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Pulmonary Edema following Direct Current Cardioversion
PULMONARY EDEMA FOLLOWING DC CARDIOVERSION
191
ated with exertion. Because of increasing exertional dyspnea and the onset of paroxysmal nocturnal dyspnea and pedal edema, he was admitted for the first time October 17, 1966. The blood pressure was 115/70 mm Hg, the pulse rate Richard B. Sutton, M.D.,** and Theofdos J. Tsagaris, M.D.f 100 and the respiratory rate 22. There was slight distension of the neck veins at 45° recumbency. The cardiac apex was of a sustained character and was displaced slightly to the left of the midclavicular line in the fifth left intercostal The most common complications of direct current (DC) space. An early diastolic and a presystolic gallop were shock for die treatment of cardiac arrhythmias are heard but there were no murmurs. Rales were heard over arrhythmias and embolic episodes. Pulmonary edema, a both lower lung fields posteriorly. The liver was not poorly understood complication of DC shock, has enlarged but slight pedal edema was present. been reported in eight patients following reversion from Results of hemogram, urinalysis, serum electrolytes, blood atrial fibrilation to sinus rhythm. This report describes urea nitrogen, serologic test for syphilis, and tests for lupus a 32-year-old white man with cardiomyopathy of unerythematosus were negative. known etiology who experienced pulmonary edema on The electrocardiogram was interpreted to show sinus two separate occasions seven months apart following rhythm with occasional premature atrial and ventricular DC cardioversion despite significant slowing of the complexes, left intra-atrial conduction defect, right axis deviation, and nonspecific ST-T changes. ventricular rate. To our knowledge, this is the first reThe chest roentgenogram and cardiac fluoroscopy were ported case in which pulmonary edema occurred more interpreted to show pulmonary congestion and left atrial than once following reversion to sinus rhythm. Although and left ventricular enlargement. tiie mechanism of pulmonary edema in this and die Right and left heart catheterization was performed on other reported cases is unknown, some workers have November 17, 1966. The results are listed in Table 1. The suggested that the mechanism is related to the reversion salient features were a wide arteriovenous O z difference, to sinus rhythm. low cardiac index, elevated ventricular diastolic pressure and pulmonary hypertension. There was no evidence of valvular disease, intracardiac shunts, or pericardial disease. T \ i r e c t current (DC) cardioversion used in the The diagnosis of a cardiomyopathy of unknown etiology was made. treatment of various cardiac arrhythmias, par-
Pulmonary Edema following Direct Current Cardioversion*
ticularly atrial fibrillation, is a highly effective and relatively simple procedure which can be performed quickly with infrequent serious complications. 110 The most common complications of DC shock are arrhythmias and embolic episodes.2-5'7' 915 An uncommon and poorly understood complication is the occurrence of pulmonary edema. 18 20 Pulmonary edema following DC shock with reversion to sinus rhythm has been reported in at least eight patients. Pulmonary edema following spontaneous reversion from atrial fibrillation to sinus rhythm also has been described in one case.21 The purpose of this report is to describe a patient who experienced pulmonary edema on two separate occasions seven months apart following DC cardioversion. CASE REPORT
A 32-year-old white married man was admitted to the Salt Lake Veterans Administration Hospital for the third and final time September 14, 1967, because of increasing shortness of breath. He was well until 1964 when he noted the onset of dyspnea, diaphoresis and dull aching anterior chest pain associ*From the Department of Internal Medicine, University of Utah College of Medicine, and the Veterans Administration Hospital, Salt Lake City, Utah. "Instructor of Medicine, University of Utah College of Medicine, and Research and Education Associate, Veterans Administration Hospital, Salt Lake City, Utah, f Assistant Professor of Medicine, University of Utah College of Medicine, and Chief, Cardiology Division, Veterans Administration Hospital, Salt Lake City, Utah.
CHEST, VOL. 57, NO. 2, FEBRUARY 1970
Table 1—Cardiac Catheterization Data, November 17,1980. VE (L/min) Voi (ml/min) SaO. (%) Ca-vO, (Vol %) C.O. (L/min) C.I. (L/min/M 2 ) Rate (beats/min) S.V. (ml/beat) PRESSURES (mm Hg): PAW PA RV
Rest
Exercise
9.6 266 92 8.0 3.3 1.7 89 37
32.5 696 94 11.9 5.8 3.0 120 48
27-35 1-12
—
(18)
1(29) 49 3
RA
(10)
Ao LV PARI (mm Hg/L/min/M*) SARI (mm Hg/L/min/M^)
13-37 (*L> 88-127 — 36-64 ( 6 9 ) 93-128 18-36
92-106 18-29 ed 7.6 48
128-147—— 84-90 ( 1 0 0 > 130-149 51-62 ed 9.3 30
VE = ventilation; Vo» = oxygen consumption; Sao» = arterial oxyhemoglobin saturation; Ca-vO« = arterio-venous Oi difference; C.O. = cardiac output; C.I. = cardiac index; S.V. = stroke volume; PAW = pulmonary artery wedge; PA = pulmonary artery; RV = right ventricle; RA = right atrium; Ao = aorta; LV = left ventricle; PARI = pulmonary arteriolar resistance index; and SARI = systemic arteriolar resistance index.
