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Prolonged paroxysmal tachycardia
Department PROLONGED
of Clinical PAROXYSMAL CASE
B. E.
HAMILTON,
Reports
TACHYCARDIA
REPORT*
M.D., AND D, HURWITZ, BOSTON, CASE
M.D.
MASS. REPORT
M.
B., cobbler, aged fifty years, 211 Armenian, entered the Second Medical Service of the Boston City Hospital on September 22, 1930. The history was obtained with difficulty because the patient spoke very little English. He had been in good health and had worked eorminuously until two weeks before entrance. At this time, following a heavy meal, the patient was seized with cramp-like pains in the umbilical region, later rising to the epigastric region. The pain fluctuated in severity, but persisted.
At entrance, the physical examination rate’ was 180 per minute. The rhythm was millimeters of mercury. The respirations &es were heard at both bases posteriorly. epigastrium. An electrocardiogram taken cardia, probably auricular in origin. The
was unimportant, except that the pulse regular. The blood pressure was 95/85 were 28 per minute. A few crepitant Slight tenderness ‘was elicited in the September 22 showed paroxysmal tachyrate was 200 per minute.
Though it was believed that the patient had had a coronary occlusion, no evidence appeared to support this suspicion. There was no fever. The white blood cell count at entrance was 10,500 per cubic millimeter of blood. ‘Later, it fell to 4,000 per cubic millimeter of blood. The paroxysmal tachyeardia persisted for thirty-five days. The only change in his condition throughout the thirty-five days was gradually increasing eongestive failure until the liver was definitely engorged and slightly tender; the &es at the lung bases increased, and a small amount of demonstrable fluid appeared at both bases. Curiously, there was more on the left than on the right. During the thirty-five days, he received the following medication: quinidine sulphate, 30 grains each day for two days, was given first, without effect on the This was stopped because of nausea and vomiting. Two doses of digalen heart. were given intravenously. The first dose was 9 grains. The second dose, given twenty-four hours later, was 10 grains. There was no appreciable effect. The following day powdered digitalis, 9 grains, was given by mouth. This dose -was repeated each day for three days. The dose was then reduced to 41/2 grains daily. This was continued for eleven days. The dose was then reduced to 1% grains daily. Throughout this time, the patient was under close observation. His heart rate was counted every hour throughout the twenty-four hours. ~There was no The digitalis was discontinued three days appreciable effect from the digitalis. *From Services
the Thorndike (Harvard) of
the
Memorial Boston
Laborator and City HOSP Ptal.
274
the
Second
and
Fourth
Medical
HAMILTON
AND
HURWITZ
:
PROLONGED
PAROXYSMAL
TACHYCARDIA
275
b’efore the ,paroxysm ceased. Quinidine sulphate, 6. grains in one dose, was given intravenously fourteen days after admission, two days after the dose of digitalis had bseen reduced to 4rh grains daily. The cardiac rate dropped from 180 per minute to 150 per minute in five minutes and then returned to 180 per minute gradually in twenty minutes. Forty-eight hours before the paroxysm ceased, quinine hydrochloride was given by mouth in lo-grain doses. An electrocardiogram taken after the first two or three doses showed a rate of 176 per minute, which was slightly lower than the average rate. After he had had a total of 70 grains of quinine h;ydrochloride over a period of forty-eight hours, his heart suddenly resumed a normal rhythm with a rate of 80 per minute. There was immediate improvement in
Fig. 1.-S&. l.-Sept. 22, 1930. l! Paroxysmal tachycardia, probably auricular. Rate ZOO. ? P-waves Lead III. QRS = 0.12 sec., slurred in all leads. T omosite main deflection in all leads. Right bundle-branch block (if tachycardia is auricular in origin.) symptoms. During the next few weeks, his was discharged in apparently good condition return to normal cardiac rhythm.
congestive four and
failure a half
cleared, and weeks after
he his
On April 4, 1931, five months after discharge, he was readmitted to the. hospital acutely ill. Following his first discharge from the hospital, he had been able to return to work and had been without symptoms until a few hours before his readmittance. He entered the hospital in a condition of shock. The temperature, by mlouth, was 96 degrees Fahrenheit. The pulse rate was 65 per minute. The respirations were 30 per minute. The white blood count was 20,000 per cubic milhmeter of blood. He’ lived only six hours following admission to the hospit& .’
