- Email: [email protected]
Electroshock therapy and cardiac pacemakers
Electroshock Therapy and Cardiac Pacemakers C. ROGER YOUMANS, Jr., M.rD., GLEB BOURIANOFF, DANIEL C. ALLENSWORTH, M.D., WINSTON L. MARTIN, JOHN R. DERRICK, M.D., Galveston, Texas
Considerable attention has been given to cardiovascular alternations after electroshock therapy. Little, however, has been written about the practical clinical application of makers. Safe application of two electrical devices in the same patient requires an understanding not only of the hazards of each technic, but also of the effects of both units used simultaneously. The influence of environmental factors on pacemaker function and the risk of electrocution in these patients from seemingly small electrical currents has been previously evaluated [l-8]. Cardiac effects of electroshock are well recorded [9-J 61. The risk of electroshock therapy (EST) in
patients with pacemakers involves the application of 170 volts of alternating current shocks of one-second duration, frequently lasting through the vulnerable myocardial repolarization phase, in patients with low resistance pathways to the heart. When EST was recommended in a pacemaker patient, a number of questions arose: (1) Would EST influence the function of the pacemaker? (2) Would the heart be more susceptible to EST-induced arrhythmias? (3) Would the pacemaker be damaged? (4) Would electrical necrosis or thrombosis possibly result at the contact points of the electrodes? (5) Would transvenous electrode displacement occur during the convulsive stage? This experiment was designed to answer these
From the Division of Thoracic and Cardiovascular Surgery, Department of Internal Medicine, and the Department of Psychiatry at the University of Texas Medical Branch, Galveston, Texas. Presented at the Twenty-First Annual Meeting of the Southwestern Surgical Congress, Stateline. Nevada, June Z-5,1969. Vol. 118. December
1969
B.A., M.D.,
questions and to establish guidelines of safety for treating patients with pacemakers.
Material
and Methods
Complete heart block was produced in five dogs during inflow occlusion by the atrioventricular node suture encircling technic described by Taufic et al. [17]. Electrocardiographic monitoring was used to confirm complete atrioventricular dissociation. When heart block was ascertained, electrical cardiac pacing was immediately instituted. Four dogs were paced with General Electric batterypowered pacemakers (Models A2070AA and A2072AA) which were placed in a cervical incision. General Electric (Model A-2070DA) bipolar transvenous electrodes were put into the apex of the right ventricle by way of the right external jugular vein. In the fifth dog a Medtronic (Model 68’70) epicardial pacemaker was used. The electrodes (Model 5814) were sutured to an avascular portion of the anterior surface of the heart and tunnelled subcutaneously to a battery pack implanted in the abdominal wall below the right costal margin. On the seventh postoperative day each dog was matched with a dog of normal stock of approximately the same weight and age. Each pair of animals was then given an identical course of electroshock therapy. (Fig. 1.) Every dog received an average of six electroshock treatments daily for a period of three days, a total of eighteen treatments per dog or ninety treatments for each group of animals. With the animals under light pentobarbital anesthesia after the administration of .5 mg. of intravenous succinylcholine chloride, EST was applied, using Medcraft’s electroshock therapy unit (Model B-24). This is the same model used in treating patients on the psychiatric unit, at our Hospital. EST electrodes were placed over the temporal regions bilaterally in the usual fashion. Shocks of one-second duration and of 170 volts were applied. Each dog of a pair received 931
Youmans et al.
TABLE
I
Cardiac Arrhythmias after 180 Applications of Electroshock Therapy Dogswith Heart
Block and Control Pacemaker Dogs
Arrhythmias
Dangerous Arrhythmias Ventricular tachycardia ldioventricular beats Competing with paced beats Ventricular asystole Sinoatrial arrest Total
Fig. 1. Schematic representation of method of EST in dogs with heart block and pacemakers. the same number of shocks at each session. This level of electrical stimulation produced generalized convulsions in every case. One pair of dogs was premeditated intravenously with 0.1 mg. of atropine sulfate. If respiratory arrest occurred, the animals were artificially ventilated with a Bird respirator. Femoral arterial blood pressure and electrocardiograms were recorded during each treatment session on a Grass polygraph. Persistence of complete heart block was confirmed at each session by brief disconnection of an electrode from the pulse generator. (Fig. 2.) At the end of each test period, each pulse generator was removed from contact
Other Arrhythmias Sinus bradycardia Sinus tachycardia Sinus arrhythmia Premature ventricular
beats
Bigeminy Atrioventricular dissociation Wandering pacemaker Total Total of all arrhythmias
Total NO. of Dogs
2 0 5 1 3 11
3 0 0 5 3 11
5 0 5 6 6 22
1 0 0 1 0 0 0 2
6 1 3 3 4 2 2 21
7 1 3 4 4 2 2 23
13
32
45
with the animal and deliberately stimulated directly with standard one-second 170 volt shocks. After a three day course of treatments, the animals were allowed to recover, then sacrificed, and autopsied one week later. Hearts and brains were examined grossly and microscopically. After each course of therapy the function of each pulse generator was evaluated according to rate and ampli-
Polygraph recording of electrocardiogram and arterial pressure demonFig. 2. strating complete atrioventricular block during seven second period of disconnection of electrode from pulse generator. 932
The American Journal of Surgery
Electroshock
tudt:. All electrocardiograms our cardiologist.
