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Recurrent ventricular fibrillation precipitated by quinidine
86
AuSrRAcrS
criterion, lasts 2-5 hours, with I0 mg only half as long. If 20 mg of orciprcnalin were given as a second dose after the effect of the first dose was over, the effect was up to twice as long. The effect seems to be additive. As a conclusion the authors suggest the permanent prophylactic therapy with orciprenalin for all patients with artificial pacemakers. W. J. Hausen Avenhaus, H., Grohmann, H. and Seibel, K. Refractor3" time measurements of the heart in man by electric stimulation (Ger.). Klin. Wochenschr. 46: 1267-1272, 1968. (I. Med. Kiln. Univ. Miinchen 15, Zienssenstr. 1, Germany) In 36 patients the authors investigated the refractory period of the heart by artificial stimulation either with a pacemaker catheter or an implanted pacemaker. The experience with several kinds of stimulation is reported, i.e. spontaneous parasystole paired and double stimulation. None of the patients was treated with glycosides, procainamide or quinidine. Independently of the methods the results show an approximately linear correlation between the preceeding R-R interval and the refractory period. The quotient of refractory period to Q-T duration is relatively constant under normal circumstances, with a range of 0.81 to 0.85. W. J. Hausen Christmann, W. Pacemaker implantation in cases ~ith Adams-Stokes seizures due to sino-auricular block (Ger.). M~inchen. Med. Wochenschr. 1101 2416--2417, 1968. (Stadtkrankenhaus, D 609 Russelsheim, Germany) A report is made on a 70-year-old patient with a sino-auricular block and 2:1 conduction, suffering from seizures of dizziness and short unconsciousness. During those attacks a slow A-V rhythm was taking place. There was no improvement after several months of drug therapy. After implantation of a fixed rate pacemaker the patient became asymptomatic. W. J. Hausen Furman, S., Parker, B., Krauthamer, M. and Escher, D.J.W. The influence of electromagnetic environment on the performance of artificial cardiac pacemakers, Ann. Thorac. Surg. 6: 90-5, 1968. (Montefiore Hosp. Bronx, N.Y.) Ten cardiac pacemakers were tested on the bench and in vivo for sensitivity to radio-frequency signals and intraeorporeal 60 cycle alternating current. All untriggercd units were insensitive in vivo, except for those designed for radio-frequency signals. The triggered units (demand, atrial or ventricular synchronous pacers) exhibited greater sensitivity and greater reversion to inactivity, fixed-rate operation, or maximum synchronous rate in the presence of interference. Two demand units were unaffected by interference in vivo. R. E. London Belier, B.M., Frater, R.W.M. and Wulfsohn, N. Cardiac pacemaking in the management of postoperalive arrhythmias, Ann. Thorac. Surg., 6: 68-76, 1968. (Albeta Einstein Coll. Med., Bronx, N.Y.) Because of the frequency of various arrhythmias complicating the postoperative period after cardiopulmonary bypass, a technique was evolved in 35 patients in whom pacing wires were implanted in the left or right ventricle or in the atrium during surgery. Pacing was found useful in 10 patients in whom bradycardia with low cardiac output, frequent ventricular
ectopic beats or heart block or standstill occurred spontaneously, or following drug therapy or electrical defibrillation. In the authors' experience, raising the heart rate in cases of severe bradycardia by either ventricular or atrial pacing will increase cardiac output. In relative bradycardia, atrial pacing may be more beneficial. When hypotension and bradycardia followed drug therapy of an ectopic rhythm, the implanted electrodes allowed pacing until the conditions were corrected. In one case, with runs of ineffective ectopic ventricular systoles, the superimposition of a pacemaker rhythm faster than the sinus rate suppressed the ectopie focus. A case of ventricular tachycardia, treated with a combination of propranolol and a pacer rhythm, pointed up the value of a basic pacemaker rhythm when highly toxic doses of suppressive agents are required or when digitalis toxicity is present. R. E. London FIBRILLATION A N D DEFIBRILLATION Witzel, D.A., Geddes, L.A., Hoff, H.E. and MacFarlane, J. Electrical defibrillation of tile equine heart. Am. J. Vet. Res. 29: 1279-1285, 1968. (Nat. Animal Dis. Lab. ADP, Agric. Res. Serv. U.S. Dept. Agriculture, Ames, Iowa 