192
SUTTON AND TSAGARIS
F I G U R E 1. Electrocardiogram (lead II) taken immediately before (A) and after (B) DC cardioversion performed on December 19, 1966. The rhythm in the upper strip is atrial fibrillation while that in the lower is sinus.
The patient improved on a regimen of salt restriction, digitalis and diuretics. On December 15, 1966, the patient was admitted for the second time with recurrent congestive heart failure. On this occasion the rate was 130 per minute and the rhythm irregular. The electrocardiogram was interpreted to show atrial fibrillation. Although pulmonary congestion improved, the rapid ventricular rate persisted despite an increase in the digitoxin dose (1.0 mg of digitoxin orally over a three day period in addition to his usual maintenance dose of 0.1 mg per day). The patient underwent DC cardioversion in the recumbent position following light anesthesia with intravenous sodium methohexital (60 mg). Following one shock of 200 watt-seconds the rhythm reverted from atrial fibrillation (ventricular rate 140 beats per minute) to sinus tachycardia with a rate of 110-120 beats per minute (Fig 1). The patient remained in the recumbent position for approximately 10 minutes preceding the cardioversion and 10 minutes afterwards. Two hours later the patient became extremely dyspneic and manifested the clinical picture of pulmonary edema despite persistence of normal sinus rhythm with a rate less than the
ventricular rate during atrial fibrillation. With vigorous therapy the patient slowly improved and was discharged on a regimen of digitoxin, procaine amide and diuretics still remaining in normal sinus rhythm. The pertinent physical findings at the time of his last admission on September 14, 1967, included a blood pressure of 110/70 mm Hg, irregular heart rate of 200, respiratory rate of 24 per minute, distended neck veins, rales throughout all lung fields, cardiomegaly, diastolic gallop, hepatomegaly and mild pedal edema. The serum transaminase was 622 and the lactic dehydrogenase was 1,026 units. The chest roentgenogram was interpreted to show pulmonary edema. The electrocardiogram was interpreted to show atrial fibrillation with a ventricular rate of 200 (at the time of his last clinic visit August 16, 1967 his rhythm was sinus). An intensive cardiopulmonary regimen including 0.7 mg of intravenous deslanoside in addition to maintenance oral digitoxin, 0.1 mg, resulted in marked relief of the dyspnea after 12 hours associated with slowing of the ventricular rate to 120-150 per minute. Twenty-four hours after admission the ventricular rate again rose to 200 per minute. Following light anesthesia with sodi-
2. Pre-conversion (A) and post-conversion (B) rhythm strips taken from lead II on September 15, 1967. The rhythm in the upper strip is atrial fibrillation and that in the lower is sinus. FICURE
CHEST, VOL. 57, NO. 2, FEBRUARY 1970
PULMONARY EDEMA FOLLOWING DC CARDIOVERSION um methohexital (70 mg) the cardiac rhythm was converted with a DC shock of 200 watt-seconds from atrial fibrillation with a ventricular rate of 200 beats per minute to sinus tachycardia with a rate of 140 beats per minute (Fig 2). As before, cardioversion was performed with the patient recumbent. Procaine amide (500 mg) was given intramuscularly 10 minutes after cardioversion. Twenty minutes following cardioversion pulmonary edema again ensued. Gradual improvement with relief of dyspnea occurred following the use of venous tourniquets, intravenous ethacrynic acid, and positive pressure breathing. Thirty-six hours later hypotension with oliguria occurred. The complication was followed by uremia, severe gastrointestinal bleeding, jaundice and coma. The patient died on the sixth hospital day, five days after DC cardioversion. Postmortem examination revealed an enlarged heart weighing 520 gm, the cardiac enlargement caused by biventricular hypertrophy with only modest ventricular dilatation. The right ventricular thickness was 0.5-0.6 mm and the left ventricular wall thickness was 1.4 mm. The left ventricle exhibited considerable endocardial thickening and small areas of scarring within the myocardium. The cardiac valves and coronary arteries were normal. Congestion was present in the lungs, spleen and liver. The liver exhibited central necrosis and bile stasis. There were multiple infarctions in kidneys as well as tubular necrosis. DISCUSSION
