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Anesthesia & Clinical Research

Anesthesia & Clinical Research
Open Access

ISSN: 2155-6148

+44 1223 790975

Abstract

Remifentanil can Prevent the Increase in Qt Dispersion During Modified Electroconvulsive Therapy: A Randomized Controlled Clinical Trial

Megumi Kageyama, Shinsuke Hamaguchi and Shigeki Yamaguchi

Objective: To clarify the hemodynamic-stabilizing effect of remifentanil in the context of modified electroconvulsive therapy (mECT), we measured electrocardiographic alterations in the corrected QT interval (QTc) and corrected QT dispersion (QTcD), considered predictive of ventricular arrhythmia, during mECT.

Methods: Sixty patients scheduled for mECT were divided randomly into 3 groups. Patients in the low-dose remifentanil administration group (group L, N=20) were administered 0.5 μg/kg of remifentanil before mECT. Patients in the high-dose group (group H, N=20) were administered 1.0 μ g/kg of remifentanil, and those in the control (group C, N=20) were administered a similar volume of normal saline solution. Modified ECT was performed in the same manner in all groups with propofol and suxamethonium. Changes in QTc and QTcD values were analyzed using a repeated measures analysis of variance, and between-group comparisons were conducted using the Bonferroni method.

Results: During mECT, an increase in the mean arterial pressure, decrease in the R wave-to-R wave interval, elongation of QTc, and increase in QTcD were observed in group C, whereas these alterations were attenuated in group L and were not observed in group H. The differences observed in group C relative to the other groups were statistically significant (P<0.05).

Conclusion: Compared with the control treatment and a 0.5 μ g/kg dose, a 1.0 μ g/kg dose of remifentanil had a preventive effect on ventricular arrhythmia after mECT, as well as on hemodynamic changes, according to the observed alterations in QTc and QTcD. Therefore, our results indicate that a 1.0 μ g/kg dose of remifentanil could suppress hemodynamic changes, prevent myocardial ischemia or cerebral hemorrhage, and minimize the development of fatal arrhythmias such as ventricular tachycardia and/or ventricular fibrillation.

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