50010.) Defibrillation experiments were carried out on 7 horses, 1 burro and 1 pony, weighing 140 to 500kg. each. Both 60 c.p.s, alternating current and capacitor discharge were used independently in each of several horses during the experiments. The alternating current was derived from the power line via an autotransformer and a 12:1 step-up transformer providing output voltages ranging from 0 to 1,320. Duration was controlled between 0.05 and 5.0 sec. The capacitor discharge was obtained from a bank of condensors totaling 1,500 microfarad (u.f.) charged to 450 volts. The electrodes were formed from elliptical sheets of copper which were large enough to surround the ventricles of each animal. Following induced fibrillation, defibrillation attempts were carried out until the heart was deteriorated to a degree that restoration of a normal rhythm was unlikely. It was possible to defibrillate the 760-Gm. heart of the 150 kg. pony with a 60 c.p.s. alternating current, lasting 0.05 see. at voltages of 600 and 600, delivering thus 250 and 360 watt-see, of energy at amperages of 10 and 12. The larger equine hearts could not be defibrillated even though large amounts of electrical energy were delivered to the ventricles. Failure probably resulted from inability to deliver the requisite energy to the ventricles within the utilization time. By extrapolation from experiments described in the published literature, defibrillation of the heart of equines weighing 450 to 500 kg. would require an energy level of approxim~ely 3 million watt-scc. By linear projection made on the basis of body weight, the 140 kg. pony defibrillated in this study would have required about 8,300 watt-see. Energy of this value did not, however, defibrillate. These data are discussed in relation to such factors as heart size, duration of current, and current theories of the mechanisms of ventricular fibrillation. D. K. Detweiler Oravetz, J. and Slodki, S.J. Recurrent ventricular fibrillation precipitated by quiuldine. Arch. Int. Med. 122:63-65 (1968). (Nit. Sinai Hosp., California Ave. 15th St., Chicago, IlL 60608.) A report is given of a 38-year-old white female with rheumatic heart disease and atrial fibrillation who
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
AuSrRAcrS
criterion, lasts 2-5 hours, with I0 mg only half as long. If 20 mg of orciprcnalin were given as a second dose after the effect of the first dose was over, the effect was up to twice as long. The effect seems to be additive. As a conclusion the authors suggest the permanent prophylactic therapy with orciprenalin for all patients with artificial pacemakers. W. J. Hausen Avenhaus, H., Grohmann, H. and Seibel, K. Refractor3" time measurements of the heart in man by electric stimulation (Ger.). Klin. Wochenschr. 46: 1267-1272, 1968. (I. Med. Kiln. Univ. Miinchen 15, Zienssenstr. 1, Germany) In 36 patients the authors investigated the refractory period of the heart by artificial stimulation either with a pacemaker catheter or an implanted pacemaker. The experience with several kinds of stimulation is reported, i.e. spontaneous parasystole paired and double stimulation. None of the patients was treated with glycosides, procainamide or quinidine. Independently of the methods the results show an approximately linear correlation between the preceeding R-R interval and the refractory period. The quotient of refractory period to Q-T duration is relatively constant under normal circumstances, with a range of 0.81 to 0.85. W. J. Hausen Christmann, W. Pacemaker implantation in cases ~ith Adams-Stokes seizures due to sino-auricular block (Ger.). M~inchen. Med. Wochenschr. 1101 2416--2417, 1968. (Stadtkrankenhaus, D 609 Russelsheim, Germany) A report is made on a 70-year-old patient with a sino-auricular block and 2:1 conduction, suffering from seizures of dizziness and short unconsciousness. During those attacks a slow A-V rhythm was taking place. There was no improvement after several months of drug therapy. After implantation of a fixed rate pacemaker the patient became asymptomatic. W. J. Hausen Furman, S., Parker, B., Krauthamer, M. and Escher, D.J.W. The influence of electromagnetic environment on the performance of artificial cardiac pacemakers, Ann. Thorac. Surg. 6: 90-5, 1968. (Montefiore Hosp. Bronx, N.Y.) Ten cardiac pacemakers were tested on the bench and in vivo for sensitivity to radio-frequency signals and