The absence of clinical and postmortem evidence of usual causes of acute pulmonary edema such as myocardial infarction or pulmonary emboli in this patient and others reported, suggests the possibility of a causal relationship between the occurrence of pulmonary edema and reversion from atrial fibrillation to sinus rhythm despite slowing of the ventricular rate. Pulmonary edema following cardioversion is rare but it has been observed in both sexes over a wide range of ages, and in patients with a variety of underlying cardiac diseases including rheumatic, arteriosclerotic, congenital and primary myocardial. The time of recognition of pulmonary edema varied from immediately to 36 hours after cardioversion. Serum enzyme or electrocardiographic changes have not been observed in the majority of these patients. The duration of atrial fibrillation prior to cardioversion is not stated in the reported cases. In our patient the duration could not have exceeded three weeks on the first occasion and one month on the second occasion. At the present time it is difficult to attribute the occurrence of pulmonary edema to such factors as the administration of quinidine or procaine amide, use of a short acting anesthetic agent, blood gas alterations during the brief period of anesthesia or the discontinuation of a cardiac glycoside. Furthermore, there is no evidence that myocardial damage results from the application of direct current to the chest wall as used clinically. CHEST, VOL. 57, NO. 2, FEBRUARY 1970
193
It has been suggested that pulmonary edema is related to the return to sinus rhythm. 2023 The mechanism proposed is that left ventricular failure occurs because left atrial contraction is ineffective and thus the left ventricle is unable to accommodate increased flow from the right heart caused by effective right atrial contraction.10 22 However, the hemodynamic pattern of right atrial A waves without left atrial A waves has been demonstrated following cardioversion in patients in whom pulmonary edema did not occur,24 25 and this hemodynamic pattern has not been demonstrated in any of the cases in which pulmonary edema did occur. If this is the mechanism, it is difficult to understand why it should lead to pulmonary edema in some patients but not in others. The present case and the one reported by Hollman and Nicholson21 suggests support of the concept that the actual change in rhythm may be responsible. To our knowledge there have been no instances of pulmonary edema following direct current shock in which the rhythm did not revert to sinus. However, the absence of the occurrence of pulmonary edema in those patients whose rhythm reverted to sinus following the administration of quinidine in the days before the use of direct current shock is an argument against this concept. Had our patient survived and experienced another bout of atrial fibrillation it would have been of interest to attempt reversion with quinidine alone. Since both cardioversions in our patient were performed with the patient recumbent, the question arises whether placing the patient in the recumbent position may have been a factor in producing the pulmonary edema. Although we cannot quantitate the degree of orthopnea experienced by our patient, he tolerated the recumbent position before and immediately following the first cardioversion without complaint (pulmonary edema did not occur until two hours after the cardioversion). However, he developed pulmonary edema 20 minutes following the second cardioversion. Since the possibility that recumbency may play a role in the development of pulmonary edema following cardioversion cannot be excluded, it is suggested that DC cardioversion in patients with left ventricular disease be carried out with the patient upright. To our knowledge this is the first reported case in which pulmonary edema occurred more than once following reversion to sinus rhythm. We would be interested to know if repeat cardioversion was associated with the recurrence of pulmonary edema in any of the previously reported cases.
194 24
REFERENCES 1
L O W N , B . , A M A R A S I N G H A M , R . , AND N E U M A N , J . :
New
method for terminating cardiac arrhythmias: use of synchronized capacitor discharge, J.A.M.A., 182:548, 1962. 2 HURST,
J.W.,
PAULK,
E.A.,
JR.,
PROCTOR,
H.D.,
AND
Management of patients with atrial fibrillation, Amer. J. Med., 37:728, 1964. 3 H A L M O S , P . B . : Direct current conversion of atrial fibrillation, Brit. Heart }., 28:302, 1966. 4 SZEKELY, P., BATSON, G.A., AND STARX, D.C.C.: Direct current shock therapy of cardiac arrhythmias, Brit. Heart ]., 28:366, 1966. 5 Kn.r.rp, T.: Synchronized D. C. precordial shock for arrhythmias. Safe new technique to establish normal rhythm may be utilized on elective or an emergency basis, J.A.M.A., 186:1, 1963. SCHLANT,
R.C.:
W.F.W.E., ROWLANDS, D . J . , H O W T I T , G., AND A.M.: Left atrial activity following cardioversion (Preliminary Communications), Lancet, 2:471, 1965. 25 ROWLANDS, D . J . , L O G A N , W.F.W.E., AND H O W I T T , G.: Atrial function after cardioversion, Amer. Heart J., 74: 149, 1967. LOGAN,
HOLMES,
Reprint requests: Richard B. Sutton, M.D., Cardiovascular Division, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah 84112
Pacemakers for Digitalis Associated Bradyarrhythmia*
AND
Robert D. Patton, M.D., Mark L. Solovay, M.D., Anthony N. Damato, M.D., and Emanuel Stein, M.D., F.C.C.P.
