Muscle relaxants change myocardial metabolism in patients with ischemic heart disease during high‐dose fentanyl anesthesia

Abstract

Although not unanimously accepted, high-dose fentanyl anesthesia has been associated with hemodynamic stability and little derangement of myocardial oxygen balance. This apparent inconsistency inspired us to investigate the effects on cardiac function and myocardial metabolism of stepwise increasing doses of fentanyl, accumulating to 15, 30, and 50 micrograms.kg-1, with the least possible interference from other drugs. Subjects were unpremedicated patients with ischemic cardiac disease scheduled for coronary artery bypass grafting or major vascular surgery. In an initial study employing succinylcholine for muscle relaxation, we found that heart rate (HR), coronary sinus blood flow (CSF) and coronary vascular resistance (CVR) remained unchanged, while systemic arterial pressure (SBP), rate-pressure product (RPP), coronary perfusion pressure (CPP) and left ventricular work (LVW) decreased. Myocardial uptake of oxygen (MVO2) and free fatty acids (FFA) both decreased in a dose-dependent manner. Arterial lactate concentration and myocardial lactate uptake both increased. These findings opposed the postinduction myocardial ischemia noted by some other investigators. In most of these studies pancuronium bromide had been used for muscle relaxation. Since the latter agent has been claimed to increase cardiac work, a second group of correspondingly diseased patients was studied in which succinylcholine was replaced by pancuronium bromide. In this group HR, RPP, CSF and MVO2 all increased at the lowest dose of fentanyl and HR additionally also at 30 micrograms.kg-1. The cardiac index was higher in the pancuronium group at the lowest and middle dose steps of fentanyl. Lactate uptake decreased with higher doses of fentanyl and relative myocardial lactate extraction declined.(ABSTRACT TRUNCATED AT 250 WORDS)