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ANESTHETIC PHARMACOLOGY

Esmolol Promotes Electroencephalographic Burst Suppression During Propofol/Alfentanil Anesthesia

Department of Anesthesiology, Emory University School of Medicine, Atlanta, Georgia

Address correspondence and reprint requests to Jay W. Johansen, MD, PhD, Department of Anesthesiology, Grady Health System of Emory University, 80 Butler Street, S.E., Atlanta, GA 30335-3801. Address e-mail to jay_johansen{at}emory.org

This study examined the effects of an esmolol infusion on the electroencephalogram during propofol/alfentanil IV anesthesia. After informed consent, 20 patients were randomly assigned into four groups on the basis of two target alfentanil concentrations (alfentanil 50 or 150 ng/mL) and of a saline or esmolol infusion. Bispectral index (BIS), burst suppression ratio (SR), and physiologic variables were continuously monitored. A 30-min blinded infusion of saline or esmolol was started after establishing a stable baseline and followed by a washout period. The electroencephalogram was significantly suppressed by esmolol (BIS, 37 ± 6 to 22 ± 6, 40% decrease [mean ± SD]; SR, 5 ± 7 to 67 ± 23, 13.4-fold increase) compared with baseline in the small-dose alfentanil groups. Discontinuation of esmolol reversed the response. BIS and SR were unaffected by placebo infusion. Twelve-minute to 16-min hysteresis between esmolol administration and the onset of half-maximal cortical suppression was observed. Physiologic variables and serum propofol and alfentanil concentrations were not significantly altered by esmolol. Although the mechanism remains unclear, significant cortical depression and the onset of burst suppression during a stable, computer-controlled propofol/alfentanil anesthetic was associated with esmolol infusion.

IMPLICATIONS: This study demonstrated the suppression of cerebral cortical electrical activity after blinded esmolol infusion during propofol/alfentanil anesthesia. A significant lag was noted between infusion and half-maximal effect (12–16 min). Whether esmolol, a metabolite, or a secondary process was responsible for this cortical suppression remains unknown and requires further study.

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