"Cardioversion" of atrial fibrillation, a report on the treatment of 65 episodes in 50 patients, New Eng. J. Med., 269:325, 1963. 7 O R A M , S., AND DAVIES, J.P.: Further experience of electrical conversion of atrial fibrillation to sinus rhythm: analysis of 100 patients, Lancet, 1:1294, 1964.
Three patients with refractory congestive heart failure are described in whom the use of digitalis was associated with serious bradyarrhythmias. In each, die implantation of a demand transvenons pacemaker permitted safe resumption of the drag with marked clinical improvement.
6
L O W N , B . , P E R L R O T H , M . G . , KAIDBEY, S . , A B E , T . , HARKEN, D . E . :
8
L E M B E R C , L . , CASTELLANOS, A . , J R . , S W E N S O N , J . , AND
A.: Arrhythmias related to cardioversion, Circulation, 30:163, 1964. GOSSELIN,
9
MORRIS, J . J . , JR.,
PETER,
R.H.,
AND M C I N T O S H ,
H.D.:
Electrical conversion of atrial fibrillation, Ann. Intern. Med.,
65:216,
1966.
Directcurrent shock in treatment of drug-resistant cardiac arrhythmias, Brit. Med. J., 1:1468, 1964. P A U L K , E . A . , J R . , AND H U R S T , J . W . : Clinical problems of cardioversion, Amer. Heart J., 70:248, 1965. K L E I C E R , R . , AND L O W N , B . : Cardioversion and digitalis. I I . Clinical studies, Circulation, 3 3 : 8 7 8 , 1 9 6 6 . G I L B E R T , R . , AND CUDDY, R . P . : Digitalis intoxication following conversion to sinus rhythm, Circulation, 32:
1 0 M C D O N A L D , L . , RESNEKOV, L . , AND O B R I E N , K . :
11 12 13
f
1 1 he advent of demand transvenous pacemakers has widened the applicability of pacemaker therapy in poor risk patients with a variety of arrhythmias. The onset of a bradyarrhythmia may limit the use of digitalis in the occasional patient requiring large doses of the drug, and in whom no other manifestation of toxicity is present. Implanting a demand pacemaker in three such patients has permitted us to circumvent this difficulty, and forms the basis of this report. C A S E REPORTS
58, 1965.
14
A., AND L A D U E , J.S.: Postconversion systemic arterial embolism, Amer. ]. Card., 16:452, 1965. NAVAB,
1 5 RABBINO, M . D . , L I K O F F , W . , AND D R E I F U S , L . S . :
16
plications and limitations of direct-current countershock, J.A.M.A., 1 9 0 : 4 1 7 , 1 9 6 4 . RESNEKOV, L . , AND M C D O N A L D , L . : Pulmonary edema following treatment of arrhythmias by direct-current shock, Lancet, 1 : 5 0 6 , 1 9 6 5 .
17 HONEY,
18 19 20
21
22 23
Com-
M.,
N I C H O L L S , T . T . , AND T O W E R S ,
M.K.:
Pul-
monary edema following direct-current defibrillation, in Letter to the Editor, Lancet, 1 : 7 6 5 , 1 9 6 5 . P A L O H E I M O , J.A.: Pulmonary edema after defibrillation, in Letter to the Editor, Lancet, 2:439, 1965. T U R N E R , J.R.B., AND T O W E R S , J.R.H.: Complications of cardioversion, Lancet, 2:612,1965. LINDSAY, J . , JR.: Pulmonary edema following cardioversion, (Annotations), Amer. Heart ]., 74:434, 1967. HOLLMAN, A., AND N I C H O L S O N , H . : Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2:801, 1966. I K R A M , H., N I X O N , P.G.F., AND ARCAN, T.: Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2:911, 1966. BELL, H.E.: Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2 : 9 1 1 , 1 9 6 6 .
CASE 1
A 61-year-old white woman with rheumatic heart disease presented with progressive exertional dyspnea and intermittent palpitations with symptoms of near syncope. Every time the arrhythmia was treated with digitalis, an intense sinus bradycardia ensued. Pertinent physical findings included bilateral basilar rales, cardiomegaly and the murmurs of aortic stenosis and insufficiency, and mitral stenosis and insufficiency. An electrocardiogram demonstrated sinus bradycardia of 42 beats/min with frequent nodal and ventricular escape beats. The chest x-ray film revealed massive cardiomegaly and bilateral pleural effusions. When digitalis was discontinued, the supraventricular tachycardia at 150 beats/min returned. Use of temporary transvenous pacemaker was followed by the implantations of a permanent demand pacemaker. The patient has been maintained free of congestive failure and tachycardia on digoxin 0.25 mg four times a day and procaine amide, 750 mg every six hours. CASE 2
An 82-year-old white man with three previous myocardial infarctions was admitted with refractory congestive heart •From the U. S. Public Health Service Hospital, Staten Island, N. Y.