were interpreted
Therapy
and Cardiac
Pacemakers
by
Results Ellectroshock therapy was well tolerated by the dogs with pacemakers. Less than half as many cardiac arrhythmias were noted in this group as in the others. (Table I.) During the 180 electroshock treatments forty-five cardiac arrhythmias were noted. The dogs with heart block and pacemakers experienced thirteen abnormal cardiac rhythms as compared to thirty-two in the control group. Arrhythmias were classified as either dangerous or otherwise. (Fig. 3.) There was a similar number of potentially dangerous rhythm disturbances in each group. Sinoatrial arrest, listed as a dangerous arrhythmia, was of no consequence to the dogs with pacing. One of the arrhythmias in the dogs with pacemakers was an escape rhythm (ventricular asystole) and may have been related to temporary displacement of the endocardial electrode. All arrhythmias in the dogs with heart block occurred in those dogs with transvenous electrodes. The animal with the epicardial electrodes experienced no arrhythmias at any time. Competition with paced beats was recorded during five treatments. Dogs with pacing usually maintained effective heart beats throughout EST, whereas in several instances the control dogs showed transient cardiac standstill with concomitant drop in blood pressure. (Fig. 4 and 5.) Atropine given before EST did not affect the response of the dog with heart block. The control dog who received this drug had fewer subsequent arrhythmias. Respiratory arrest occurred in about half of the sessions and was equally common in both groups. Application of electric shocks directly across the pulse generator produced no effect. No pacemaker was noticeably damaged. They paced at the same rate and amplitude at the end of the test period. Only one dog demonstrated any behavioral disturbance after EST. This dog thrashed about in his cage after awakening from anesthesia. He was quiet and responsive to environmental stimuli twenty-four hours later. In all dogs microscopic examination of the brain showed moderate edema of the type usually produced by electroshock. Examination of the heart both grossly and microscopically Vol. 118, December 1969
Polygraph recording of a dangerous arFig. 3. rhythmia (ventricular tachycardia) after EST in a pacemaker dog.
gave no evidence of thrombi or coagulation necrosis. Several dogs not included in this test series and not having pacemakers were given standard one second shocks of 170 volts across the shoulders and chest. Ventricular fibrillation resulted immediately in all cases. Similar electric shocks across the cervical region produced ventricular fibrillation about half of the time.
Polygraph recording of dog in control group Fig. 4. during EST. Effective cardiac output has ceased during two one-second shocks. 933
Youmans et al.
Fig. 5. Polygraph recording of pacemaker dog during EST. Note continued cardiac output in spite of three one-second shocks.
It should be noted that none studied experienced ventricular a result of EST. When, however, of an electrode was deliberately therapy ventricular fibrillation produced.
of the dogs fibrillation as the insulation broken, shock was uniformly
Case Report A sixty-two year old woman was hospitalized with a diagnosis of severe psychotic depression. Her history included coronary artery disease. In 1964 she had experienced complete heart block which kept her confined to bed with symptoms of congestive failure. In early 1965 an epicardial Medtronic cardiac pacemaker was implanted with good results. After initial unsuccessful attempts to control the patient’s psychiatric problem with medical therapy, EST was considered. After consultation with the manufacturer of the pacemaker, several courses of EST were administered. No cardiac arrhythmias were noted and there was no evidence of damage to the pacemaker. Mental status improved after therapy.
