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The mechanism of digitalis-induced ventricular fibrillation
ABSTRACTS
developed 28 episodcs of recurrent ventricular fibrillation after receiving 3 doses of 0.2 gin. Quinidine SO4 (given at 4-hour intervals) prior to elective electrocardioversion. Daily maintenance doses of Digoxin (0.25 rag.) and Ethacrynic acid (100 rag.) were discontinued one day before Quinidine administration. As with other cases of"Quinidine Syncope" described in the literature, the patient's arrhythmia was characterized by a sudden onset, lack of relationship to dose, a repetitive nature and its usual spontaneous termination, with only the last episode treated with D. C. eountershock, which resulted in sinus rhythm. However, concomitant digitalis toxicity could not be ruled out since the admitting serum K level was 3.2 mEq/L, and especially when the arrhythmia was completely suppressed following K replacement. It is felt, therefore, that the recurrent ventricular fibrillation this patient manifested is due to combined effects of hypokalemia and digitalis toxicity, with direct sensitization of the myocardium to Quinidine resulting in the reduction of the fibrillation threshold. L. Lemberg Castellanos, Jr., A., Lemberg, L. and Centurion, M. J. The medlanism of digitalis-induced ventricular fibrillation. Dis. Chest 54: 53-57,1968.(Sect. Cardiol. Univ. Miami Sch. Med. Miami, Florida) Two cases of ventricular fibrillation induced by digitalis are recordcd. In the first case the fibrillation evolved from a rapidly progressing bidirectional ventricular tachycardia. The second case of vcntricular fibrillation occurred when a ventricular extrasystole fell in the vulnerable phase of the preceding contraction. These two cases demonstrate two types of digitalis-related ventricular fibrillation, one appearing suddenly and responding to electric shock and the other being preceded by a gradual widening of the QRS complexes. The latter cannot be abolished electrically. M. M. Halpern Baedecker, W., Henselmann, L., Kiefhaber, F. and Bl6mer, H. Electrotherapy of atrial fibrillation after mitral commissurotomy (Ger.). Mtinchen. Med. Wochensehr. 110: 1981-1987, 1968. (Med. Kiln. Techn. Hochsch., D 8 Mtlnchen 80, Ismaningerstr. 22. Germany) 68 patients were treated with electroreduction after having undergone surgery for mitral stenosis. In 81 ~o of these patients with atrial fibrillation sinus rhythm could be established by electrical defibrillation, but only in 14~ of the whole patient number did the sinus rhythm persist more than one year. Immediately after defibrillation the following rhythm disturbances were observed in a certain number of patients: P-R prolongation, bradycardia with slow A-V nodal rhythm, "and atrial or ventricular premature beats. Quinidine 9should be given before defibrillation in doses up to 1.5 g/day, after reduction 600-800 mg/day for three to four months. The patients were also treated with anticoagulants for two to three weeks before defibrillation. 9The studies showed that the long-term results of electroreduction were good in patients with only slight post-operative residual stenosis, but there is no direct correlation between the results of the electroreduction and the results of the operation. Furihermore, good results are to be expected if the left auricle diminishes in size after operation, and if there is no additional
87
mitral insufficiency. On the other hand, the preoperative severity of the stenosis, pulmonary hypertension, the preoperative pulmonary wedge pressure, electrocardiographic signs of myocardial damage and the time interval between commissurotomy and electrical reduction show no significant correlation with the units. W. J. Hausen VAGAL EFFECTS Toda, N.: Cholinergie actions in the sinoatrial node of the reserpine-pretreated rabbit. J. Pharmacol. & Exp. Therap. 