(916 Jllfi 1 TRANSIENT AURICULAR FIBRILLATION An Electrocardiographic Study Thesis presented to the Faculty of the Graduate School of the University of Pennsylvania in partial fulfilment of the requirements for the degree of Ph.D., 1916. BY EDWARD B. KRUMBHAAR, M.D. (From the John Herr Musser Department of Research Medicine, University._ol_Eennsylvania, Philadelphia.) OFT UN I VE K 3T TY _ _ ^ ' ! CHICAGO AMERICAN MEDICAL ASSOCIATION FIVE HUNDRED AND THIRTY-FIVE NORTH DEARBORN STREET 1916 TRANSIENT AURICULAR FIBRILLATION An Electrocardiographic Study Thesis presented to the Faculty of the Graduate School of the University of Pennsylvania in partial fulfilment of the requirements for the degree of Ph.D., 1916. BY EDWARD B. KRUMBHAAR, M.D. (From the John Herr Musser Department of Research Medicine, University of Pennsylvania, Philadelphia.) CHICAGO AMERICAN MEDICAL ASSOCIATION FIVE HUNDRED AND THIRTY-FIVE NORTH DEARBORN STREET 1916 B)C UBHARY TRANSIENT AURICULAR FIBRILLATION AN ELECTROCARDIOGRAPHIC STUDY * EDWARD B. KRUMBHAAR, M.D. PHILADELPHIA In this communication are presented the results of a detailed study, by means of the electrocardiograph, of six individuals exhibiting the change from a normal heart rhythm to that of auricular fibrillation. Although the disturbance of cardiac mechanism that causes this type of cardiac irregularity incoordinate contraction or fibrillation of the auricular musculature has been understood only during the past few years, its clinical prototype, the pulsus irregularis perpetuus of Hering, or the totally irregular pulse, has for years been recognized as one of the commonest as well as one of the gravest forms of cardiac arrhyth- mia. Perhaps from the widespread use of Hering's terminology, how- ever, the erroneous impression has been prevalent that this condition once present is practically always permanent. Already a sufficient num- ber of cases have been published to combat this view, so that we must now consider that auricular fibrillation, like the other disturbances of the cardiac mechanism premature contractions, heart block and alter- nation may, though less frequently, occur in a transitory as well as a permanent form. My main thesis will be to show not only that tran- sient auricular fibrillation constitutes a well recognized condition, but that it may be subdivided into three well-defined groups. REVIEW OF THE LITERATURE Cushny and Edmunds, 1 in the paper that first propounded the theory that a totally irregular pulse is due to fibrillation of the auricles, were led to their experimental work by the study of a woman who had had numerous paroxysmal attacks of fibrillation during several years of observation. No determining factor was discovered clinically, but the conclusion was reached that the attacks were due to reflex vagus inhi- bition. * From the John Herr Musser Department of Research Medicine, Univer- sity of Pennsylvania, Philadelphia. 1. Cushny, A. R., and Edmunds, C. W. : Paroxysmal Irregularity of the Heart and Auricular Fibrillation, Am. Jour. Med. Sc., 1907, cxxxiii, 66. *i I > v > ** > v AiV?HY*H j Very similar cases have been reported by Fox, 2 Hornung, 3 G. C. Robinson, 4 Popper, 5 and Lewis and Schleiter. 6 These patients, as was Cushny and Edmund's patient, were all over 50 years of age and had had numerous attacks, lasting from a few minutes or hours to several days, and extending over many years. In none was a valvular defect present, but hypertension and preponderance of the left ventricles were found in all. Another interesting group of ten cases has been reported by Heitz, 7 together with polygraphic records, which unfortunately do not absolutely preclude the existence of some other form of arrhythmia. In another series, out of a total of 120 patients with auricular fibrilla- tion examined electrocardiographically, Fahrenkamp 8 found only four in whom the trouble was transient (3.3 per cent.). Though paroxysmal in character, the attacks were all single and short (one fatal), seen in acute conditions, such as Graves' disease, pneumonia and septicemia. Further details of these cases will be considered later, in connection with the discussion of the cases here reported. The cases reported by Falconer and Dean 9 and by Schwarzmann 10 developed transient attacks of fibrillation in the presence of an already existing heart block. The complication that this causes makes it inadvisable to include them in this discussion. The older theory that a temporarily but totally irregular pulse (delirium cordis) is not uncommon and frequently disappears under digitalis medication was in most cases due to imperfect observation. The probability is that in such cases the slight degree of arrhythmia, which became still less with the improvement of the patient, became unnoticeable to the touch, in spite of the fact that the underlying con- dition of fibrillation persisted. In some cases, also, as Fahrenkamp and others have pointed out, the occurrence of complicated groups of extra- systoles may (in the absence of electrocardiograms) present a picture indistinguishable from auricular fibrillation. 