Cardiovascular Effects of EST Although deaths from EST are relatively rare, Ebaugh, Barnacle, and Neubuerger [lo] and Will, Rehfeldt, and Neumann [ll] recently reviewed thirty-five fatalities. Two such deaths have been previously reported from this hospital. Kalinowsky and Hock [12] be934
lieved that most fatalities were of cardiovascular origin. The types of EKG alteration recorded with electroshock therapy were similar to those noted in this study. The changes could be arranged roughly into two groups : (1) vagotonia, or increase in P-R interval, bradycardia, sinus standstill, and atrioventricular dissociation-30 per cent incidence; and (2) etopic rhythms, such as premature atria1 contractions, premature ventricular contractions, ventricular tachycardia, and wandering pacemaker-18 per cent incidence [9]. These cardiovascular alterations may be induced by postconvulsive vagotonia, direct stimulation of central nervous system autonomic centers [18], local stimulation of the myocardium, and right heart overload secondary to increased return of blood to the right side of the heart during convulsions [19-j. Currently it is the usual practice to administer atropine before therapy to avert many of these changes
[14,16]. Electroshock Hazards with Pacemakers
in Patients
It has been recognized for several years that cardiac pacemakers that operated from line voltage could be hazardous to the patient [J--8]. As determined by Ohm’s law, current is a factor of the voltage delivered and the reThe American Journal of Surgery
Electroshock Therapy and Cardiac Pacemakers
sistance to flow (current = V/R). Body tissues that act as resistors to electrical flow protect the heart from voltage applied externally. When, however, low resistance pathways to the myocardium exist (such as endocardial electrodes, endocardial catheters with guide wire, and pericardiocentesis needles), improperly grounded hospital equipment, whether in the “on” or the “off” position may induce ventricular fibrillation [Z $1. This complication has been reported in pacemaker patients after contact with electrocardiographic machines [5,7,8] during intracardiac catheterization [SO] and when electrocautery was used during thoracotomy [4,5]. When a machine using linepower is improperly grounded, a voltage potential may develop on the chassis in relation to true ground. An external temporary pacemaker that is properly grounded in the same patient will allow current flow from the machine (electrocardiograph, electric bed, oxygen tent, and the like), through the pacemaker to ground. The reverse situation is also possible. When battery-stimulated pacemakers are used, either internal or external, the pacing system is isolated from the power-line ground circuit. Thus, voltage potential on electrical equipment cannot run to ground by way of the cardiac electrodes. If, however, an uninsulated portion of the electrode is touched by a person who is in contact with true ground, current flow and ventricular fibrillation may result without even a shock to the person who has completed the circuit. Wiggers and Wegria [21] in 1939, in elaboration of observations originally recorded by King [22], described a vulnerable period during late systole, roughly corresponding to the T wave of the electrocardiogram, at which point ventricular fibrillation could most easily be produced. Seemingly, alternating current was most likely to cause fibrillation. An electrical impulse passing through a low resistance cardiac electrode and falling during the myocardial repolarization phase can induce ventricular fibrillation in dogs with currents as low as 0.20 ma. [I] to 0.35 ma. [SS]. The human heart can be fibrillated during heart surgery with currents in the range of 0.180 ma. [I 1. Even the impulse from the pacemaker has been thought to induce fatal arrhythmias occasionally when the stimulus falls on the T wave of a previous premature contraction Ci 1. Vol. 118, December 1969
These factors appear pertinent when it is considered that in EST alternating current shocks of one-second duration undoubtedly fall in many cases during the vulnerable period. The obvious conclusion from this point is that in EST, electrical impulses are applied far enough from the heart to allow body tissue resistance to protect the heart.
Environmental Influence on Pacemaker Function The influence of a number of environmental factors on pacemaker function has been investigated [4,5,6,91. Some early pa&makers were found susceptible to such radiofrequency-wave interference as surgical diathermy or physical therapy short-wave units [5]. Totally implanted units manufactured currently in this country have been tested with a variety of electric, radiation and radiofrequency devices that might be encountered in hospital, home, or work environment [4,6’,9]. The only deleterious pacemaker effects were seen with electric cautery or with spark plugs in immediate proximity (1 to 2 inches) to the pulse generator [4]. In June 1966 the National Institute of Health issued a statement to the effect that radiofrequency interference is no longer a hazard to patients with modern pacemakers manufactured in the United States [241.
Comments Electroshock therapy appears to be well tolerated in animals with heart block and pacemakers. The pacemaker units employed in this procedure were so well insulated that neither pulse generators nor electrodes received sufficient current to allow the low resistance pathway to initiate fibrillation. As indicated in the experiment, an unsuspected break in electrode insulation, perhaps most likely to occur after multiple battery changes, could easily bring about ventricular fibrillation with EST. It is recommended that myocardial defibrillator be readily available and that all patients be constantly monitored. The possibility has been suggested of temporary electrode dislodgement of pacemakers that utilize endocardial catheter electrodes. Possibly a longer wait after pacemaker implantation before electroshock therapy might have decreased the incidence of cardiac arrhythmias in these animals. On the basis of this experiment, however, no conclu-
Youmans et al.
sions can be drawn about electrode displacement or myocardial stability as related to different types of pacemakers and electrodes. Because of the apparent protection from cardiac rhythm disturbances by the pacemaker in some dogs, it seems feasible to speculate that future patients in whom rhythm disturbances are likely to develop may receive a prophylactic standby pacing catheter before EST. If electroshock therapy is considered in a patient who has an external pacemaker stimulated by line voltage, it would seem prudent to delay EST until a totally implantable battery-stimulated pacemaker can be inserted. If delay is not possible, the external unit should be converted to a battery power source and all points in contact with the conductive portions of the cardiac electrode be well insulated before initiation of therapy. The use of atropine before electroconvulsive therapy in patients with pacemakers does not seem to be necessary since the heart rate remains the same in spite of vagotonia. Indeed, it may be contraindicated. This drug may increase the patient’s own heart rate to a point of competition with the pacemaker rate and thus produce an additional potential source of arrhythmias [25].
3. 4.
5. 6.
10.
11.