276
THE
AMERICAN
HEART
JOURNAL
Post-mortem
Eza&%ution of Hear&-The weight was 360 gm. The organ was normal in size. The epicardium was smooth but showed slight discoloration over the posterior portion of the left ventricle. The myocardium was pale greyish red in color and was markedly scarred. Immediately below the mitral ring, extending posteriorly as far as the interventricular septum, and inferiorly as far as the apex, there was a pear-shaped area approximately 5 or 6 cm. in diameter where the myocardium was thinned, mottled yellowish grey in color, eon taining hyalin appearing bands ; the thickness at this point was 0.7 cm. The valves were negative with the exception of slight atberoma of the aortic. The aorta immediately above showed marked thickening of the intima, with the formation of plaques and nodules some of which were yellow in color and appeared atheromatous; others were bluish in color and hyalin in appearance, giving the appearance essentially
Fig. 2.-O& 10, 1930. Paroxysmal tachycardia, probably auricular. P-wave Lead III. QRS = 0.12 sec. slurred in all leads. Right bundle-branch Low amplitude (maximum 5 mm.). tachycarcl.ia is auricular in origin).
Rate
200.
block
?
(if
of syphilis. The mouths of both coronaries were patent but thickened. The right coronary at the level of the tricuspid valve showed almost complete occlusion. Tbe vessel at this point was yellowish grey in color and appeared hyalinized. Beyond this point the lumen was patent but very narrow. The interventricular portion of the left coronary about 2.5 cm. from its point of origin showed an occlusion by a red, soft tbrombus; beyond, the vessel wall was thickened but patent. The circumflex branch of the left coronary 1 cm. from its point of origin showed complete occlusion, from an old process. The healed infarcted area. described above lay below. During the patient’s stay in the hospital. he was under the care of Drs. L. B. Ellis, B. E. Hamilton, DL Hum&z, W. R. Ohler, W. H. Robey, and I?. W. White. The electrocardiograms were taken and interpreted under the direction of Dr. J. M. Faulkner. The post-portem examination was made by Dr. J. M. WoodalL
278
THE
AMERICAN
HEART
JOURNAL
COMMENT
The important
findings
are:
1. Dz&r%tio% of paroxymml tachycar&a.-Though it is known that paroxysmal tachycardia may continue indefinitely, a duration of more than a few days is rare and very few caseshave been reported with a known duration of thirty-five days with recovery-. The attack may have been present during the two weeks before admission, making a possible total of forty-nine days. 2. The patient was not conscious of his tachyeardia. He complained only of gastrointestinal disturbance. 3. The paroxysmal ta,chycardia was probably associated with a coronary occlusion with infarction. This was indicated by the subsequent post-mortem examination. There was no clinical evidence to confirm this diagnosis, except the unexplained paroxysmal tachycardia itself. The gastrointestinal discomfort might have been the result of the paroxysmal tachycardia alone. So far as, is known, this is the first and only attack of paroxysmal tachycardia that the patient had. 4. Di,gitalis and quinidine sulphate by mouth and digalen intravenously were not followed by any appreciable change in rate. Quinidine sulphate intravenously caused a reduction in rate for twenty minutes only. Quinine hydrochloride by mouth was accompanied by some slowing of rate and a return to normal rhythm. REFERENCES Clinical Disorders of the Heart Beat, ed: 5, London, 1920, pp. 64, 71. Lewis, T.: Heart Disease, Macmillan Co., 1931, p.’ 640. White, P. D.: Tachycardie, Wien. med. Wchnschr. 78: 254, 1928. Wenckebach, K. F. : Paroxysmale Tachycardie Paroxystique A Ace&s Gallavardin, L., Veil, P., and Froment, Roger: Tr6s Prolong&, Lyon mded. 145: 3, 1930. Unusual Example of Paroxysmal Tachycardia With Gradual SlowMarvin, H. M.: ing of the Rate, Heart 10: 279, 1923. Quinidine in the Treatment of Extrasystolic Arrhythmia Musser, John H., Jr.: and Paroxysmal TacZyeardia, Ann. Clin. Med. 2: 209, 1924. Paroxysmal Tachycardia With Myocardial Major, Ralph H., and Wahl, H. R.: Lesion, AM. HEART J. 5: 477, 1930.
of Clinical PAROXYSMAL CASE
B. E.
HAMILTON,
Reports
TACHYCARDIA
REPORT*
M.D., AND D, HURWITZ, BOSTON, CASE
M.D.