intraeorporeal 60 cycle alternating current. All untriggercd units were insensitive in vivo, except for those designed for radio-frequency signals. The triggered units (demand, atrial or ventricular synchronous pacers) exhibited greater sensitivity and greater reversion to inactivity, fixed-rate operation, or maximum synchronous rate in the presence of interference. Two demand units were unaffected by interference in vivo. R. E. London Belier, B.M., Frater, R.W.M. and Wulfsohn, N. Cardiac pacemaking in the management of postoperalive arrhythmias, Ann. Thorac. Surg., 6: 68-76, 1968. (Albeta Einstein Coll. Med., Bronx, N.Y.) Because of the frequency of various arrhythmias complicating the postoperative period after cardiopulmonary bypass, a technique was evolved in 35 patients in whom pacing wires were implanted in the left or right ventricle or in the atrium during surgery. Pacing was found useful in 10 patients in whom bradycardia with low cardiac output, frequent ventricular
ectopic beats or heart block or standstill occurred spontaneously, or following drug therapy or electrical defibrillation. In the authors' experience, raising the heart rate in cases of severe bradycardia by either ventricular or atrial pacing will increase cardiac output. In relative bradycardia, atrial pacing may be more beneficial. When hypotension and bradycardia followed drug therapy of an ectopic rhythm, the implanted electrodes allowed pacing until the conditions were corrected. In one case, with runs of ineffective ectopic ventricular systoles, the superimposition of a pacemaker rhythm faster than the sinus rate suppressed the ectopie focus. A case of ventricular tachycardia, treated with a combination of propranolol and a pacer rhythm, pointed up the value of a basic pacemaker rhythm when highly toxic doses of suppressive agents are required or when digitalis toxicity is present. R. E. London FIBRILLATION A N D DEFIBRILLATION Witzel, D.A., Geddes, L.A., Hoff, H.E. and MacFarlane, J. Electrical defibrillation of tile equine heart. Am. J. Vet. Res. 29: 1279-1285, 1968. (Nat. Animal Dis. Lab. ADP, Agric. Res. Serv. U.S. Dept. Agriculture, Ames, Iowa 50010.) Defibrillation experiments were carried out on 7 horses, 1 burro and 1 pony, weighing 140 to 500kg. each. Both 60 c.p.s, alternating current and capacitor discharge were used independently in each of several horses during the experiments. The alternating current was derived from the power line via an autotransformer and a 12:1 step-up transformer providing output voltages ranging from 0 to 1,320. Duration was controlled between 0.05 and 5.0 sec. The capacitor discharge was obtained from a bank of condensors totaling 1,500 microfarad (u.f.) charged to 450 volts. The electrodes were formed from elliptical sheets of copper which were large enough to surround the ventricles of each animal. Following induced fibrillation, defibrillation attempts were carried out until the heart was deteriorated to a degree that restoration of a normal rhythm was unlikely. It was possible to defibrillate the 760-Gm. heart of the 150 kg. pony with a 60 c.p.s. alternating current, lasting 0.05 see. at voltages of 600 and 600, delivering thus 250 and 360 watt-see, of energy at amperages of 10 and 12. The larger equine hearts could not be defibrillated even though large amounts of electrical energy were delivered to the ventricles. Failure probably resulted from inability to deliver the requisite energy to the ventricles within the utilization time. By extrapolation from experiments described in the published literature, defibrillation of the heart of equines weighing 450 to 500 kg. would require an energy level of approxim~ely 3 million watt-scc. By linear projection made on the basis of body weight, the 140 kg. pony defibrillated in this study would have required about 8,300 watt-see. Energy of this value did not, however, defibrillate. These data are discussed in relation to such factors as heart size, duration of current, and current theories of the mechanisms of ventricular fibrillation. D. K. Detweiler Oravetz, J. and Slodki, S.J. Recurrent ventricular fibrillation precipitated by quiuldine. Arch. Int. Med. 122:63-65 (1968). (Nit. Sinai Hosp., California Ave. 15th St., Chicago, IlL 60608.) A report is given of a 38-year-old white female with rheumatic heart disease and atrial fibrillation who
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