Summary Complete heart block was surgically produced in five dogs by atrioventricular node suture ligature. Battery-powered totally implantable cardiac pacemakers were immediately installed. After one week of convalescence each dog was paired with a normal control animal and both animals were started on identical courses of electroshock therapy. The dogs with heart blocks with pacemakers not only tolerated EST well, they experienced less than half as many arrhythmias as dogs in the control group. Experimental evidence from this study and the successful clinical application of multiple courses of EST to a patient with a pacemaker would indicate that electroconvulsive therapy is not contraindicated in patients with permanent cardiac pacemakers.
12.
References
17.
1. 2. 936
WHALEN, R. E. and STARMER,C. F. Electric shock hazards in clinical cardiology. Mod. Cardiovas. D&T.,36 : ?,1967. WHALEN, R. E., STARMER, C. F., and Mc-
13.
14.
15.
16.
18.
INTOSH,H. D. Electrical hazards associated with cardiac pacing. Ann. New York Acad. Sci., 111: 922, 1964. BURCHELL.H. B. Hidden hazards of cardiac pacemakers. Circulation, 24: 161, 1961. CARLETON, R. R., SESSIONS, R. W., and GRAETINGER, J. S. Environmental influence of implantable pacemakers. J.A.M.A., 190; 928, 1964. LICHTER, I., BORRIE,J., and MILLER, W. M. Radiofrequency hazards with cardiac pacemakers. B&t. M. J., 1: 1513, 1965. FEIN, R. L. Transuretheral electrocautery procedures in patients with cardiac pacemakers. J.A.M.A., 202: 101,1967. NOORDIJK,J. A., FIT, O., and TEBRA,W. Myocardial electrodes and the danger of ventricular fibrillation. Lancet. 1: 975. 1961. FURMAN, S., SCHE~E~EL, J: B., RABINSON, G., and HTJRWITTES, E. S. Use of an intracardiac pacemaker in the control of heart block. Surgery, 49: 98, 1961. HEJTMANICK, M. R., BANKHEAD,A. J., and HERRMANN, G. R. Electrocardiographic changes following electroshock therapy in curarized patients. Am. Heart J., 36: 790, 1948. EBAUGH, F. G., BARNACLE,C. H., and NEUBUERGER, K. T. Fatalities following electric convulsive therapy. Report of 2 cases with autopsy. Arch. Neurol. & Psychiat., 49: 107, 1943. WILL, 0. A., JR., REHFELDT,F. C., and NEUMANN, M. A, A fatality in electroshock therapy. Report of a case and review of certain previously described cases. J. Nerv. d Ment. Dis., 107: 106,1948. KALINOWSKY,L. B. and HOCK, P. H. Shock Treatments and Other Somatic Procedures in Psychiatry, p. 168, New York, 1946. Grune and Stratton, Inc. BELLET, S., KERSHBAUM,A., and FTJRST,W. The electrocardiogram during electric shock treatment of mental disorders. Am. J. M. Sci., 201: 167,194l. VON NYMAN, E. and SILFVERSKIOLD, B. P. Kreislaufstorungen bei Krampfanfall.en Epileptischen Typs. III. Das Elektrokardiogramm beim Elecktroshock. Acta med. scandinav., 114: 223, 1943. ALTSCHULE, M. D., SULZBACH,W. M., and TILLOTSON,K. J. Significance of changes in the electrocardiogram after electrically induced convulsions in man. Arch. Neural. & Psychiat., 58 : 716,1947. BANKHEAD,A. J., TORENS,J. K., and HARRIS, T. H. The anticipation and prevention of cardiac complications in electroconvulsive therapy. Am. J. Psychiat., 106: 911,195O. TAUFIC,M., BASHOUR,F. A., and LEWIS, F. J. Production of heart block in dogs under direct vision. S. Forum, 6: 96, 1964. WEINBERG,S. J. Cardiac arrhythmias of central origin. Ann. West. Med. & Surg., 2: 83,194s. The American
Journalof
Surgery
Electroshock Therapy and Cardiac Pacemakers 19.
20.
21.
SILFVERSKIOLD, B. P. and AMARK, C. Disturbances of circulation in convulsions of the epileptic type: arterial and venous pressure during electroshock. Acta med. scunczi?zaw.,113: 191, 1943. WEINBERG,D. I., ARTLEY, J. L., WHALEN, R. E., and MCINTOSH, H. D. Hazards in cardiac catheterization. Circulation Res., 2: 1004,1962. WIGGERS,C. J. and WEGRIA, R. Ventricular fibrillation due to single, localized induction and condenser shocks applied during
Vol. 118, December
1969
22. 23. 24. 25.
the vulnerable phase of ventricular systole. Am. J. Ph&ol., 134: 500, 1940. KING, B. G. Thesis, 1934. Cited by Wiggers and Wegria [21]. WEINBERG,D. I., et al: Electric shock hazards in cardiac catheteization. Elec. Eng., 82: 30,1963. Pacemakers not influenced by outside electric current. Texas Med., 62: 58, 1966. BELLET, S. The drug treatment of complete atrio-ventricular heart block. Ann. New York Acad. Sci., 111: 848,1964.
