In patients undergoing electroconvulsive therapy (ECT) an intense circulatory reaction takes place, which includes marked changes in arterial pressure (Silfverskiöld and Åmark1; Holmberg et al.2; Richardson et al.3) and cardiac rate and rhythm (Bellet, Kershbaum, and Furst4; Bankhead, Torrens, and Harris5; Green and Woods6). These cardiovascular effects are of considerable practical importance, since circulatory strain is reported to be the leading cause of death in electroconvulsive therapy (Maclay8; L. Alexander7; S. P. Alexander, Gahagan, and Lewis10; Lewis11; Impastato9).
The typical cardiovascular response to ECT is diphasic. Immediately after the stimulus a sharp, but short-lasting, fall in arterial pressure occurs, accompanied by bradycardia or, in some cases, by asystole, of several seconds' duration. This is followed by a phase of acute arterial hypertension, which persists for five minutes or more. Tachycardia is prominent during the hypertensive phase. The general pattern