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Hemodynamic Effects of Esmolol in Chronically $bT-Blocked Patients Undergoing Aortocoronary Bypass Surgery

Division of Cardiothoracic Anesthesia, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina.

Abstract

The hemodynamic effects of esmolol were studied in 40 patients scheduled for elective coronary artery surgery to determine whether the administration of esmolol in chronically ß-blocked patients would result in additional attenuation of sympathetically mediated hemodynamic stress responses to noxious stimuli. Patients were randomly assigned to receive IV infusions of esmolol or 5% dextrose in water (D₅W). All received their regular dose of ß-adrenergic blocker within 6 hr of surgery and were anesthetized with diazepam, pancuronium, and enflurane. Increases (>25% above baseline) in systolic blood pressure were treated with sodium nitroprusside (SNP). Esmolol was started before induction of anesthesia and continued until 5 min after maximal sternal spread. There were no statistically significant differences between the esmolol and control groups in any hemodynamic parameter during induction, intubation, skin incision, and sternotomy. Only at 5 min after maximal sternal spread was there a statistically significant lower systolic blood pressure in the esmolol-treated group. However the incidence and magnitude of SNP use in the control group was significantly (P < 0.05) greater. Thus, the lower blood pressure, in the absence of changes in systemic vascular resistance, cardiac index, heart rate, and pulmonary capillary wedge pressure points toward a decrease in myocardial contractility, suggesting that the addition of esmolol to chronically used ß-blockers resulted in an additional negative inotropic effect. We conclude that in patients with coronary artery disease in whom chronic ß-blocker therapy is continued until the time of surgery, esmolol does not further attenuate the heart rate response but does attenuate the increase in blood pressure. The presumed reason for this finding is that esmolol in the dose employed does not occupy sufficient additional ß-receptors to produce added ß-adrenergic blockade and therefore does not further attenuate heart rate response to sympathetic nervous system stimulation. Blood pressure is probably decreased because of esmolol's negative inotropic effect.

Key Words: SYMPATHETIC NERVOUS SYSTEM—ß-adrenergic antagonists, esmolol. • HEART—myocardial function, ß-adrenergic blockade.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999