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Electroconvulsive therapy and cardiac pacemakers
Electroconvulsive Therapy and Cardiac Pacemakers JAMES
C.
BALLENGER,
The use of cardiac pacemakers in recent years raises a new clinical problem for physicians involved when these patients need electroconvulsive therapy. There have been very few published reports of electroconvulsive treatment of these patients and little experimental work. A patient with a cardiac pacemaker who was successfully treated with ECT is reported here. CASE REPORT
Mr. O. is a fifty-year-old married caucasian male and was first admitted to the psychiatric ward at the Massachusetts General Hospital on August 22, 1971 after one month history of personality change. He had become quite irritable, and at times irrational, seemed to have boundless energy, needed little sleep and spent large amounts of money buying gifts. On admission he was frankly manic and was agitated, angry, abusive, and exhibited flight of ideas and grandiose ideation. He was oriented and spoke in a forceful voice. He had had no previous affective illness, but his family described his as a hypomanic life style. His physical exam was essentially normal except for a permanently implanted cardiac pacemaker and frequent irregular beats. His EKG had frequent premature atrial beats with occasional blocked premature beat and nodal escapes, occasional premature ventricular contractions, left axis deviation and incomplete right bundle branch block. He was treated with chlorpromazine and lithium carbonate and the frank manic behavior disappeared, but the patient, although appropriate and cooperative, remained somewhat hypomanic. He was readmitted approximately six weeks after discharge, again manic with little sleep in the previous four days, with excitement, and rapid, at times unintelligible speech, and anorexia. He was more depressed during this episode and over the next few weeks developed a mixed manic-depressive picture, despite treatment on chlorpromazine and lithium. He became withdrawn and transiently developed auditory and visual hallucinations. His cardiac difficulties were discovered in February 1971, five months before his first manic episode. He had no previous history of congestive heart failure or suggested coronary artery disease. However, he was seen in February, 1971 in atrial flutter with complete heart block and a ventricular rate of 30. He had a confusing EKG picture but was presumed to have Dr. Ballenger is a resident in the Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. July-August, 1973
M.D.
trifasicular disease.· He subsequently had two syncopal episodes with ventricular rates of 30 and episodes of asystole lasting 9-12 seconds. He had a temporary pacer, then permanent demand pacemaker placed (I\Jedtronic Model 5842) in February, 1971. He went into atrial flutter soon afterward but was cardioverted to normal sinus rhythm without incident. The patient was given seven ECT (150 V, 0.75 sec.) on a three per week basis which he tolerated without incident. He was monitored during the treatment by an Electrodyne cardiac monitor (Model #CB51B) and there was no evidence of pacemaker dysfunction at any time. Because of the interference of the muscle artifact on the monitor, the 1 or 2 beats after the shock were monitored by palpation of the femoral pulse, and these remained regular. Subsequently, there were several opportunities to see normal pacemaker function when it would fire after a premature atrial beat and capture for a few beats before returning to normal sinus rhythm. The patient developed atrial flutter after administration of the atropine pre-medication before his first ECT but was successfully treated by cardioversion and then procaineamide and propranolol. Atropine was subsequently omitted. The patient clearly improved after the first and second ECT and then developed an increasingly severe posttreatment organic psychosis. This resolved after completion of ECT course and the patient improved and was discharged four weeks after his last treatment. DISCUSSION
The primary considerations in this special clinical situation would seem to be: (l) Will the presence of the pacemaker increase the danger of arrhythmias in these patients (2) Will the shock itself or electromagnetic fields generated by the ECT machine adversely affect the functioning of the pacemaker (3) What should be considered because of the increased danger of inducing ventricular fibrillation in the presence of the pacemaker. In the two previously reported cases1.8 and in this case, there was no evidence of ECT induced arrhythmias. In fact, the presence of the pacemaker removes the threat of the most dangerous arrhythmias accompanying ECT, the bradyarrhythmias. In the one published laboratory investigation Youmans, et al.,1.2 using six • Conduction difficulties in all three fasicles of the Bundle of His. 233
PSYCHOSOMATICS