937
Considerable attention has been given to cardiovascular alternations after electroshock therapy. Little, however, has been written about the practical clinical application of makers. Safe application of two electrical devices in the same patient requires an understanding not only of the hazards of each technic, but also of the effects of both units used simultaneously. The influence of environmental factors on pacemaker function and the risk of electrocution in these patients from seemingly small electrical currents has been previously evaluated [l-8]. Cardiac effects of electroshock are well recorded [9-J 61. The risk of electroshock therapy (EST) in
patients with pacemakers involves the application of 170 volts of alternating current shocks of one-second duration, frequently lasting through the vulnerable myocardial repolarization phase, in patients with low resistance pathways to the heart. When EST was recommended in a pacemaker patient, a number of questions arose: (1) Would EST influence the function of the pacemaker? (2) Would the heart be more susceptible to EST-induced arrhythmias? (3) Would the pacemaker be damaged? (4) Would electrical necrosis or thrombosis possibly result at the contact points of the electrodes? (5) Would transvenous electrode displacement occur during the convulsive stage? This experiment was designed to answer these
From the Division of Thoracic and Cardiovascular Surgery, Department of Internal Medicine, and the Department of Psychiatry at the University of Texas Medical Branch, Galveston, Texas. Presented at the Twenty-First Annual Meeting of the Southwestern Surgical Congress, Stateline. Nevada, June Z-5,1969. Vol. 118. December
1969
B.A., M.D.,
questions and to establish guidelines of safety for treating patients with pacemakers.
Material
and Methods
Complete heart block was produced in five dogs during inflow occlusion by the atrioventricular node suture encircling technic described by Taufic et al. [17]. Electrocardiographic monitoring was used to confirm complete atrioventricular dissociation. When heart block was ascertained, electrical cardiac pacing was immediately instituted. Four dogs were paced with General Electric batterypowered pacemakers (Models A2070AA and A2072AA) which were placed in a cervical incision. General Electric (Model A-2070DA) bipolar transvenous electrodes were put into the apex of the right ventricle by way of the right external jugular vein. In the fifth dog a Medtronic (Model 68’70) epicardial pacemaker was used. The electrodes (Model 5814) were sutured to an avascular portion of the anterior surface of the heart and tunnelled subcutaneously to a battery pack implanted in the abdominal wall below the right costal margin. On the seventh postoperative day each dog was matched with a dog of normal stock of approximately the same weight and age. Each pair of animals was then given an identical course of electroshock therapy. (Fig. 1.) Every dog received an average of six electroshock treatments daily for a period of three days, a total of eighteen treatments per dog or ninety treatments for each group of animals. With the animals under light pentobarbital anesthesia after the administration of .5 mg. of intravenous succinylcholine chloride, EST was applied, using Medcraft’s electroshock therapy unit (Model B-24). This is the same model used in treating patients on the psychiatric unit, at our Hospital. EST electrodes were placed over the temporal regions bilaterally in the usual fashion. Shocks of one-second duration and of 170 volts were applied. Each dog of a pair received 931
Youmans et al.
TABLE
I
Cardiac Arrhythmias after 180 Applications of Electroshock Therapy Dogswith Heart
Block and Control Pacemaker Dogs
Arrhythmias
Dangerous Arrhythmias Ventricular tachycardia ldioventricular beats Competing with paced beats Ventricular asystole Sinoatrial arrest Total
Fig. 1. Schematic representation of method of EST in dogs with heart block and pacemakers. the same number of shocks at each session. This level of electrical stimulation produced generalized convulsions in every case. One pair of dogs was premeditated intravenously with 0.1 mg. of atropine sulfate. If respiratory arrest occurred, the animals were artificially ventilated with a Bird respirator. Femoral arterial blood pressure and electrocardiograms were recorded during each treatment session on a Grass polygraph. Persistence of complete heart block was confirmed at each session by brief disconnection of an electrode from the pulse generator. (Fig. 2.) At the end of each test period, each pulse generator was removed from contact
Other Arrhythmias Sinus bradycardia Sinus tachycardia Sinus arrhythmia Premature ventricular
beats
Bigeminy Atrioventricular dissociation Wandering pacemaker Total Total of all arrhythmias
Total NO. of Dogs
2 0 5 1 3 11
3 0 0 5 3 11
5 0 5 6 6 22
1 0 0 1 0 0 0 2
6 1 3 3 4 2 2 21
7 1 3 4 4 2 2 23
13
32
45
with the animal and deliberately stimulated directly with standard one-second 170 volt shocks. After a three day course of treatments, the animals were allowed to recover, then sacrificed, and autopsied one week later. Hearts and brains were examined grossly and microscopically. After each course of therapy the function of each pulse generator was evaluated according to rate and ampli-
Polygraph recording of electrocardiogram and arterial pressure demonFig. 2. strating complete atrioventricular block during seven second period of disconnection of electrode from pulse generator. 932
The American Journal of Surgery
Electroshock
tudt:. All electrocardiograms our cardiologist.