159: 290--297,1968. (Dept. Pharmacol. Kyoto, Univ., Kyoto, Japan.) Isolated preparations of vagus and atrial wall from the rabbit were used. Transmembrane potentials were recorded from sinoatrial nodal pacemaker fibers in the steady state and during stimulation of extracardiae vagus nerves. Pretreatment with reserpine had no effect on normal slowing due to vagal stimulation, but did cause a slower rate before stimulation when compared with normal preparations. Soldium ion depletion decreased sinoatrial nodal electrical activity, but increased chronotropic response to vagal stimulation. Under these conditions, cholinergie stimulation induced hyperpolarization followed by transient recovery of activity. The recovery was not inhibited either by pretreatment with reserpine or by application of propranolol. Atropine decreased the hyperpolarization but not the recovery of activity. The author proposes that endogenous acetylcholine possessed cardioexcitatory action which was independent of the release of catecholamines and was atropine-resistant. J. G. Ellis Gerhard, W., Paulussen, F., Frowein, R. and V. Smekal, P. The neurogenle paneordial asystolia. A case of brain stem tumor with Adams-Stokes seizures (Ger.) Dtsch. med. Wschr. 93: 242-246, 1968 (I Med. Univ. Klinik, D15 KiSln-Lindenthal, Germany) This report concerns a 54-year-old patient with history of nausea, vomiting, weight loss and dizziness, later seizures of unconsciousness. These occurred particularly with certain manipulations like shaking the bed, elevation of the head and drinking. These seizures were shown to be caused by asystolia of 5 to 10 seconds with an otherwise normal ECG. No ventricular beats took place. While the stimulus of an electrode-pacemaker produced a response with 5 to 8 V. during the interval, 30 V. were required during asystolia. The patient died from circulatory shock. The necropsy did not reveal any heart muscle necrosis nor changes in the conduction system. However, a small tumor in the medulla oblongata near the vagal nucleus was found. This was considered to be the cause for the extreme vagal irritation since other vagal effects could be ruled out. W. J. Hausen ELECTROLYTES Johnson, J. D. and Jennings, R. Hypocalcemia and cardiac arrhythmias. Amer. J. Dis. Child. 115: 373376, 1968 (Lab. Clin. Sci., Nat. Inst. Mental Health, Bethesda, Md. 20014) Cardiac arrhYthmias in a 5-year-old mentally retarded undernourished boy with hypocalcemla varied from supraventricular tachycardia to sinus bradycardia with intermittent sinoatrial block and nodal escape. After infusion of 175 rag. Ca Gluconate at a
developed 28 episodcs of recurrent ventricular fibrillation after receiving 3 doses of 0.2 gin. Quinidine SO4 (given at 4-hour intervals) prior to elective electrocardioversion. Daily maintenance doses of Digoxin (0.25 rag.) and Ethacrynic acid (100 rag.) were discontinued one day before Quinidine administration. As with other cases of"Quinidine Syncope" described in the literature, the patient's arrhythmia was characterized by a sudden onset, lack of relationship to dose, a repetitive nature and its usual spontaneous termination, with only the last episode treated with D. C. eountershock, which resulted in sinus rhythm. However, concomitant digitalis toxicity could not be ruled out since the admitting serum K level was 3.2 mEq/L, and especially when the arrhythmia was completely suppressed following K replacement. It is felt, therefore, that the recurrent ventricular fibrillation this patient manifested is due to combined effects of hypokalemia and digitalis toxicity, with direct sensitization of the myocardium to Quinidine resulting in the reduction of the fibrillation threshold. L. Lemberg Castellanos, Jr., A., Lemberg, L. and Centurion, M. J. The medlanism of digitalis-induced ventricular fibrillation. Dis. Chest 54: 53-57,1968.(Sect. Cardiol. Univ. Miami Sch. Med. Miami, Florida) Two cases of ventricular fibrillation induced by digitalis are recordcd. In the first case the fibrillation evolved from a rapidly progressing bidirectional ventricular tachycardia. The second case of vcntricular fibrillation occurred when a ventricular extrasystole fell in the vulnerable phase of the preceding contraction. These two cases demonstrate two types of digitalis-related ventricular fibrillation, one appearing suddenly and responding to electric shock and the other being preceded by a gradual widening of the QRS complexes. The latter cannot be abolished electrically. M. M. Halpern Baedecker, W., Henselmann, L., Kiefhaber, F. and Bl6mer, H. Electrotherapy of atrial fibrillation after mitral commissurotomy (Ger.). Mtinchen. Med. Wochensehr. 