2. Fox, G. H. : Transitory Delirium Cordis, Am. Jour. Med. Sc., 1910, cxl, 815. 3. Hornung, O. : Ueber atypische tachykardische Paroxysmen, Deutsch. Arch, f. klin. Med., 1907, xci, 469. 4. Robinson, G. C. : Paroxysmal Auricular Fibrillation, THE ARCHIVES INT. MED., 1914, xiii, 298. 5. Popper, H. : Ueber Anfalle von Vorhofflimmern, Med. Klin., 1915, xi, 885. 6. Lewis, T., and Schleiter, H. G. : The Relation of Regular Tachycardias of Auricular Origin to Auricular Fibrillation, Heart, 1911-1912, iii, 173. 7. Heitz, J. : La forme paroxystique de 1'arythmie complete, Ann. de med., 1914, i. 483. 8. Fahrenkamp, K. : Voriibergehende komplette Herzunregelmassigkeiten unter dem klinischen Bilde der Arythmia Perpetua mit Beobachtungen iiber Vaguswirkung, Deutsch. Arch. f. klin. Med., 1914, cxvii, 1. 9. Falconer, A. W., and Dean, G. : Observations on a Case of Heart Block Associated with Intermittent Attacks of Auricular Fibrillation, Heart, 1911- 1912, iii, 247. 10. Schwarzmann. G. S. : Ueber ein Fall von Herz Block mit Paroxysmalem Vorhofflimmern. Zentralbl. f. inn. Med., 1914, xxxv, 1001. The six cases of fibrillation mentioned above are here reported in detail, in the hope that they may throw some light on the poorly under- stood pathogenesis of this common and serious condition and on the prognosis of such transient cases. The fibrillation in four of the cases was found to be transient, and in the other two cases developed while the patients were under observation. These four represent 7.5 per cent, of the total number of cases of auricular fibrillation studied electro- cardiographically at the University Hospital during a period of two Fig. 1 (Case 1). Electrocardiogram of V. W., showing transient auricular fibrillation in lobar pneumonia. In this, as in other electrocardiograms of this series, records were taken from the three customary leads. The tension of the string was so standardized that 1 millivolt caused a deflection of 1 cm. As the string could not be standardized with the patient in circuit, 1,400 ohms were added as an arbitrary equivalent of the patient's resistance. Platinum string, resistance about 3,500 ohms. Time intervals are expressed in fifths of second and occasionally by vertical lines indicating % and ^5 second. In this figure, note (1) absence of sign of auricular contraction (P wave) ; (2) ventricular arrhythmia (irregular occurrence of R) ; and (3) occasional coarse waves of fibrillation. and a half years. While this is apparently an unusually high percen- tage of transient fibrillation, it is very probable that the wider use of graphic methods of registration will in the near future demonstrate its greater frequency. X> .* J *.." I [ I P T -P > T -p f T *^^^h>^k^ - Fig. 2 (Case 1). Electrocardiogram of same patient as in Figure 1, show- ing normal rhythm during convalescence from pneumonia. Note reappear- ance of P wave, regular occurrence of R and absence of fibrillation waves. (The print of Lead II, as in a few other instances, has been retouched for purposes of reproduction.) I. TRANSIENT AURICULAR FIBRILLATION IN LOBAR PNEUMONIA CASE 1. V. M., a white man, married, S3 years old, a tinsmith by trade, was admitted to the hospital March 17, 1915, on the third day of a typical attack of lobar pneumonia, involving the left lower lobe. A total arrhythmia was noticed on admission, although the patient had never noticed such arrhythmia before and had never to his knowledge had any previous cardiac trouble Cardiac dulness was not increased and there were no valvular murmurs. Except for two attacks of gonorrhea twenty-five years before, he had never been seriously ill. He had never had rheumatism, tonsillitis or other fever, although a later blood examination gave a positive Wassermann reaction. The systolic blood pressure on admission was 120, diastolic 95. After the reestablishment of normal rhythm, the systolic pressure was 115, diastolic 85. An electrocardiogram (Fig. 1) taken