Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy.

STUDY OBJECTIVE: To examine the acute hemodynamic effects of intravenous (i.v.) nicardipine and its ability to attenuate the hyperdynamic response to electroconvulsive therapy (ECT), when used alone or in combination with labetalol. DESIGN: Prospective, randomized, double-blind, positive-control, clinical investigation. SETTING: University hospital. PATIENTS: 36 patients undergoing ECT. INTERVENTIONS: In a series of three studies, the hemodynamic effects of nicardipine were assessed prior to, during, and after ECT. After administration of glycopyrrolate 0.1 mg i.v., placebo (saline) or nicardipine was administered by rapid infusion (1, 2.5, 5, 10, and 15 mg) or bolus injection (1.25, 2.5, and 5 mg), either alone or in combination with labetalol 10 mg i.v. Unconsciousness was induced with methohexital 1 mg/kg i.v.; succinylcholine 1.2 to 1.5 mg/kg i.v. was administered for muscle relaxation. A bilateral electrical stimulus was delivered and the durations of motor and electroencephalographic (EEG) seizures were noted. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure (MAP) and heart rate (HR) values were recorded at 1- to 5-minute intervals throughout the study period. When administered as a rapid infusion, nicardipine 5 mg i.v. produced a significant decrease in MAP; however, nicardipine dosages of 10 to 15 mg i.v. did not produce a significantly greater decrease in MAP than 5 mg. Bolus administration of nicardipine 1.25 to 5 mg produced a rapid onset of its hemodynamic effects without exacerbating the cardiovascular depressant effects of methohexital. However, the decrease in MAP was accompanied by an increase in HR after administration of the 5 mg i.v. bolus dose. The acute hyperdynamic response to ECT was most effectively controlled by nicardipine 2.5 to 5 mg i.v. bolus, in combination with labetalol 10 mg i.v. Seizure duration was not significantly altered by the use of nicardipine as part of the anesthetic regimen for ECT. CONCLUSION: Nicardipine 2.5 mg i.v. bolus in combination with labetalol 10 mg i.v. was the most effective pretreatment regimen for preventing the acute hyperdynamic response to ECT. However, this combination produced a 20% decrease in MAP immediately prior to ECT and a lower MAP at the time of discharge.

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

UNLABELLED: 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. IMPLICATIONS: 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.

Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity.

STUDY OBJECTIVE: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (i.v.) lidocaine. DESIGN: Randomized, double-blind, placebo-controlled, cross-over study. SETTING: University-affiliated hospital. PATIENTS: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression. INTERVENTIONS: Patients received lidocaine 50 mg, 100 mg, 200 mg i.v., or saline prior to induction of anesthesia via a standardized anesthetic technique. MEASUREMENTS AND MAIN RESULTS: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means +/- SD) were 37 +/- 13 sec and 64 +/- 21 sec, 25 +/- 11 sec and 52 +/- 43 sec, 17 +/- 12 sec and 32 +/- 17 sec, 1 +/- 3 sec and 18 +/- 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups. CONCLUSIONS: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity.