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Paroxysmal auricular fibrillation in the course of right heart failure due to chronic pulmonary tuberculosis
PAROXYSMAL AURICULAR OF RIGHT HEART
FIBRILLATION FAILURE DUE
PULMONARY
IN THE COURSE TO CHRONIC
TUBERCULOSIS
CASE
REPORT’
MILTON B. ROSENBLATT, M.D. NEW YORK, N. Y.
T HAS been well established that cardiac failure may be produced by a hypertension of the lesser circulation. In this type of failure the increased resistance in the pulmonary circulation results in hypertrophy and dilatation of the right side of the heart. While this condition may be due to a primary obliterating pulmonary arterial disease, it is more commonly due to chronic diseasesof the lung. One of the notable features of this form of cardiac insufficiency is the extreme infrequency of disturbances in cardiac rhythm. This point has been emphasized by White1 and also by Smith,2 who showed that the heart in pulmonary disease characteristically failed with normal rhythm. In a study of right heart failure previously reported3 and in observation of these cases on the Tuberculosis Division for the past five years, this is the first instance of cardiac arrythmia that we have encountered due only to right ventricular failure.
I
S. G., a fifty-five-year-old baker, was admitted to the Montefiore Hospital on Sept. 20, 1936, with a history of pulmonary tuberculosis of twenty years’ duration. With the exception of a brief period of hospitalization at the onset he had been able to work all the time and complained only of a moderate productive cough. In 1934, following an hemoptysis, there was an exacerbation of the pulmonary tuberculosis, and his condition became progressively worse up to the time of admission. In addition to his pulmonary symptoms he had experienced recurrent attacks of syneope since 1931. These seizures were brief, occasionally associated with convulsions, occurred about twice monthly, and recovery was spontaneous each time. Physical examination showed the patient to be well developed, well nourished, and comfortable. There were no cardiac symptoms. The heart was not enlarged, there were no murmurs, and the rhyt,hm was regular. The systolic blood pressure was 110 and the diastolic pressure was 60. The liver edge was palpable 2 cm. below the costal border but was not tender. There was no peripheral edema. Roentgen ray examination of the chest disclosed an extensive bilateral tuberculosis of the upper lobes with several large cavities. The cardiac outlines were within normal limits. The important laboratory data are summarized as follows: Sputum, positive; Wassermann reaction,, negative; urine, negative; blood chemistry, negative; red blood cells, 4,290,OOO; hemoglobin, 82 per cent; white blood cells, 12,500 with normal differential; sedimentation rate, 26 mm. in one hour; venous pressure, 4 cm. of water ; electrocardiogram, normal except for low voltage. *From
the
Tuberculosis
Divisim
of
the
114
Montefiore
Hospital.
ROSENBLATT
:
PAROXYSMAL
AURICULAR
FIBRILLATION
115
The clinical course in the hospital was characterized chiefly by recurrent large hemoptyses. However there was no remarkable change in his general condition until Nov. 3, 1936, when he suddenly became dyspneic, and examination revealed the pulse to be totally irregular. The cardiac rate at the apex was 140 per minute and the pulse rate was 116. There was no visible venous engorgement or peripheral edema. No electrocardiogram was taken at that time. The patient was rapidly digitalized and completely recovered within twenty-four hours. An electrocardiogram on the following day showed a normal rhythm. On November 14 the patient experienced a similar attack and a tracing taken during the seizure showed auricular fibrillation with a rapid ventricular rate (Fig. 1). These episodes were repeated at approximately weekly intervals without any manifestations of congestive heart failure until Dec. 7, 1936, when, in the course of another paroxysmal attack, the dyspnea became progressively worse, and the patient became markedly cyanotic. The liver was enlarged to 4 cm. below the eostal There was no response to therapy, border, but there was no edema of the extremities. and the patient died on Dec. 9, 1936. On post-mortem examination the heart weighed 450 gm. There was no pericardial fluid. The right auricle and right ventricle were markedly dilated and hypertrophied, but the left auricle and ventricle were normal in size. The maximum thickness of the right ventricular wall was 10 mm. There was no valvular disease.
Fig.
The coronary arteries showed out. Microscopic examination Of interest in the examination which was indicative of the patient.
1.
slight sclerotic thickening but were patent throughshowed hypertrophy of the fibers of the right ventricle. of the lungs was the finding of extensive bronchiectasis long duration of the pulmonary tuberculosis in this
Auricular fibrillation, in itself, has been found on many occasions in patients on the tuberculosis wards. However, it has always been associated with hypertension, coronary artery disease, fibrinous pericarditis, or valvular disease. This is the first instance we have observed in which the only pathological condition found on autopsy was hypertrophy and dilatation of the right side of the heart. REFERENCES
1. White, Paul: Heart Disease, ed. 2, New York, 1937, The Macmillan Co., p. 739. 2. Smith, K. 5.: The Heart in Pulmonary Disease, Post-Graduate M. J. 6: 43, 1930. 3. Nemet, G., and Rosenblatt, M. B.: Cardiac Failure Secondary to Chronic Pulmonary Tuberculosis, Am. Rev. Tuberc. 35: 713, 1937.