MASS. REPORT
M.
B., cobbler, aged fifty years, 211 Armenian, entered the Second Medical Service of the Boston City Hospital on September 22, 1930. The history was obtained with difficulty because the patient spoke very little English. He had been in good health and had worked eorminuously until two weeks before entrance. At this time, following a heavy meal, the patient was seized with cramp-like pains in the umbilical region, later rising to the epigastric region. The pain fluctuated in severity, but persisted.
At entrance, the physical examination rate’ was 180 per minute. The rhythm was millimeters of mercury. The respirations &es were heard at both bases posteriorly. epigastrium. An electrocardiogram taken cardia, probably auricular in origin. The
was unimportant, except that the pulse regular. The blood pressure was 95/85 were 28 per minute. A few crepitant Slight tenderness ‘was elicited in the September 22 showed paroxysmal tachyrate was 200 per minute.
Though it was believed that the patient had had a coronary occlusion, no evidence appeared to support this suspicion. There was no fever. The white blood cell count at entrance was 10,500 per cubic millimeter of blood. ‘Later, it fell to 4,000 per cubic millimeter of blood. The paroxysmal tachyeardia persisted for thirty-five days. The only change in his condition throughout the thirty-five days was gradually increasing eongestive failure until the liver was definitely engorged and slightly tender; the &es at the lung bases increased, and a small amount of demonstrable fluid appeared at both bases. Curiously, there was more on the left than on the right. During the thirty-five days, he received the following medication: quinidine sulphate, 30 grains each day for two days, was given first, without effect on the This was stopped because of nausea and vomiting. Two doses of digalen heart. were given intravenously. The first dose was 9 grains. The second dose, given twenty-four hours later, was 10 grains. There was no appreciable effect. The following day powdered digitalis, 9 grains, was given by mouth. This dose -was repeated each day for three days. The dose was then reduced to 41/2 grains daily. This was continued for eleven days. The dose was then reduced to 1% grains daily. Throughout this time, the patient was under close observation. His heart rate was counted every hour throughout the twenty-four hours. ~There was no The digitalis was discontinued three days appreciable effect from the digitalis. *From Services
the Thorndike (Harvard) of
the
Memorial Boston
Laborator and City HOSP Ptal.
274
the
Second
and
Fourth
Medical
HAMILTON
AND
HURWITZ
:
PROLONGED
PAROXYSMAL
TACHYCARDIA
275
b’efore the ,paroxysm ceased. Quinidine sulphate, 6. grains in one dose, was given intravenously fourteen days after admission, two days after the dose of digitalis had bseen reduced to 4rh grains daily. The cardiac rate dropped from 180 per minute to 150 per minute in five minutes and then returned to 180 per minute gradually in twenty minutes. Forty-eight hours before the paroxysm ceased, quinine hydrochloride was given by mouth in lo-grain doses. An electrocardiogram taken after the first two or three doses showed a rate of 176 per minute, which was slightly lower than the average rate. After he had had a total of 70 grains of quinine h;ydrochloride over a period of forty-eight hours, his heart suddenly resumed a normal rhythm with a rate of 80 per minute. There was immediate improvement in
Fig. 1.-S&. l.-Sept. 22, 1930. l! Paroxysmal tachycardia, probably auricular. Rate ZOO. ? P-waves Lead III. QRS = 0.12 sec., slurred in all leads. T omosite main deflection in all leads. Right bundle-branch block (if tachycardia is auricular in origin.) symptoms. During the next few weeks, his was discharged in apparently good condition return to normal cardiac rhythm.
congestive four and
failure a half
cleared, and weeks after
he his
On April 4, 1931, five months after discharge, he was readmitted to the. hospital acutely ill. Following his first discharge from the hospital, he had been able to return to work and had been without symptoms until a few hours before his readmittance. He entered the hospital in a condition of shock. The temperature, by mlouth, was 96 degrees Fahrenheit. The pulse rate was 65 per minute. The respirations were 30 per minute. The white blood count was 20,000 per cubic milhmeter of blood. He’ lived only six hours following admission to the hospit& .’