on the day of admission showed the presence of auricular fibrillation (of the coarse type), absence of the P wave, and a moderate degree of arrhythmia. The form of the electrocardiogram shows no other deviation from the normal, except that the T wave is inverted in Lead III. Tincture of digitalis (0.6 c.c. three times a day) was begun at once and continued during the patient's stay in the hospital of more than a month. Although the pneumonic crisis was reached in four days after admis- sion, with normal resolution of the involved lobe, the pulse rate remained over 100 for another ten days. The arrhythmia became less and less marked, until, one month after admission, with the pulse rate varying between 60 and 90, arrhythmia was imperceptible. An electrocardiogram (Fig. 2) taken at this time showed a regular rhythm, with the reappearance of the P wave. The T wave in Lead III is no longer inverted and is more pronounced in the other two leads than in the former record. The patient was discharged in good condition and since then has had no return of any cardiac irregularity. A polygram (Fig. 3) taken three months later revealed a regular radial pulse (rate 62 beats per minute) with a normal jugular pulse. The fact that the myocardium had not yet returned to normal, however, was shown by the persistence of pretibial edema and dyspnea on exertion. 4 Fig. 3 (Case 1). Normal polygram three months after pneumonia. Note regular radial rhythm and normal "a, c, v" type of venous pulse, with promi- nent "a" wave. Summary of Case. A patient in the third day of an attack of lobar pneumonia was found to have auricular fibrillation with considerable arrhythmia, although there had been no previous history of heart dis- ease. After recovery from the pneumonia, the arrhythmia gradually decreased, until one month later the electrocardiogram showed a nor- mal P wave and regular rhythm. The exact time at which the auricle began again to beat coordinately was not determined, but was appar- ently not accompanied by any noticeable subjective symptoms or change in rate. That the return to a normal rhythm was permanent is shown, by polygraphic records taken three months later. II. TRANSIENT AURICULAR FIBRILLATION OF NERVOUS ORIGIN IN SYPHILITIC MYOCARDITIS CASE 2. B. A., a white woman, married, 38 years old, was admitted to the. hospital March 2, 1915, for the removal of a uterine fibroid. She had had measles, mumps, appendicitis and typhoid, but had totally recovered from each, and had otherwise been healthy. Her husband was living and well, but she. had had no children, one miscarriage, and the Wassermann reaction was. strongly positive. She had never complained of any cardiac trouble until three^ weeks before admission, at which time after a hard day's work she had an attack of palpitation, dyspnea and irregular heart action. Another attack occurred the next evening and the symptoms continued more or less marked until admission to the hospital. On the day of admission she had a similar Fig. 4 (Case 2). Electrocardiogram of Mrs. B. A., taken March 2, 1915, showing transient auricular fibrillation in syphilitic myocarditis. Note same disturbances of mechanism as in Figure 1. attack, but more serious than any previous one, and the extreme rapidity and irregularity of the heart action necessitated the abandonment of the operation. The patient attributed this attack to the nervous excitement aroused by con- templation of the operation. At the time of the electrocardiographic study she was in a very nervous state, with warm, flushed skin, and marked tremor of the hands. The radial pulse was distinctly irregular, rapid (180 per minute), quick, full, with increased tension, the wall slightly sclerotic. The cardiac dulness was slightly increased T T * i*Ji^^ . Q T ' ~ Fig. 5 (Case 2). Electrocardiogram of same patient as in Figure 4, taken March 3, showing normal rhythm. to the left, the apex beat distinct in fifth space, 12 cm. from the mid- line. There was a distinct apical systolic murmur transmitted to the axilla, with accentuated second aortic and pulmonic sounds. An electrocardiogram (Fig. 4) showed the arrhythmia to be due to an auricular fibrillation of the 10 coarse type. With the fear of operation removed, and after a quiet night in bed, the patient awoke the next morning without any disagreeable subjective sensations, and the pulse was regular and much slower. The systolic blood pres- sure, which during the attack of fibrillation had been 165, was found during the period of regular rhythm