FIBRILLATION FAILURE DUE
PULMONARY
IN THE COURSE TO CHRONIC
TUBERCULOSIS
CASE
REPORT’
MILTON B. ROSENBLATT, M.D. NEW YORK, N. Y.
T HAS been well established that cardiac failure may be produced by a hypertension of the lesser circulation. In this type of failure the increased resistance in the pulmonary circulation results in hypertrophy and dilatation of the right side of the heart. While this condition may be due to a primary obliterating pulmonary arterial disease, it is more commonly due to chronic diseasesof the lung. One of the notable features of this form of cardiac insufficiency is the extreme infrequency of disturbances in cardiac rhythm. This point has been emphasized by White1 and also by Smith,2 who showed that the heart in pulmonary disease characteristically failed with normal rhythm. In a study of right heart failure previously reported3 and in observation of these cases on the Tuberculosis Division for the past five years, this is the first instance of cardiac arrythmia that we have encountered due only to right ventricular failure.
I
S. G., a fifty-five-year-old baker, was admitted to the Montefiore Hospital on Sept. 20, 1936, with a history of pulmonary tuberculosis of twenty years’ duration. With the exception of a brief period of hospitalization at the onset he had been able to work all the time and complained only of a moderate productive cough. In 1934, following an hemoptysis, there was an exacerbation of the pulmonary tuberculosis, and his condition became progressively worse up to the time of admission. In addition to his pulmonary symptoms he had experienced recurrent attacks of syneope since 1931. These seizures were brief, occasionally associated with convulsions, occurred about twice monthly, and recovery was spontaneous each time. Physical examination showed the patient to be well developed, well nourished, and comfortable. There were no cardiac symptoms. The heart was not enlarged, there were no murmurs, and the rhyt,hm was regular. The systolic blood pressure was 110 and the diastolic pressure was 60. The liver edge was palpable 2 cm. below the costal border but was not tender. There was no peripheral edema. Roentgen ray examination of the chest disclosed an extensive bilateral tuberculosis of the upper lobes with several large cavities. The cardiac outlines were within normal limits. The important laboratory data are summarized as follows: Sputum, positive; Wassermann reaction,, negative; urine, negative; blood chemistry, negative; red blood cells, 4,290,OOO; hemoglobin, 82 per cent; white blood cells, 12,500 with normal differential; sedimentation rate, 26 mm. in one hour; venous pressure, 4 cm. of water ; electrocardiogram, normal except for low voltage. *From
the
Tuberculosis
Divisim
of
the
114
Montefiore
Hospital.
ROSENBLATT
:
PAROXYSMAL
AURICULAR
FIBRILLATION
115
The clinical course in the hospital was characterized chiefly by recurrent large hemoptyses. However there was no remarkable change in his general condition until Nov. 3, 1936, when he suddenly became dyspneic, and examination revealed the pulse to be totally irregular. The cardiac rate at the apex was 140 per minute and the pulse rate was 116. There was no visible venous engorgement or peripheral edema. No electrocardiogram was taken at that time. The patient was rapidly digitalized and completely recovered within twenty-four hours. An electrocardiogram on the following day showed a normal rhythm. On November 14 the patient experienced a similar attack and a tracing taken during the seizure showed auricular fibrillation with a rapid ventricular rate (Fig. 1). These episodes were repeated at approximately weekly intervals without any manifestations of congestive heart failure until Dec. 7, 1936, when, in the course of another paroxysmal attack, the dyspnea became progressively worse, and the patient became markedly cyanotic. The liver was enlarged to 4 cm. below the eostal There was no response to therapy, border, but there was no edema of the extremities. and the patient died on Dec. 9, 1936. On post-mortem examination the heart weighed 450 gm. There was no pericardial fluid. The right auricle and right ventricle were markedly dilated and hypertrophied, but the left auricle and ventricle were normal in size. The maximum thickness of the right ventricular wall was 10 mm. There was no valvular disease.
Fig.
The coronary arteries showed out. Microscopic examination Of interest in the examination which was indicative of the patient.
1.
slight sclerotic thickening but were patent throughshowed hypertrophy of the fibers of the right ventricle. of the lungs was the finding of extensive bronchiectasis long duration of the pulmonary tuberculosis in this
Auricular fibrillation, in itself, has been found on many occasions in patients on the tuberculosis wards. However, it has always been associated with hypertension, coronary artery disease, fibrinous pericarditis, or valvular disease. This is the first instance we have observed in which the only pathological condition found on autopsy was hypertrophy and dilatation of the right side of the heart. REFERENCES
1. White, Paul: Heart Disease, ed. 2, New York, 1937, The Macmillan Co., p. 739. 2. Smith, K. 5.: The Heart in Pulmonary Disease, Post-Graduate M. J. 6: 43, 1930. 3. Nemet, G., and Rosenblatt, M. B.: Cardiac Failure Secondary to Chronic Pulmonary Tuberculosis, Am. Rev. Tuberc. 35: 713, 1937.