276
THE
AMERICAN
HEART
JOURNAL
Post-mortem
Eza&%ution of Hear&-The weight was 360 gm. The organ was normal in size. The epicardium was smooth but showed slight discoloration over the posterior portion of the left ventricle. The myocardium was pale greyish red in color and was markedly scarred. Immediately below the mitral ring, extending posteriorly as far as the interventricular septum, and inferiorly as far as the apex, there was a pear-shaped area approximately 5 or 6 cm. in diameter where the myocardium was thinned, mottled yellowish grey in color, eon taining hyalin appearing bands ; the thickness at this point was 0.7 cm. The valves were negative with the exception of slight atberoma of the aortic. The aorta immediately above showed marked thickening of the intima, with the formation of plaques and nodules some of which were yellow in color and appeared atheromatous; others were bluish in color and hyalin in appearance, giving the appearance essentially
Fig. 2.-O& 10, 1930. Paroxysmal tachycardia, probably auricular. P-wave Lead III. QRS = 0.12 sec. slurred in all leads. Right bundle-branch Low amplitude (maximum 5 mm.). tachycarcl.ia is auricular in origin).
Rate
200.
block
?
(if
of syphilis. The mouths of both coronaries were patent but thickened. The right coronary at the level of the tricuspid valve showed almost complete occlusion. Tbe vessel at this point was yellowish grey in color and appeared hyalinized. Beyond this point the lumen was patent but very narrow. The interventricular portion of the left coronary about 2.5 cm. from its point of origin showed an occlusion by a red, soft tbrombus; beyond, the vessel wall was thickened but patent. The circumflex branch of the left coronary 1 cm. from its point of origin showed complete occlusion, from an old process. The healed infarcted area. described above lay below. During the patient’s stay in the hospital. he was under the care of Drs. L. B. Ellis, B. E. Hamilton, DL Hum&z, W. R. Ohler, W. H. Robey, and I?. W. White. The electrocardiograms were taken and interpreted under the direction of Dr. J. M. Faulkner. The post-portem examination was made by Dr. J. M. WoodalL
278
THE
AMERICAN
HEART
JOURNAL
COMMENT
The important
findings
are:
1. Dz&r%tio% of paroxymml tachycar&a.-Though it is known that paroxysmal tachycardia may continue indefinitely, a duration of more than a few days is rare and very few caseshave been reported with a known duration of thirty-five days with recovery-. The attack may have been present during the two weeks before admission, making a possible total of forty-nine days. 2. The patient was not conscious of his tachyeardia. He complained only of gastrointestinal disturbance. 3. The paroxysmal ta,chycardia was probably associated with a coronary occlusion with infarction. This was indicated by the subsequent post-mortem examination. There was no clinical evidence to confirm this diagnosis, except the unexplained paroxysmal tachycardia itself. The gastrointestinal discomfort might have been the result of the paroxysmal tachycardia alone. So far as, is known, this is the first and only attack of paroxysmal tachycardia that the patient had. 4. Di,gitalis and quinidine sulphate by mouth and digalen intravenously were not followed by any appreciable change in rate. Quinidine sulphate intravenously caused a reduction in rate for twenty minutes only. Quinine hydrochloride by mouth was accompanied by some slowing of rate and a return to normal rhythm. REFERENCES Clinical Disorders of the Heart Beat, ed: 5, London, 1920, pp. 64, 71. Lewis, T.: Heart Disease, Macmillan Co., 1931, p.’ 640. White, P. D.: Tachycardie, Wien. med. Wchnschr. 78: 254, 1928. Wenckebach, K. F. : Paroxysmale Tachycardie Paroxystique A Ace&s Gallavardin, L., Veil, P., and Froment, Roger: Tr6s Prolong&, Lyon mded. 145: 3, 1930. Unusual Example of Paroxysmal Tachycardia With Gradual SlowMarvin, H. M.: ing of the Rate, Heart 10: 279, 1923. Quinidine in the Treatment of Extrasystolic Arrhythmia Musser, John H., Jr.: and Paroxysmal TacZyeardia, Ann. Clin. Med. 2: 209, 1924. Paroxysmal Tachycardia With Myocardial Major, Ralph H., and Wahl, H. R.: Lesion, AM. HEART J. 5: 477, 1930.