to be 132. The diastolic fell from 85 to 78. No. 3t :fc E -^R-^R----*: Fig. 6 (Case 2). Electrocardiogram of same patient as in Figure 4, taken March 9, showing normal rhythm occasionally disturbed by an auricular pre- mature contraction. An electrocardiogram (Fig. 5) taken the same morning showed a regular rhythm, with a normal P wave. The complexes were practically the same as in the former record (the more rapid passage of the film being shown by the increased intervals of the time marker), except that systole (as indicated by 11 the end of T) lasted more than 0.3 second and was immediately followed by thg next P wave. For several days the patient's improvement continued, the pulse being either quite regular or showing only an occasional slight irregu- larity. The nature of this irregularity is shown in Figure 6 to be due to an occasional extrasystole. Although there is practically a complete compensatory pause, this is probably an auricular extrasystole merging with the preceding T, because the following ventricular complex shows no ectopic origin. Fig. 7 (Case 2). Electrocardiogram of same patient as in Figure 4, taken March 10, showing another period of transient auricular fibrillation. After one week's improvement, the patient awoke one morning from a ter- rifying dream, and felt her heart pounding violently. Auscultation disclosed a total arrhythmia, with disappearance of all murmurs, a cardiac rate of 130, and a pulse deficit of 50. The systolic pressure was found to have risen to 155, the diastolic remaining at 70. An electrocardiogram (Fig. 7) showed that 12 coarse fibrillation had again supervened. In Lead I, especially, the fibrillatory waves were so marked and regular that at first the condition of auricular flutter was suggested. This was rejected, however, as the rhythm of the waves of fibrillation was not absolutely regular and the ventricular response was totally irregular, and not explainable by any combination of heart block. During the same afternoon, the patient suddenly announced that the trouble had stopped, and the rate was found to be much slower (80 per minute) and less irregular. Occasional extrasystoles, however, persisted for forty-eight hours. After one week of normal heart action, the patient was returned to the surgical wards for myomectomy and from this time on she flatly refused to allow further cardiac examination. It is of interest that the patient later volunteered the information that she had had a strong psychic disturbance before each cardiac attack. It is of course possible for a third and unknown factor to have been responsible for both the nightmare and the paroxysmal attack of fibrillation, but the pre- sumption is strong that the cardiac attack was induced by nervous excite- ment. The chronic endocarditis, enlarged heart and positive Wassermann would all indicate a basic myocardial involvement requiring only the nervous excita- tion to produce the paroxysm of fibrillation. The appearance of auricular extrasystoles for a few days after each attack is also of interest. It is impos- sible to say whether these also were of nervous origin or a sign of myocardial degeneration, but here again the time of their appearance affords a strong presumption that the psychic element was at least one factor in their production. A recent report, one year after the period of observation, states that the patient is now in a state of chronic decompensation and that the arrhythmia has become permanent. Summary of Case. In a highly excitable, nervous woman, on sev- eral occasions strong emotional excitement was observed to be followed by transient attacks of auricular fibrillation. Though the blood pres- sure was higher during the periods of fibrillation, the state of the pres- sure just preceding the attacks could not be determined. After the nor- mal auricular activity had returned, the regular rhythm was disturbed for one or two days by occasional auricular extrasystoles. After repeated attacks during the next year, the fibrillation, which had a probable syphilitic myocarditis as a basis, became permanent. III. TRANSIENT AURICULAR FIBRILLATION OF TOXIC ORIGIN CASE 3. W. W., a white man, single, aged 40 years, was referred to me for examination on Oct. 12, 1915, by Dr. Newlin, on account of extreme palpitation, dyspnea and arrhythmia of two days' duration. One brother had died of heart disease, following over-indulgence in alcohol, and there was a general family tendency toward overeating and overdrinking. Except for occa- sional attacks of