CHEST, VOL. 57, NO. 2, FEBRUARY 1970
191
ated with exertion. Because of increasing exertional dyspnea and the onset of paroxysmal nocturnal dyspnea and pedal edema, he was admitted for the first time October 17, 1966. The blood pressure was 115/70 mm Hg, the pulse rate Richard B. Sutton, M.D.,** and Theofdos J. Tsagaris, M.D.f 100 and the respiratory rate 22. There was slight distension of the neck veins at 45° recumbency. The cardiac apex was of a sustained character and was displaced slightly to the left of the midclavicular line in the fifth left intercostal The most common complications of direct current (DC) space. An early diastolic and a presystolic gallop were shock for die treatment of cardiac arrhythmias are heard but there were no murmurs. Rales were heard over arrhythmias and embolic episodes. Pulmonary edema, a both lower lung fields posteriorly. The liver was not poorly understood complication of DC shock, has enlarged but slight pedal edema was present. been reported in eight patients following reversion from Results of hemogram, urinalysis, serum electrolytes, blood atrial fibrilation to sinus rhythm. This report describes urea nitrogen, serologic test for syphilis, and tests for lupus a 32-year-old white man with cardiomyopathy of unerythematosus were negative. known etiology who experienced pulmonary edema on The electrocardiogram was interpreted to show sinus two separate occasions seven months apart following rhythm with occasional premature atrial and ventricular DC cardioversion despite significant slowing of the complexes, left intra-atrial conduction defect, right axis deviation, and nonspecific ST-T changes. ventricular rate. To our knowledge, this is the first reThe chest roentgenogram and cardiac fluoroscopy were ported case in which pulmonary edema occurred more interpreted to show pulmonary congestion and left atrial than once following reversion to sinus rhythm. Although and left ventricular enlargement. tiie mechanism of pulmonary edema in this and die Right and left heart catheterization was performed on other reported cases is unknown, some workers have November 17, 1966. The results are listed in Table 1. The suggested that the mechanism is related to the reversion salient features were a wide arteriovenous O z difference, to sinus rhythm. low cardiac index, elevated ventricular diastolic pressure and pulmonary hypertension. There was no evidence of valvular disease, intracardiac shunts, or pericardial disease. T \ i r e c t current (DC) cardioversion used in the The diagnosis of a cardiomyopathy of unknown etiology was made. treatment of various cardiac arrhythmias, par-
Pulmonary Edema following Direct Current Cardioversion*
ticularly atrial fibrillation, is a highly effective and relatively simple procedure which can be performed quickly with infrequent serious complications. 110 The most common complications of DC shock are arrhythmias and embolic episodes.2-5'7' 915 An uncommon and poorly understood complication is the occurrence of pulmonary edema. 18 20 Pulmonary edema following DC shock with reversion to sinus rhythm has been reported in at least eight patients. Pulmonary edema following spontaneous reversion from atrial fibrillation to sinus rhythm also has been described in one case.21 The purpose of this report is to describe a patient who experienced pulmonary edema on two separate occasions seven months apart following DC cardioversion. CASE REPORT
A 32-year-old white married man was admitted to the Salt Lake Veterans Administration Hospital for the third and final time September 14, 1967, because of increasing shortness of breath. He was well until 1964 when he noted the onset of dyspnea, diaphoresis and dull aching anterior chest pain associ*From the Department of Internal Medicine, University of Utah College of Medicine, and the Veterans Administration Hospital, Salt Lake City, Utah. "Instructor of Medicine, University of Utah College of Medicine, and Research and Education Associate, Veterans Administration Hospital, Salt Lake City, Utah, f Assistant Professor of Medicine, University of Utah College of Medicine, and Chief, Cardiology Division, Veterans Administration Hospital, Salt Lake City, Utah.
CHEST, VOL. 57, NO. 2, FEBRUARY 1970
Table 1—Cardiac Catheterization Data, November 17,1980. VE (L/min) Voi (ml/min) SaO. (%) Ca-vO, (Vol %) C.O. (L/min) C.I. (L/min/M 2 ) Rate (beats/min) S.V. (ml/beat) PRESSURES (mm Hg): PAW PA RV
Rest
Exercise
9.6 266 92 8.0 3.3 1.7 89 37
32.5 696 94 11.9 5.8 3.0 120 48
27-35 1-12
—
(18)
1(29) 49 3
RA
(10)
Ao LV PARI (mm Hg/L/min/M*) SARI (mm Hg/L/min/M^)
13-37 (*L> 88-127 — 36-64 ( 6 9 ) 93-128 18-36
92-106 18-29 ed 7.6 48
128-147—— 84-90 ( 1 0 0 > 130-149 51-62 ed 9.3 30
VE = ventilation; Vo» = oxygen consumption; Sao» = arterial oxyhemoglobin saturation; Ca-vO« = arterio-venous Oi difference; C.O. = cardiac output; C.I. = cardiac index; S.V. = stroke volume; PAW = pulmonary artery wedge; PA = pulmonary artery; RV = right ventricle; RA = right atrium; Ao = aorta; LV = left ventricle; PARI = pulmonary arteriolar resistance index; and SARI = systemic arteriolar resistance index.