dogs with implanted pacemakers, found that the pacemaker dogs actually had one-third the arrhythmias of the control dogs during ECT. There were no fatal arrhythmias in either group and all arrhythmias occurred in the dogs with transvenous electrodes; the one with epicardial electrodes experienced no arrhythmias. Despite the previously well documented adverse effects on pacemaker function of some environmental electrical factors, we saw no evidence that the ECT current affected pacemaker function, nor was this seen in the two patients reported by Youmans and Wharton. Additionally, Youmans applied the ECT shocks directly to the pulse generators of his experimental animals and produced no damage. Also, theoretically one would not expect serious dysfunction of the newer pacemakers which are designed to revert to a fixed rate during electrical interference, which in this instance could be only during the shock itself (0.5 - 0.75 seconds). The electromagnetic fields generated by the transformers in the ECT machine might also be suspect. Under continuous cardiac monitoring in our patient, the machine was repeatedly operated within twelve inches of the pacemaker itself without effect. The need for cardiac monitoring devices in this situation poses what is probably the greatest danger, that is the possibility that inadvertently a current might pass from the eletcrical monitoring device over the implanted low resistance pathway to the myocardium and induce ventricular fibrillation. The mechanism has been well demonstrated4 with external pacemakers. In this situation a current might develop on the chassis of an improperly grounded machine (e.g.EKG) and then travels to true ground through the pacemaker and myocardium. This is less likely with internally placed pacemakers, although still possible if there is contact between ground and an exposed portion of the pacemaker wiring or electrodes. Care should therefore be exerted to insure that there are no breaks in the insulation of the pacemaker and
234
that there is no possible contact between the patient (grounded EKG, electrical bed, an assistant in contact with the patient and ground) and ground. It would seem that experience to date with the three patients mentioned and the limited experimental work would support the safety of ECT in patients with pacemakers. Because of the subtleties of the electronics involved, engineering consultation would seem wise. Also capabilities to treat cardiac emergencies should be available. The only modification in the standard ECT procedures would be that there would seem to be no need for atropine premedication. The availability of the pacemaker almost eliminates the danger of possible vagotonically induced bradycardias and the atropine induced tachycardias can lead to competition with fixed rate pacemakers or atrial tachyarrhythmias as in the above patient. SUMMARY
A patient with a cardiac pacemaker who was successfully treated with ECT for a manic episode is reported. The author feels that clinical and laboratory experience to date suggests that properly administered electroconvulsive therapy is a safe procedure in patients with cardiac pacemakers. Address for reprints: James C. Ballenger, M.D., Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts 02114. REFERENCES I. Youmans, C. R., Bourianotf, B. A., Allensworth, D. l::. et at: Electroshock Therapy and Cardiac Pacemakers, Amer. J. Surgery, 118:931-937, Dec.
1969. 2. Youmans, C. R., Bourianotf, B. A., Allensworth, D. C., et al: Cardiovascular Alterations during Electroconvulsive Therapy in Patients with Cardiac Pacemakers, SOil. Med. J., 65: No.3, 361365, March 1972. 3. Wharton, R. N.: Electroshock Treatment: Two Novel Problems, Amer. J. Psychiat., 125: 3, 397398, Sept. 1968. 4. Noordijk, J. A., Oey, F. T., Tebra, W.: Myocardial Electrodes and the Danger of Ventricular Fibrillation, Lancet, 1:975-977, 1961.
Volume XIV
C.
BALLENGER,
The use of cardiac pacemakers in recent years raises a new clinical problem for physicians involved when these patients need electroconvulsive therapy. There have been very few published reports of electroconvulsive treatment of these patients and little experimental work. A patient with a cardiac pacemaker who was successfully treated with ECT is reported here. CASE REPORT
Mr. O. is a fifty-year-old married caucasian male and was first admitted to the psychiatric ward at the Massachusetts General Hospital on August 22, 1971 after one month history of personality change. He had become quite irritable, and at times irrational, seemed to have boundless energy, needed little sleep and spent large amounts of money buying gifts. On admission he was frankly manic and was agitated, angry, abusive, and exhibited flight of ideas and grandiose ideation. He was oriented and spoke in a forceful voice. He had had no previous affective illness, but his family described his as a hypomanic life style. His physical exam was essentially normal except for a permanently implanted cardiac pacemaker and frequent irregular beats. His EKG had frequent premature atrial beats with occasional blocked premature beat and nodal escapes, occasional premature ventricular contractions, left axis deviation and incomplete right bundle branch block. He was treated with chlorpromazine and lithium carbonate and the frank manic behavior disappeared, but the patient, although appropriate and cooperative, remained somewhat hypomanic. He was readmitted approximately six weeks after discharge, again manic with little sleep in the previous four days, with excitement, and rapid, at times unintelligible speech, and anorexia. He was more depressed during this episode and over the next few weeks developed a mixed manic-depressive picture, despite treatment on chlorpromazine and lithium. He became withdrawn and transiently developed auditory and visual hallucinations. His cardiac difficulties were discovered in February 1971, five months before his first manic episode. He had no previous history of congestive heart failure or suggested coronary artery disease. However, he was seen in February, 1971 in atrial flutter with complete heart block and a ventricular rate of 30. He had a confusing EKG picture but was presumed to have Dr. Ballenger is a resident in the Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. July-August, 1973
M.D.