tonsillitis, the patient had not had any severe infections, but had always eaten too much, and had been a steady consumer of alcohol, but seldom to the point of intoxication. For years he had had some distress after eating and had occasional attacks of heartburn. He had always considered himself in excellent health, however, had not overworked, and had been able to under- take violent exercise without the slightest embarrassment. The present illness began two months previously while the patient was on a hunting trip in the Rocky Mountains (altitude 5,000 feet). Following an attack of acute bronchitis, the patient noticed that he easily became dyspneic and tired, and that his heart occasionally "skipped" beats. The trip was aban- doned, and with appropriate treatment the symptoms disappeared. Systolic blood pressure at this time was 150. In three weeks' time the patient felt 13 entirely well, except for a mild afebrile tonsillitis, which persisted for several weeks. On a carbohydrate-poor diet he succeeded in losing 50 pounds and the systolic blood pressure dropped to 140. He then began three days of increased alcohol consumption, and became nervous and irritable for several days, but without cardiac symptoms. Then without adequate explanation, after one week of total abstinence, extreme palpitation and arrhythmia developed, with dizzi- ness on standing. The systolic pressure at this time was only 110, diastolic 90. This attack had continued for the two days immediately preceding his visit to the hospital, but he had improved sufficiently to walk without distress. Fig. 8 (Case 3). Electrocardiogram of patient W. W., who had no discover- able organic lesion, showing transient auricular fibrillation of toxic origin Physical Examination. The patient was a large, powerful, well-nourished man, weighing 25S pounds. Although normally rather lethargic, he was at that time apprehensive and slightly dyspneic. The eyes were negative. The tongue was moderately coated, the tonsils red and swollen, but without exudate. There were irregular heavings of the neck, but no distinct venous pulsation. The pulse rate was about 120 and very irregular in force and rhythm. The vessel wall was indefinitely palpable. The heart rate by auscultation was 160, also irregular in force and rhythm, giving a pulse deficit of 25 per cent. The 14 'apex beat was not visible or palpable ; the cardiac dulness extended to the right border of the sternum in the fourth space, and 1 cm. to the left of the midclavicular line at the fifth space. No murmurs were audible, but the muscle sounds were rumbling and of poor quality. Examination of the lungs and abdomen was negative. The legs showed very slight pitting on sustained To. 3. Fig. 15 (Case 5). Electrocardiogram of same patient as in Figure 14, taken January 14, showing permanent auricular fibrillation. Though this symptom has not been of long duration, the waves of fibrillation are not visible. confirmed the diagnosis of fibrillation and recorded the response of the heart to digitalis (slowing of rate, lessening of arrhythmia, change in form and Q and T waves). At no time were the waves of fibrillation of the coarse type. The patient, however, failed to improve clinically, and succumbed in three days with the signs of acute dilatation. Necropsy was refused. Summary of Case. A woman with mitral stenosis of at least four years' duration had such severe signs of decompensation during her fourth pregnancy that labor had to be induced. She improved during the first week of the puerperium, but then a second and more severe 22 stage of decompensation set in. In the third day of this attack a very rapid pulse rate was initiated (auricular flutter?) and this progressed to auricular fibrillation, which persisted until death three days later. The development of auricular fibrillation after a transient period of flutter has been frequently observed ; in fact the administration of large doses of digitalis has been recommended in cases of auricular flutter in the hope that the disturbance may pass on to fibrillation and thence, perhaps, return to normal rhythm. The contingency must at least be considered, therefore, in the present case that digitalis was a con tributing factor to the causation of fibrillation. VI. DEVELOPMENT OF PERMANENT AURICULAR FIBRILLATION DURING CARDIAC DECOMPENSATION Another case is reported in which auricular fibrillation developed after three years occasional observation. CASE 6. M. H., an American woman, 35 years old, married, was admitted to