192
SUTTON AND TSAGARIS
F I G U R E 1. Electrocardiogram (lead II) taken immediately before (A) and after (B) DC cardioversion performed on December 19, 1966. The rhythm in the upper strip is atrial fibrillation while that in the lower is sinus.
The patient improved on a regimen of salt restriction, digitalis and diuretics. On December 15, 1966, the patient was admitted for the second time with recurrent congestive heart failure. On this occasion the rate was 130 per minute and the rhythm irregular. The electrocardiogram was interpreted to show atrial fibrillation. Although pulmonary congestion improved, the rapid ventricular rate persisted despite an increase in the digitoxin dose (1.0 mg of digitoxin orally over a three day period in addition to his usual maintenance dose of 0.1 mg per day). The patient underwent DC cardioversion in the recumbent position following light anesthesia with intravenous sodium methohexital (60 mg). Following one shock of 200 watt-seconds the rhythm reverted from atrial fibrillation (ventricular rate 140 beats per minute) to sinus tachycardia with a rate of 110-120 beats per minute (Fig 1). The patient remained in the recumbent position for approximately 10 minutes preceding the cardioversion and 10 minutes afterwards. Two hours later the patient became extremely dyspneic and manifested the clinical picture of pulmonary edema despite persistence of normal sinus rhythm with a rate less than the
ventricular rate during atrial fibrillation. With vigorous therapy the patient slowly improved and was discharged on a regimen of digitoxin, procaine amide and diuretics still remaining in normal sinus rhythm. The pertinent physical findings at the time of his last admission on September 14, 1967, included a blood pressure of 110/70 mm Hg, irregular heart rate of 200, respiratory rate of 24 per minute, distended neck veins, rales throughout all lung fields, cardiomegaly, diastolic gallop, hepatomegaly and mild pedal edema. The serum transaminase was 622 and the lactic dehydrogenase was 1,026 units. The chest roentgenogram was interpreted to show pulmonary edema. The electrocardiogram was interpreted to show atrial fibrillation with a ventricular rate of 200 (at the time of his last clinic visit August 16, 1967 his rhythm was sinus). An intensive cardiopulmonary regimen including 0.7 mg of intravenous deslanoside in addition to maintenance oral digitoxin, 0.1 mg, resulted in marked relief of the dyspnea after 12 hours associated with slowing of the ventricular rate to 120-150 per minute. Twenty-four hours after admission the ventricular rate again rose to 200 per minute. Following light anesthesia with sodi-
2. Pre-conversion (A) and post-conversion (B) rhythm strips taken from lead II on September 15, 1967. The rhythm in the upper strip is atrial fibrillation and that in the lower is sinus. FICURE
CHEST, VOL. 57, NO. 2, FEBRUARY 1970
PULMONARY EDEMA FOLLOWING DC CARDIOVERSION um methohexital (70 mg) the cardiac rhythm was converted with a DC shock of 200 watt-seconds from atrial fibrillation with a ventricular rate of 200 beats per minute to sinus tachycardia with a rate of 140 beats per minute (Fig 2). As before, cardioversion was performed with the patient recumbent. Procaine amide (500 mg) was given intramuscularly 10 minutes after cardioversion. Twenty minutes following cardioversion pulmonary edema again ensued. Gradual improvement with relief of dyspnea occurred following the use of venous tourniquets, intravenous ethacrynic acid, and positive pressure breathing. Thirty-six hours later hypotension with oliguria occurred. The complication was followed by uremia, severe gastrointestinal bleeding, jaundice and coma. The patient died on the sixth hospital day, five days after DC cardioversion. Postmortem examination revealed an enlarged heart weighing 520 gm, the cardiac enlargement caused by biventricular hypertrophy with only modest ventricular dilatation. The right ventricular thickness was 0.5-0.6 mm and the left ventricular wall thickness was 1.4 mm. The left ventricle exhibited considerable endocardial thickening and small areas of scarring within the myocardium. The cardiac valves and coronary arteries were normal. Congestion was present in the lungs, spleen and liver. The liver exhibited central necrosis and bile stasis. There were multiple infarctions in kidneys as well as tubular necrosis. DISCUSSION