were interpreted
Therapy
and Cardiac
Pacemakers
by
Results Ellectroshock therapy was well tolerated by the dogs with pacemakers. Less than half as many cardiac arrhythmias were noted in this group as in the others. (Table I.) During the 180 electroshock treatments forty-five cardiac arrhythmias were noted. The dogs with heart block and pacemakers experienced thirteen abnormal cardiac rhythms as compared to thirty-two in the control group. Arrhythmias were classified as either dangerous or otherwise. (Fig. 3.) There was a similar number of potentially dangerous rhythm disturbances in each group. Sinoatrial arrest, listed as a dangerous arrhythmia, was of no consequence to the dogs with pacing. One of the arrhythmias in the dogs with pacemakers was an escape rhythm (ventricular asystole) and may have been related to temporary displacement of the endocardial electrode. All arrhythmias in the dogs with heart block occurred in those dogs with transvenous electrodes. The animal with the epicardial electrodes experienced no arrhythmias at any time. Competition with paced beats was recorded during five treatments. Dogs with pacing usually maintained effective heart beats throughout EST, whereas in several instances the control dogs showed transient cardiac standstill with concomitant drop in blood pressure. (Fig. 4 and 5.) Atropine given before EST did not affect the response of the dog with heart block. The control dog who received this drug had fewer subsequent arrhythmias. Respiratory arrest occurred in about half of the sessions and was equally common in both groups. Application of electric shocks directly across the pulse generator produced no effect. No pacemaker was noticeably damaged. They paced at the same rate and amplitude at the end of the test period. Only one dog demonstrated any behavioral disturbance after EST. This dog thrashed about in his cage after awakening from anesthesia. He was quiet and responsive to environmental stimuli twenty-four hours later. In all dogs microscopic examination of the brain showed moderate edema of the type usually produced by electroshock. Examination of the heart both grossly and microscopically Vol. 118, December 1969
Polygraph recording of a dangerous arFig. 3. rhythmia (ventricular tachycardia) after EST in a pacemaker dog.
gave no evidence of thrombi or coagulation necrosis. Several dogs not included in this test series and not having pacemakers were given standard one second shocks of 170 volts across the shoulders and chest. Ventricular fibrillation resulted immediately in all cases. Similar electric shocks across the cervical region produced ventricular fibrillation about half of the time.
Polygraph recording of dog in control group Fig. 4. during EST. Effective cardiac output has ceased during two one-second shocks. 933
Youmans et al.
Fig. 5. Polygraph recording of pacemaker dog during EST. Note continued cardiac output in spite of three one-second shocks.
It should be noted that none studied experienced ventricular a result of EST. When, however, of an electrode was deliberately therapy ventricular fibrillation produced.
of the dogs fibrillation as the insulation broken, shock was uniformly
Case Report A sixty-two year old woman was hospitalized with a diagnosis of severe psychotic depression. Her history included coronary artery disease. In 1964 she had experienced complete heart block which kept her confined to bed with symptoms of congestive failure. In early 1965 an epicardial Medtronic cardiac pacemaker was implanted with good results. After initial unsuccessful attempts to control the patient’s psychiatric problem with medical therapy, EST was considered. After consultation with the manufacturer of the pacemaker, several courses of EST were administered. No cardiac arrhythmias were noted and there was no evidence of damage to the pacemaker. Mental status improved after therapy.
