Troup P J, Small J G, Milstein V, Small I F, Zipes D P
Pacing Clin Electrophysiol. 1978 Apr;1(2):172-7. doi: 10.1111/j.1540-8159.1978.tb03461.x.
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-hout 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 less than .001), PR interval decreased (149 +/- 3.3 to 131 +/- 3.7 msec, p less than .001) and QTc interval increased (132 +/- 6.5 to 454 +/- 9.7 msec, p less than .001) compared to values obtained after atropine administration. Mean PVC or PAC frequently 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 effects of ECT and QTc increase may be due to imbalanced 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.