the University Hospital on March 21, 1916, with the usual signs and symp- toms of cardiac decompensation. This was a recurrence similar to those seen in her previous admissions in the spring of 1913 and the autumn of 1914. She had had measles, mumps, scarlet fever and acute articular rheumatism. Her cardiac symptoms were first noted at the time of a second attack of acute polyarthritis thirteen years before, and reappeared during an attack of "grippe" nine years before. For the past four years she has suffered from some shortness of breath and puffiness of the ankles, which on the two occasions mentioned became bad enough to make her seek the hospital. At both these times she improved quickly under hospital care, and she had never noticed any irregularities of her heart further than an occasional dropped beat. The present illness started two weeks before admission with greatly increased dyspnea, palpitation and pericardial pain. Four days later the patient suffered a "stroke," losing the power of speech and of moving the left arm, but not becoming unconscious. Speech returned after sleep, but the left thumb, index finger and left side of the face have remained numb and weak. Four days after that, sudden pain developed low in the right chest with cough and hemop- tysis, and the lesion was later shown by the Roentgen ray to be a pulmonary infarct. Social and family history irrelevant. Physical Examination. It was found on examination that the patient was more emaciated than on previous admissions ; the tongue was dry and coated, with herpes on the lips. The cardiac dulness extended 3 cm. to the right of the midline and 13 cm. to the left. The apex beat was well localized in the fifth space 2 cm. outside of the midclavicular line. There was a harsh systolic murmur, best heard at the apex and transmitted to the base and axilla. No arrhythmia was noted. The liver was palpable 4 cm. below the costal margin and the right kidney was also palpable. There was dulness and rales at the bases of both lungs, but more marked on the right. The leukocytes varied between 10,000 and 14,000; hemoglobin 95 per cent., red blood cells 5,480,000. The urine was acid, specific gravity 1.018, contained a cloud of albumin, urates, but no casts. The Wassermann reaction was negative. The systolic blood pressure varied between 115 and 120, the diastolic between 77 and 90. The signs of decompensation decreased steadily during the patient's stay in the hospital, so that she was able to leave in one month in very good condition. The cardiac arrhythmia, which was first discovered by electrocardiographic examination, was still present, but frequently had been so slight that it could not be detected by simple digital examination of the pulse. Fig. 16 (Case 6). Electrocardiogram of patient M. H., a case of mitral stenosis with decompensation, taken April 14, 1913, showing normal rhythm (sinus arrhythmia). Fig. 17 (Case 6). Electrocardiogram of same patient as in Figure 16, taken in November, 1914. The figure shows occasional auricular premature con- tractions. 24 Electrocardiograms (Fig. 16) were taken during each stay at the hospital. The one taken in 1913 showed a normal rhythm and complexes, with a P-R interval of 0.18 second. No abnormalities of rhythm were noted either dur- ing the examination or during the patient's stay in the hospital. The electro- cardiogram (Fig. 17) taken in 1914 showed, besides some small changes in the form of the ventricular complex, the same P-R interval as on the first admis- sion, but two definite auricular extrasystoles in addition. The large P wave Ak.fega.jLwJ <. 3. H3C *" * Fig. 18 (Case 6). Electrocardiogram of same patient as in Figure 16. show- ing permanent auricular fibrillation (waves of coarse type). characteristic of mitral stenosis persisted. On the patient's last admission in March, 1916, electrocardiograms (Fig. 18) taken on several occasions con- stantly showed a coarse type of auricular fibrillation. The form of the ven- tricular complexes, however, had changed very little from that of the two former admissions. Although the patient improved steadily from a clinical point of view, fibrillation persisted with a gradual decrease of the coarseness of the fibrillation waves. 