Cardiovascular Effects of EST Although deaths from EST are relatively rare, Ebaugh, Barnacle, and Neubuerger [lo] and Will, Rehfeldt, and Neumann [ll] recently reviewed thirty-five fatalities. Two such deaths have been previously reported from this hospital. Kalinowsky and Hock [12] be934
lieved that most fatalities were of cardiovascular origin. The types of EKG alteration recorded with electroshock therapy were similar to those noted in this study. The changes could be arranged roughly into two groups : (1) vagotonia, or increase in P-R interval, bradycardia, sinus standstill, and atrioventricular dissociation-30 per cent incidence; and (2) etopic rhythms, such as premature atria1 contractions, premature ventricular contractions, ventricular tachycardia, and wandering pacemaker-18 per cent incidence [9]. These cardiovascular alterations may be induced by postconvulsive vagotonia, direct stimulation of central nervous system autonomic centers [18], local stimulation of the myocardium, and right heart overload secondary to increased return of blood to the right side of the heart during convulsions [19-j. Currently it is the usual practice to administer atropine before therapy to avert many of these changes
[14,16]. Electroshock Hazards with Pacemakers
in Patients
It has been recognized for several years that cardiac pacemakers that operated from line voltage could be hazardous to the patient [J--8]. As determined by Ohm’s law, current is a factor of the voltage delivered and the reThe American Journal of Surgery
Electroshock Therapy and Cardiac Pacemakers
sistance to flow (current = V/R). Body tissues that act as resistors to electrical flow protect the heart from voltage applied externally. When, however, low resistance pathways to the myocardium exist (such as endocardial electrodes, endocardial catheters with guide wire, and pericardiocentesis needles), improperly grounded hospital equipment, whether in the “on” or the “off” position may induce ventricular fibrillation [Z $1. This complication has been reported in pacemaker patients after contact with electrocardiographic machines [5,7,8] during intracardiac catheterization [SO] and when electrocautery was used during thoracotomy [4,5]. When a machine using linepower is improperly grounded, a voltage potential may develop on the chassis in relation to true ground. An external temporary pacemaker that is properly grounded in the same patient will allow current flow from the machine (electrocardiograph, electric bed, oxygen tent, and the like), through the pacemaker to ground. The reverse situation is also possible. When battery-stimulated pacemakers are used, either internal or external, the pacing system is isolated from the power-line ground circuit. Thus, voltage potential on electrical equipment cannot run to ground by way of the cardiac electrodes. If, however, an uninsulated portion of the electrode is touched by a person who is in contact with true ground, current flow and ventricular fibrillation may result without even a shock to the person who has completed the circuit. Wiggers and Wegria [21] in 1939, in elaboration of observations originally recorded by King [22], described a vulnerable period during late systole, roughly corresponding to the T wave of the electrocardiogram, at which point ventricular fibrillation could most easily be produced. Seemingly, alternating current was most likely to cause fibrillation. An electrical impulse passing through a low resistance cardiac electrode and falling during the myocardial repolarization phase can induce ventricular fibrillation in dogs with currents as low as 0.20 ma. [I] to 0.35 ma. [SS]. The human heart can be fibrillated during heart surgery with currents in the range of 0.180 ma. [I 1. Even the impulse from the pacemaker has been thought to induce fatal arrhythmias occasionally when the stimulus falls on the T wave of a previous premature contraction Ci 1. Vol. 118, December 1969
These factors appear pertinent when it is considered that in EST alternating current shocks of one-second duration undoubtedly fall in many cases during the vulnerable period. The obvious conclusion from this point is that in EST, electrical impulses are applied far enough from the heart to allow body tissue resistance to protect the heart.
Environmental Influence on Pacemaker Function The influence of a number of environmental factors on pacemaker function has been investigated [4,5,6,91. Some early pa&makers were found susceptible to such radiofrequency-wave interference as surgical diathermy or physical therapy short-wave units [5]. Totally implanted units manufactured currently in this country have been tested with a variety of electric, radiation and radiofrequency devices that might be encountered in hospital, home, or work environment [4,6’,9]. The only deleterious pacemaker effects were seen with electric cautery or with spark plugs in immediate proximity (1 to 2 inches) to the pulse generator [4]. In June 1966 the National Institute of Health issued a statement to the effect that radiofrequency interference is no longer a hazard to patients with modern pacemakers manufactured in the United States [241.
Comments Electroshock therapy appears to be well tolerated in animals with heart block and pacemakers. The pacemaker units employed in this procedure were so well insulated that neither pulse generators nor electrodes received sufficient current to allow the low resistance pathway to initiate fibrillation. As indicated in the experiment, an unsuspected break in electrode insulation, perhaps most likely to occur after multiple battery changes, could easily bring about ventricular fibrillation with EST. It is recommended that myocardial defibrillator be readily available and that all patients be constantly monitored. The possibility has been suggested of temporary electrode dislodgement of pacemakers that utilize endocardial catheter electrodes. Possibly a longer wait after pacemaker implantation before electroshock therapy might have decreased the incidence of cardiac arrhythmias in these animals. On the basis of this experiment, however, no conclu-
Youmans et al.
sions can be drawn about electrode displacement or myocardial stability as related to different types of pacemakers and electrodes. Because of the apparent protection from cardiac rhythm disturbances by the pacemaker in some dogs, it seems feasible to speculate that future patients in whom rhythm disturbances are likely to develop may receive a prophylactic standby pacing catheter before EST. If electroshock therapy is considered in a patient who has an external pacemaker stimulated by line voltage, it would seem prudent to delay EST until a totally implantable battery-stimulated pacemaker can be inserted. If delay is not possible, the external unit should be converted to a battery power source and all points in contact with the conductive portions of the cardiac electrode be well insulated before initiation of therapy. The use of atropine before electroconvulsive therapy in patients with pacemakers does not seem to be necessary since the heart rate remains the same in spite of vagotonia. Indeed, it may be contraindicated. This drug may increase the patient’s own heart rate to a point of competition with the pacemaker rate and thus produce an additional potential source of arrhythmias [25].
3. 4.
5. 6.
10.
11.