110: 1981-1987, 1968. (Med. Kiln. Techn. Hochsch., D 8 Mtlnchen 80, Ismaningerstr. 22. Germany) 68 patients were treated with electroreduction after having undergone surgery for mitral stenosis. In 81 ~o of these patients with atrial fibrillation sinus rhythm could be established by electrical defibrillation, but only in 14~ of the whole patient number did the sinus rhythm persist more than one year. Immediately after defibrillation the following rhythm disturbances were observed in a certain number of patients: P-R prolongation, bradycardia with slow A-V nodal rhythm, "and atrial or ventricular premature beats. Quinidine 9should be given before defibrillation in doses up to 1.5 g/day, after reduction 600-800 mg/day for three to four months. The patients were also treated with anticoagulants for two to three weeks before defibrillation. 9The studies showed that the long-term results of electroreduction were good in patients with only slight post-operative residual stenosis, but there is no direct correlation between the results of the electroreduction and the results of the operation. Furihermore, good results are to be expected if the left auricle diminishes in size after operation, and if there is no additional
87
mitral insufficiency. On the other hand, the preoperative severity of the stenosis, pulmonary hypertension, the preoperative pulmonary wedge pressure, electrocardiographic signs of myocardial damage and the time interval between commissurotomy and electrical reduction show no significant correlation with the units. W. J. Hausen VAGAL EFFECTS Toda, N.: Cholinergie actions in the sinoatrial node of the reserpine-pretreated rabbit. J. Pharmacol. & Exp. Therap. 159: 290--297,1968. (Dept. Pharmacol. Kyoto, Univ., Kyoto, Japan.) Isolated preparations of vagus and atrial wall from the rabbit were used. Transmembrane potentials were recorded from sinoatrial nodal pacemaker fibers in the steady state and during stimulation of extracardiae vagus nerves. Pretreatment with reserpine had no effect on normal slowing due to vagal stimulation, but did cause a slower rate before stimulation when compared with normal preparations. Soldium ion depletion decreased sinoatrial nodal electrical activity, but increased chronotropic response to vagal stimulation. Under these conditions, cholinergie stimulation induced hyperpolarization followed by transient recovery of activity. The recovery was not inhibited either by pretreatment with reserpine or by application of propranolol. Atropine decreased the hyperpolarization but not the recovery of activity. The author proposes that endogenous acetylcholine possessed cardioexcitatory action which was independent of the release of catecholamines and was atropine-resistant. J. G. Ellis Gerhard, W., Paulussen, F., Frowein, R. and V. Smekal, P. The neurogenle paneordial asystolia. A case of brain stem tumor with Adams-Stokes seizures (Ger.) Dtsch. med. Wschr. 93: 242-246, 1968 (I Med. Univ. Klinik, D15 KiSln-Lindenthal, Germany) This report concerns a 54-year-old patient with history of nausea, vomiting, weight loss and dizziness, later seizures of unconsciousness. These occurred particularly with certain manipulations like shaking the bed, elevation of the head and drinking. These seizures were shown to be caused by asystolia of 5 to 10 seconds with an otherwise normal ECG. No ventricular beats took place. While the stimulus of an electrode-pacemaker produced a response with 5 to 8 V. during the interval, 30 V. were required during asystolia. The patient died from circulatory shock. The necropsy did not reveal any heart muscle necrosis nor changes in the conduction system. However, a small tumor in the medulla oblongata near the vagal nucleus was found. This was considered to be the cause for the extreme vagal irritation since other vagal effects could be ruled out. W. J. Hausen ELECTROLYTES Johnson, J. D. and Jennings, R. Hypocalcemia and cardiac arrhythmias. Amer. J. Dis. Child. 115: 373376, 1968 (Lab. Clin. Sci., Nat. Inst. Mental Health, Bethesda, Md. 20014) Cardiac arrhYthmias in a 5-year-old mentally retarded undernourished boy with hypocalcemla varied from supraventricular tachycardia to sinus bradycardia with intermittent sinoatrial block and nodal escape. After infusion of 175 rag. Ca Gluconate at a