Effect of Electroconvulsive Therapy on Cardiac Rhythm, Conduction and Repolarization

PAUL J. TROUP, JOYCE G. SMALL, VICTOR MILSTEIN, IVER F. SMALL, DOUGLAS P. ZIPES

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Because sympathetic stimulation has been implicated in the genesis of arrhythmias, we studied the effects on arrhythmias of electroconvulsive therapy (ECT). Fifteen psychiatric patients (male: 8, female: 7, age: 19‐51, mean: 29.8) without known heart disease underwent 24‐hour Holter recordings before, during, and after ECT (25 episodes). All patients were taking psychotropic drugs and received atropine (0.4‐1.2 mg, mean: 1.1 mg IV), methohexital, and succinylcholine prior to ECT. Following ECT, mean maximum heart rate increased (106 ± 3.2 to 142 ± 6.0 beats/min, p < .001), PR interval decreased (149 ± 3.3 to 131 ± 3.7 msec, p < .001) and QTC interval increased (432 ± 6.5 to 454 ± 9.7 msec, p < .001) compared to values obtained after atropine administration. Mean PVC or PAG frequency immediately after ECT or per 24 hours did not change significantly (PVC per 24 hours 6.8 ± 3.2 to 10.4 ± 6.4, NS; PAC per 24 hours 0.4 ± 0.3 to 0.3 ± 0.2, NS) and no complex arrhythmias were noted. Rate and PR changes suggest adrenergic effeqts of ECT and QTC increase may be due to imbaianced sympathetic discharge. Autonomic stimulation produced by ECT did not induce arrhythmias in these patients without heart disease. The possible antiarrhythmic role of psychotropic agents or premedication is unknown.

Original languageEnglish (US)
Pages (from-to)172-177
Number of pages6
JournalPacing and Clinical Electrophysiology
Volume1
Issue number2
DOIs
StatePublished - Apr 1978

Keywords

  • adrenergic stimulation
  • arrhythmias
  • electroconvulsive therapy

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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