Summary Complete heart block was surgically produced in five dogs by atrioventricular node suture ligature. Battery-powered totally implantable cardiac pacemakers were immediately installed. After one week of convalescence each dog was paired with a normal control animal and both animals were started on identical courses of electroshock therapy. The dogs with heart blocks with pacemakers not only tolerated EST well, they experienced less than half as many arrhythmias as dogs in the control group. Experimental evidence from this study and the successful clinical application of multiple courses of EST to a patient with a pacemaker would indicate that electroconvulsive therapy is not contraindicated in patients with permanent cardiac pacemakers.
12.
References
17.
1. 2. 936
WHALEN, R. E. and STARMER,C. F. Electric shock hazards in clinical cardiology. Mod. Cardiovas. D&T.,36 : ?,1967. WHALEN, R. E., STARMER, C. F., and Mc-
13.
14.
15.
16.
18.
INTOSH,H. D. Electrical hazards associated with cardiac pacing. Ann. New York Acad. Sci., 111: 922, 1964. BURCHELL.H. B. Hidden hazards of cardiac pacemakers. Circulation, 24: 161, 1961. CARLETON, R. R., SESSIONS, R. W., and GRAETINGER, J. S. Environmental influence of implantable pacemakers. J.A.M.A., 190; 928, 1964. LICHTER, I., BORRIE,J., and MILLER, W. M. Radiofrequency hazards with cardiac pacemakers. B&t. M. J., 1: 1513, 1965. FEIN, R. L. Transuretheral electrocautery procedures in patients with cardiac pacemakers. J.A.M.A., 202: 101,1967. NOORDIJK,J. A., FIT, O., and TEBRA,W. Myocardial electrodes and the danger of ventricular fibrillation. Lancet. 1: 975. 1961. FURMAN, S., SCHE~E~EL, J: B., RABINSON, G., and HTJRWITTES, E. S. Use of an intracardiac pacemaker in the control of heart block. Surgery, 49: 98, 1961. HEJTMANICK, M. R., BANKHEAD,A. J., and HERRMANN, G. R. Electrocardiographic changes following electroshock therapy in curarized patients. Am. Heart J., 36: 790, 1948. EBAUGH, F. G., BARNACLE,C. H., and NEUBUERGER, K. T. Fatalities following electric convulsive therapy. Report of 2 cases with autopsy. Arch. Neurol. & Psychiat., 49: 107, 1943. WILL, 0. A., JR., REHFELDT,F. C., and NEUMANN, M. A, A fatality in electroshock therapy. Report of a case and review of certain previously described cases. J. Nerv. d Ment. Dis., 107: 106,1948. KALINOWSKY,L. B. and HOCK, P. H. Shock Treatments and Other Somatic Procedures in Psychiatry, p. 168, New York, 1946. Grune and Stratton, Inc. BELLET, S., KERSHBAUM,A., and FTJRST,W. The electrocardiogram during electric shock treatment of mental disorders. Am. J. M. Sci., 201: 167,194l. VON NYMAN, E. and SILFVERSKIOLD, B. P. Kreislaufstorungen bei Krampfanfall.en Epileptischen Typs. III. Das Elektrokardiogramm beim Elecktroshock. Acta med. scandinav., 114: 223, 1943. ALTSCHULE, M. D., SULZBACH,W. M., and TILLOTSON,K. J. Significance of changes in the electrocardiogram after electrically induced convulsions in man. Arch. Neural. & Psychiat., 58 : 716,1947. BANKHEAD,A. J., TORENS,J. K., and HARRIS, T. H. The anticipation and prevention of cardiac complications in electroconvulsive therapy. Am. J. Psychiat., 106: 911,195O. TAUFIC,M., BASHOUR,F. A., and LEWIS, F. J. Production of heart block in dogs under direct vision. S. Forum, 6: 96, 1964. WEINBERG,S. J. Cardiac arrhythmias of central origin. Ann. West. Med. & Surg., 2: 83,194s. The American
Journalof
Surgery
Electroshock Therapy and Cardiac Pacemakers 19.
20.
21.
SILFVERSKIOLD, B. P. and AMARK, C. Disturbances of circulation in convulsions of the epileptic type: arterial and venous pressure during electroshock. Acta med. scunczi?zaw.,113: 191, 1943. WEINBERG,D. I., ARTLEY, J. L., WHALEN, R. E., and MCINTOSH, H. D. Hazards in cardiac catheterization. Circulation Res., 2: 1004,1962. WIGGERS,C. J. and WEGRIA, R. Ventricular fibrillation due to single, localized induction and condenser shocks applied during
Vol. 118, December
1969
22. 23. 24. 25.
the vulnerable phase of ventricular systole. Am. J. Ph&ol., 134: 500, 1940. KING, B. G. Thesis, 1934. Cited by Wiggers and Wegria [21]. WEINBERG,D. I., et al: Electric shock hazards in cardiac catheteization. Elec. Eng., 82: 30,1963. Pacemakers not influenced by outside electric current. Texas Med., 62: 58, 1966. BELLET, S. The drug treatment of complete atrio-ventricular heart block. Ann. New York Acad. Sci., 111: 848,1964.
937