25 Summary of Case. In a case of mitral stenosis of some years' standing with recurrent periods of decompensation* electrocardio- graphic records were made over a period of three years. At first the rhythm was normal, next was broken by occasional auricular extra- systoles and finally was found to have been replaced by a constant, coarse type of fibrillation. If the history may be relied upon, this prob- ably developed within two weeks of admission to the hospital, when decompensation was further complicated by cerebral and pulmonary emboli and infarct formation. GENERAL COMMENT A comparison of the foregoing cases with those mentioned in the literature allows the change from normal rhythm to auricular fibrilla- tion to be subdivided into three types. In the first group falls the first case of this series, twelve of Cohn's 11 pneumonia cases, all four of those reported by Fahrenkamp, Robin- son's 12 recent case, the fourth of Heitz's and the sixth of Fox's series. In these cases the predominant factor was some acute infection or intoxication (pneumonia, Septicemia, hyperthyroidism), and the attack of fibrillation was single. No organic cardiac lesion was found or need be presumed, and when the infection or intoxication was removed the rhythm returned permanently to normal. In the second group, and this comprises the larger number of those cases reported as paroxysmal auricular fibrillation, belong the second and probably the third cases of this report, also the remaining nine of Heitz's, the four of Hornung's, four of Fox's series, and the single cases of Robinson, Popper, and Lewis and Schleiter. At the time of observa- tion all but three of these patients were in the sixth or seventh decade of life, but the onset of attacks when mentioned occurred as follows : Two in the third decade, two in the fourth, five in the fifth, five in the sixth, and six in the seventh decade. The average duration of the condition was over nine years. Both sexes were equally involved. Previous dis- eases bore no relationship to the condition ; even the cardiac condition varied greatly. In eight cases mitral lesions were present, but in ten others no valvular lesion was found. In nearly all, however, there was distinct evidence of myocardial disease. The blood pressure was found increased in seven and not increased in eight. Arteriosclerosis was noted in ten. Factors determining the paroxysms were either absent or widely varying in character. In six, emotional excitement preceded attacks and in two others they were attributed to a general increase in 11. Cohn, A. E. : Certain Phases of the Action of Digitalis in Pneumonia, Meeting of Am. Soc. for the Advancement of Clin. Investigations, Washington, D. C, May 8, 1916, unpublished. 12. Robinson, G. C. : Transient Auricular Fibrillation in a Healthy Man Fol- lowing Hydrogen Sulphid Poisoning, Jour. Am. Med. Assn., 1916, Ixvi, 1611. 26 the patient's nervousness. In four, attacks were induced by exercise or fatigue, but in three others they nearly always occurred during sleep. Overeating (three cases), defecation, and asthmatic attacks were held responsible in other cases. Many of these factors might be grouped under the head of conditions that raise blood pressure, but in some cases this factor was definitely absent. The duration of the individual attacks was also extremely variable, ranging from a few minutes to several weeks; in most cases, however, they lasted a few hours. In the early stages the attacks tended to be either short or infrequent, the duration and frequency of the attacks increasing as the disease progressed. They usually began abruptly, without premonitory symp- toms, and caused more or less severe cardiac embarrassment. The attacks ended either during sleep or with such abruptness that the patient could notice the return to regular rhythm. In only one case were extrasystoles noticed between attacks, and in two cases there occurred also attacks of paroxysmal tachycardia. In this connection Lewis and Schleiter have called attention to the closely related mechanism of auricular extrasystoles, fibrillation and paroxysmal tachychardia. Six patients died while under observation (mostly from cardiac complications during regular rhythm) ; in five others fibrillation had become permanent; while six of the remaining ten were considered as improved. Venesection, digitalis and quinin have been used successfully and the ordinary treatment of cardiac failure seems advisable. In a third group, represented by the last three cases of this report and the fourth of Fox's series, the onset of fibrillation should be regarded as but one more link in the chain of cardiac failure. In all these cases the signs of mitral disease with decompensation were prom- inent and had existed for years. In two cases the first attack of fibrilla- tion