trifasicular disease.· He subsequently had two syncopal episodes with ventricular rates of 30 and episodes of asystole lasting 9-12 seconds. He had a temporary pacer, then permanent demand pacemaker placed (I\Jedtronic Model 5842) in February, 1971. He went into atrial flutter soon afterward but was cardioverted to normal sinus rhythm without incident. The patient was given seven ECT (150 V, 0.75 sec.) on a three per week basis which he tolerated without incident. He was monitored during the treatment by an Electrodyne cardiac monitor (Model #CB51B) and there was no evidence of pacemaker dysfunction at any time. Because of the interference of the muscle artifact on the monitor, the 1 or 2 beats after the shock were monitored by palpation of the femoral pulse, and these remained regular. Subsequently, there were several opportunities to see normal pacemaker function when it would fire after a premature atrial beat and capture for a few beats before returning to normal sinus rhythm. The patient developed atrial flutter after administration of the atropine pre-medication before his first ECT but was successfully treated by cardioversion and then procaineamide and propranolol. Atropine was subsequently omitted. The patient clearly improved after the first and second ECT and then developed an increasingly severe posttreatment organic psychosis. This resolved after completion of ECT course and the patient improved and was discharged four weeks after his last treatment. DISCUSSION
The primary considerations in this special clinical situation would seem to be: (l) Will the presence of the pacemaker increase the danger of arrhythmias in these patients (2) Will the shock itself or electromagnetic fields generated by the ECT machine adversely affect the functioning of the pacemaker (3) What should be considered because of the increased danger of inducing ventricular fibrillation in the presence of the pacemaker. In the two previously reported cases1.8 and in this case, there was no evidence of ECT induced arrhythmias. In fact, the presence of the pacemaker removes the threat of the most dangerous arrhythmias accompanying ECT, the bradyarrhythmias. In the one published laboratory investigation Youmans, et al.,1.2 using six • Conduction difficulties in all three fasicles of the Bundle of His. 233
PSYCHOSOMATICS
dogs with implanted pacemakers, found that the pacemaker dogs actually had one-third the arrhythmias of the control dogs during ECT. There were no fatal arrhythmias in either group and all arrhythmias occurred in the dogs with transvenous electrodes; the one with epicardial electrodes experienced no arrhythmias. Despite the previously well documented adverse effects on pacemaker function of some environmental electrical factors, we saw no evidence that the ECT current affected pacemaker function, nor was this seen in the two patients reported by Youmans and Wharton. Additionally, Youmans applied the ECT shocks directly to the pulse generators of his experimental animals and produced no damage. Also, theoretically one would not expect serious dysfunction of the newer pacemakers which are designed to revert to a fixed rate during electrical interference, which in this instance could be only during the shock itself (0.5 - 0.75 seconds). The electromagnetic fields generated by the transformers in the ECT machine might also be suspect. Under continuous cardiac monitoring in our patient, the machine was repeatedly operated within twelve inches of the pacemaker itself without effect. The need for cardiac monitoring devices in this situation poses what is probably the greatest danger, that is the possibility that inadvertently a current might pass from the eletcrical monitoring device over the implanted low resistance pathway to the myocardium and induce ventricular fibrillation. The mechanism has been well demonstrated4 with external pacemakers. In this situation a current might develop on the chassis of an improperly grounded machine (e.g.EKG) and then travels to true ground through the pacemaker and myocardium. This is less likely with internally placed pacemakers, although still possible if there is contact between ground and an exposed portion of the pacemaker wiring or electrodes. Care should therefore be exerted to insure that there are no breaks in the insulation of the pacemaker and
234
that there is no possible contact between the patient (grounded EKG, electrical bed, an assistant in contact with the patient and ground) and ground. It would seem that experience to date with the three patients mentioned and the limited experimental work would support the safety of ECT in patients with pacemakers. Because of the subtleties of the electronics involved, engineering consultation would seem wise. Also capabilities to treat cardiac emergencies should be available. The only modification in the standard ECT procedures would be that there would seem to be no need for atropine premedication. The availability of the pacemaker almost eliminates the danger of possible vagotonically induced bradycardias and the atropine induced tachycardias can lead to competition with fixed rate pacemakers or atrial tachyarrhythmias as in the above patient. SUMMARY
A patient with a cardiac pacemaker who was successfully treated with ECT for a manic episode is reported. The author feels that clinical and laboratory experience to date suggests that properly administered electroconvulsive therapy is a safe procedure in patients with cardiac pacemakers. Address for reprints: James C. Ballenger, M.D., Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts 02114. REFERENCES I. Youmans, C. R., Bourianotf, B. A., Allensworth, D. l::. et at: Electroshock Therapy and Cardiac Pacemakers, Amer. J. Surgery, 118:931-937, Dec.
1969. 2. Youmans, C. R., Bourianotf, B. A., Allensworth, D. C., et al: Cardiovascular Alterations during Electroconvulsive Therapy in Patients with Cardiac Pacemakers, SOil. Med. J., 65: No.3, 361365, March 1972. 3. Wharton, R. N.: Electroshock Treatment: Two Novel Problems, Amer. J. Psychiat., 125: 3, 397398, Sept. 1968. 4. Noordijk, J. A., Oey, F. T., Tebra, W.: Myocardial Electrodes and the Danger of Ventricular Fibrillation, Lancet, 1:975-977, 1961.
Volume XIV