Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy?

Clonidine decreases the stress-induced sympathoadrenal responses to painful stimuli and improves hemodynamic stability during general anesthesia. Because acute hypertensive responses are often observed immediately after electroconvulsive therapy (ECT), we designed a prospective, randomized, placebo-controlled, cross-over study to assess the effects of four different oral doses of clonidine (0.05-0.3 mg per os) on the acute hemodynamic response to ECT. Anesthesia was induced with methohexital 1 mg/kg followed by succinylcholine, 1.3 mg/kg i.v. A total of 110 treatments were evaluated in 22 patients. Noninvasive mean arterial pressure (MAP) and heart rate (HR) values, duration of motor and electroencephalographic (EEG) seizure activity, and recovery times were recorded. Clonidine produced a dose-related decrease in MAP before and after ECT. Although clonidine 0.2-0.3 mg per os decreased the peak MAP value after ECT, the changes in MAP from the prestimulation values were similar in all treatment groups. Clonidine produced no significant changes in HR, duration of motor and EEG seizure activity, or recovery times after anesthesia. These data suggest that clonidine decreases the peak MAP value after ECT by decreasing MAP immediately before the ECT stimulus.

Oral clonidine (0.2-0.3 mg) decreases the acute hypertensive response after electroconvulsive therapy; however, this antihypertensive effect was achieved by decreasing the blood pressure before the electrical stimulus.