The absence of clinical and postmortem evidence of usual causes of acute pulmonary edema such as myocardial infarction or pulmonary emboli in this patient and others reported, suggests the possibility of a causal relationship between the occurrence of pulmonary edema and reversion from atrial fibrillation to sinus rhythm despite slowing of the ventricular rate. Pulmonary edema following cardioversion is rare but it has been observed in both sexes over a wide range of ages, and in patients with a variety of underlying cardiac diseases including rheumatic, arteriosclerotic, congenital and primary myocardial. The time of recognition of pulmonary edema varied from immediately to 36 hours after cardioversion. Serum enzyme or electrocardiographic changes have not been observed in the majority of these patients. The duration of atrial fibrillation prior to cardioversion is not stated in the reported cases. In our patient the duration could not have exceeded three weeks on the first occasion and one month on the second occasion. At the present time it is difficult to attribute the occurrence of pulmonary edema to such factors as the administration of quinidine or procaine amide, use of a short acting anesthetic agent, blood gas alterations during the brief period of anesthesia or the discontinuation of a cardiac glycoside. Furthermore, there is no evidence that myocardial damage results from the application of direct current to the chest wall as used clinically. CHEST, VOL. 57, NO. 2, FEBRUARY 1970
193
It has been suggested that pulmonary edema is related to the return to sinus rhythm. 2023 The mechanism proposed is that left ventricular failure occurs because left atrial contraction is ineffective and thus the left ventricle is unable to accommodate increased flow from the right heart caused by effective right atrial contraction.10 22 However, the hemodynamic pattern of right atrial A waves without left atrial A waves has been demonstrated following cardioversion in patients in whom pulmonary edema did not occur,24 25 and this hemodynamic pattern has not been demonstrated in any of the cases in which pulmonary edema did occur. If this is the mechanism, it is difficult to understand why it should lead to pulmonary edema in some patients but not in others. The present case and the one reported by Hollman and Nicholson21 suggests support of the concept that the actual change in rhythm may be responsible. To our knowledge there have been no instances of pulmonary edema following direct current shock in which the rhythm did not revert to sinus. However, the absence of the occurrence of pulmonary edema in those patients whose rhythm reverted to sinus following the administration of quinidine in the days before the use of direct current shock is an argument against this concept. Had our patient survived and experienced another bout of atrial fibrillation it would have been of interest to attempt reversion with quinidine alone. Since both cardioversions in our patient were performed with the patient recumbent, the question arises whether placing the patient in the recumbent position may have been a factor in producing the pulmonary edema. Although we cannot quantitate the degree of orthopnea experienced by our patient, he tolerated the recumbent position before and immediately following the first cardioversion without complaint (pulmonary edema did not occur until two hours after the cardioversion). However, he developed pulmonary edema 20 minutes following the second cardioversion. Since the possibility that recumbency may play a role in the development of pulmonary edema following cardioversion cannot be excluded, it is suggested that DC cardioversion in patients with left ventricular disease be carried out with the patient upright. To our knowledge this is the first reported case in which pulmonary edema occurred more than once following reversion to sinus rhythm. We would be interested to know if repeat cardioversion was associated with the recurrence of pulmonary edema in any of the previously reported cases.
194 24
REFERENCES 1
L O W N , B . , A M A R A S I N G H A M , R . , AND N E U M A N , J . :
New
method for terminating cardiac arrhythmias: use of synchronized capacitor discharge, J.A.M.A., 182:548, 1962. 2 HURST,
J.W.,
PAULK,
E.A.,
JR.,
PROCTOR,
H.D.,
AND
Management of patients with atrial fibrillation, Amer. J. Med., 37:728, 1964. 3 H A L M O S , P . B . : Direct current conversion of atrial fibrillation, Brit. Heart }., 28:302, 1966. 4 SZEKELY, P., BATSON, G.A., AND STARX, D.C.C.: Direct current shock therapy of cardiac arrhythmias, Brit. Heart ]., 28:366, 1966. 5 Kn.r.rp, T.: Synchronized D. C. precordial shock for arrhythmias. Safe new technique to establish normal rhythm may be utilized on elective or an emergency basis, J.A.M.A., 186:1, 1963. SCHLANT,
R.C.:
W.F.W.E., ROWLANDS, D . J . , H O W T I T , G., AND A.M.: Left atrial activity following cardioversion (Preliminary Communications), Lancet, 2:471, 1965. 25 ROWLANDS, D . J . , L O G A N , W.F.W.E., AND H O W I T T , G.: Atrial function after cardioversion, Amer. Heart J., 74: 149, 1967. LOGAN,
HOLMES,
Reprint requests: Richard B. Sutton, M.D., Cardiovascular Division, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah 84112
Pacemakers for Digitalis Associated Bradyarrhythmia*
AND
Robert D. Patton, M.D., Mark L. Solovay, M.D., Anthony N. Damato, M.D., and Emanuel Stein, M.D., F.C.C.P.
"Cardioversion" of atrial fibrillation, a report on the treatment of 65 episodes in 50 patients, New Eng. J. Med., 269:325, 1963. 7 O R A M , S., AND DAVIES, J.P.: Further experience of electrical conversion of atrial fibrillation to sinus rhythm: analysis of 100 patients, Lancet, 1:1294, 1964.
