, 11; can- non-ball, 71; capillary. 71; Corrigan's, 71; deficient, 11; frequent, lO; infrequent, 7, 10; intermittent, 11; large, 7; paradoxical, 173; premature, 174; quick, 7; small, 7; trigeminal, 11. Pupils, inequality of the in aneurism of the transverse portion of the aorta, Pyopericardium. 167. Ramollisscment du Cccur, 124. Reduplication of sounds, 20. Regimen in chronic heart disease, 292. Index 303 Residence, choice of, 223. Respiration, Cheyne-Slokcs, II, 249. Respiration in heart disease, 11. Retraction of apex, 169. Rheumatism, relation of to endocarditis, 28. Rotter's operation, 286. Rhythm, 8; cardiac, 12, 19; double, 20; embryocardial, 20; foetal, 20; gallop, II, 20; pulse, 12; triple, 11, 20. Sarcoma of the heart, 288. Schott system of exercise, 230. Sclerosis, arterial (see Arteriosclerosis), 273. Segmentation of heart muscle, 126. Septic diseases, endocarditis in, 46. Septum, cardiac defective development of, 288. Sex, as affecting prognosis, 243. Skiagraphy, 12; Skin changes in the, in exophthalmic goitre, 199. Sodium, sulpho-carbolate of, 221. Sounds, cardiac, 21. Spanocai'dia, 181. Sparteine, 227. Sperling's tables, 31. Sphygmomanometer, 231, 293. Sphygmograph, 2,7, 175. Spleen, examination of, 12 ; embolism of in endocarditis, 48. Stellwag's sign in exophthalmic goitre, 201. Stenocardia (see Angina pectoris), 207. Stenosis, aortic, 77; mitral, 55; pulmonary, 86; tricuspid, 98. Sternalgia (see Angina pectoris), 207. Streptococcus sera, 221. Strophanthus, 227 ; as a substitute for digitalis, 227. Strychnine in heart diseases, 223. Sudden death, 39, in, 114, 246, 249. Sulpho-carbolates in infective diseases, 221. Supra-renal extract, 223. Surgery of the heart, 285. Suture of the heart, 285. Sweating, excessive, in exophthalmic goitre, 200. Syncope dolorosa, 207. Sympathetic system, changes in, in exophthalmic goitre, 197, 205. Symptom, v. Graefe's, in exophthalmic goitre, 200. Syphilis of the heart, 136; angina in, 139; aortitis in, 139; diagnosis, 139; endo- carditis in, 139; frequency, 140; frequent pulse in, 139; in aneurism of the aorta, 139; pathology, 137; treatment, 141; prognosis, 141. Systolic sounds, 18. Tachycardia, 174. Temperature in heart disease, 11. Terrain cur, 230. Thrill, 12, 161 ; purring, 2^, 63. Thrombosis of veins, 40, 131. Thyroid extract, 118. Tobacco heart, 171. Tracheal tugging, a sign of aneurism of the transverse portion, 254. Treatment of heart disease, 220. Tremor in exop-hthalmic goitre, 196. Trional, 225. Tricuspid area, 24. Tricuspid insufficiency, 92; acquired. 92; congenital, 92; diagnosis. 93, 96; frequency, 92; morbid anatomy, 93; murmurs. 96; organic lesions, 93; inorganic, 93; physiology, 93; prognosis, 97; relative, 93; statistics, 92; symptoms. 95 ; venous pulsation in. 94. 304 Index Tricuspid obstruction (stenosis), 99; age, 99; and mitral obstruction, 100; congenital form, 99; diagnosis, 100; prognosis, lOi ; sex in, 99; symp- toms. 100. Trousseau's plan, 116. Tuberculosis of the heart, 104; stenosis of the pulmonary valve associated with, 90. Tugging, tracheal, a sign of aneurism of the transverse portion of the arch of the aorta, 254. Treatment of heart disease, 220; in acute simple endocarditis, 220; in acute infective, 221; in angina pectoris, 214; in chronic valvular disease, 221; in fatty degeneration, 132; in fat heart, 115; in functional disorders, 171. Tumors of tlie heart, 288; Nauheim methods, 230. Urine, examination of, 24. Vaso-dilators, 224. Valerian, 224. Valves, relative position of, 15, 17. Vegetable-fibre paper, 13. Venesection in heart diseases, 222. Veins, distention of, 94; pulsation of 97, 100; true, 94; false, 94. Venous hum, 25. Venous murmurs, 25. Vibration, 238. Von Graefe symptom in Graves' disease, 200. Weak heart, 103. White infarct, in. "Withered-apple" heart, no. Work, muscular, cardiac hypertrophy from, 104- Worry, arteriosclerosis from, 284. DATE : DUE P-^€L '- / 1 GAYLDRO PRINTED IN U.S.A ^M^i'irirrmiiys'r'r I lili|i||n|iii||i 0048049212