proved to be permanent, one of these being preceded by auricular extrasystoles, in one other the permanent period was preceded by one transient period, and in the fourth a transient period lasting three days occurred a few days before death from cardiac failure (normal rhythm). The development of most of the cases of permanent auricu- lar fibrillation is probably of this character, but closer observation and wider use of graphic methods would probably reveal one or more pre- vious transient periods. As auricular fibrillation aggravates the prog- nosis, energetic treatment should be instituted at these times, in order to delay or avoid the onset of the permanent condition. That this should not include too large doses of digitalis is indicated by the fact that in two cases at least (Case 3 of this report and Robinson's case) digitalis was considered as a possible factor in the production of fibril- lation. Its value as a cardiac remedy, however, especially after fibril- lation is established, makes it a necessary aid in practically all such cases. 27 SUMMARY Four cases are described in which the transition of the cardiac mechanism was observed from normal rhythm to auricular fibrillation and back again. In two others the development of permanent auricular fibrillation was observed. These have been compared with similar cases in the literature. CONCLUSIONS Transient auricular fibrillation is a comparatively rare condition, although the more widespread and frequently repeated use of the string , galvanometer will probably reveal many more cases than are now available for study. The change from normal rhythm to auricular fibrillation occurs in three well-defined groups: 1. In the course of an acute infection, such as pneumonia or septi- cemia, or of an acute intoxication, such as alcohol or hyperthyroidism, or possibly from other temporary causes, one or more attacks of fibril- lation may occur for several days, but disappear permanently when the source of intoxication is removed. In this group permanent myocardial damage is probably not present. 2. In another group, probably always associated with underlying myocardial degeneration, paroxysms lasting from a few minutes to many hours or even days, may be induced by a great variety of causes and occur over a period of many years. They tend, however, to become more lasting or more frequent or both, and eventually with the progress of the myocardial disease the fibrillation becomes permanent. Death may occur, however, before permanent fibrillation has ensued, or clin- ical improvement may take place with the onset of fibrillation. The term "paroxysmal" is most aptly applied to cases of this group. 3. In a third group, in which the signs of valvular or myocardial disease are more, prominent, the original change from normal rhythm to fibrillation is liable to be permanent, or at least be preceded by only a few transient periods. A determining factor in such cases is liable to be some cardiac complication, such as pulmonary embolus, acute pericarditis, or the added strain of pregnancy, and may be preceded by a transient period of flutter. No relationship between the onset of fibrillation and changes in blood pressure could be established. In the earlier stages of fibrillation the electrocardiogram usually shows coarser waves of fibrillation, so that this evidence, when pres- ent, may be guardedly used to influence favorably the prognosis. 28 The occurrence of fibrillation, while a bad factor in prognosis, does not necessarily indicate either permanency or a fatal outcome. It is of graver significance when it occurs in valvular cases with prominent signs of decompensation, and of least significance in the cases of the first group. The usual treatment of heart failure (rest in bed, the digitalis group, removal of sources of intoxication, etc.) help to terminate attacks of fibrillation, but excessive doses of digitalis may help to induce this condition. These cases were studied in the wards and laboratory of the University Hospital, while under the care of Drs. Stengel, Hirst, Anspach and Newlin, to whom my thanks are due. UNIVEESITY OF CALIFOENIA LIBEAEY, BEEKELEY THIS BOOK IS DUE ON THE LAST DATE STAMPED BELOW Books not returned on time are subject to a fine of 50c per volume after the third day overdue, increasing to $1.00 per-volume after the sixth day. Books not in aewed if application is made before V - - i period. ; 141951 MAY 14 1951 75m-7,'30 Makers Syracuse, N. Y. PAT. JAN. 21 ,1908 UNIVERSITY OF CALIFORNIA LIBRARY