Three patients with refractory congestive heart failure are described in whom the use of digitalis was associated with serious bradyarrhythmias. In each, die implantation of a demand transvenons pacemaker permitted safe resumption of the drag with marked clinical improvement.
6
L O W N , B . , P E R L R O T H , M . G . , KAIDBEY, S . , A B E , T . , HARKEN, D . E . :
8
L E M B E R C , L . , CASTELLANOS, A . , J R . , S W E N S O N , J . , AND
A.: Arrhythmias related to cardioversion, Circulation, 30:163, 1964. GOSSELIN,
9
MORRIS, J . J . , JR.,
PETER,
R.H.,
AND M C I N T O S H ,
H.D.:
Electrical conversion of atrial fibrillation, Ann. Intern. Med.,
65:216,
1966.
Directcurrent shock in treatment of drug-resistant cardiac arrhythmias, Brit. Med. J., 1:1468, 1964. P A U L K , E . A . , J R . , AND H U R S T , J . W . : Clinical problems of cardioversion, Amer. Heart J., 70:248, 1965. K L E I C E R , R . , AND L O W N , B . : Cardioversion and digitalis. I I . Clinical studies, Circulation, 3 3 : 8 7 8 , 1 9 6 6 . G I L B E R T , R . , AND CUDDY, R . P . : Digitalis intoxication following conversion to sinus rhythm, Circulation, 32:
1 0 M C D O N A L D , L . , RESNEKOV, L . , AND O B R I E N , K . :
11 12 13
f
1 1 he advent of demand transvenous pacemakers has widened the applicability of pacemaker therapy in poor risk patients with a variety of arrhythmias. The onset of a bradyarrhythmia may limit the use of digitalis in the occasional patient requiring large doses of the drug, and in whom no other manifestation of toxicity is present. Implanting a demand pacemaker in three such patients has permitted us to circumvent this difficulty, and forms the basis of this report. C A S E REPORTS
58, 1965.
14
A., AND L A D U E , J.S.: Postconversion systemic arterial embolism, Amer. ]. Card., 16:452, 1965. NAVAB,
1 5 RABBINO, M . D . , L I K O F F , W . , AND D R E I F U S , L . S . :
16
plications and limitations of direct-current countershock, J.A.M.A., 1 9 0 : 4 1 7 , 1 9 6 4 . RESNEKOV, L . , AND M C D O N A L D , L . : Pulmonary edema following treatment of arrhythmias by direct-current shock, Lancet, 1 : 5 0 6 , 1 9 6 5 .
17 HONEY,
18 19 20
21
22 23
Com-
M.,
N I C H O L L S , T . T . , AND T O W E R S ,
M.K.:
Pul-
monary edema following direct-current defibrillation, in Letter to the Editor, Lancet, 1 : 7 6 5 , 1 9 6 5 . P A L O H E I M O , J.A.: Pulmonary edema after defibrillation, in Letter to the Editor, Lancet, 2:439, 1965. T U R N E R , J.R.B., AND T O W E R S , J.R.H.: Complications of cardioversion, Lancet, 2:612,1965. LINDSAY, J . , JR.: Pulmonary edema following cardioversion, (Annotations), Amer. Heart ]., 74:434, 1967. HOLLMAN, A., AND N I C H O L S O N , H . : Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2:801, 1966. I K R A M , H., N I X O N , P.G.F., AND ARCAN, T.: Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2:911, 1966. BELL, H.E.: Direct-current shock for atrial fibrillation, in Letter to the Editor, Lancet, 2 : 9 1 1 , 1 9 6 6 .
CASE 1
A 61-year-old white woman with rheumatic heart disease presented with progressive exertional dyspnea and intermittent palpitations with symptoms of near syncope. Every time the arrhythmia was treated with digitalis, an intense sinus bradycardia ensued. Pertinent physical findings included bilateral basilar rales, cardiomegaly and the murmurs of aortic stenosis and insufficiency, and mitral stenosis and insufficiency. An electrocardiogram demonstrated sinus bradycardia of 42 beats/min with frequent nodal and ventricular escape beats. The chest x-ray film revealed massive cardiomegaly and bilateral pleural effusions. When digitalis was discontinued, the supraventricular tachycardia at 150 beats/min returned. Use of temporary transvenous pacemaker was followed by the implantations of a permanent demand pacemaker. The patient has been maintained free of congestive failure and tachycardia on digoxin 0.25 mg four times a day and procaine amide, 750 mg every six hours. CASE 2
An 82-year-old white man with three previous myocardial infarctions was admitted with refractory congestive heart •From the U. S. Public Health Service Hospital, Staten Island, N. Y.
CHEST, VOL. 57, NO. 2, FEBRUARY 1970