M Kikura1, K Ikeda. 1. Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, Japan.
Abstract
BACKGROUND: Few studies have been reported on the direct depressive effects of sevoflurane on myocardial contractility in humans. Direct assessment of contractile state is possible by examining the slope of left ventricular end-systolic wall stress (LVESWS) versus velocity of circumferential fiber shortening with heart rate corrected (Vcfc) relationship with echocardiography. Using this contractile index, the effects of sevoflurane/nitrous oxide were compared with that of enflurane/nitrous oxide on myocardia contractility in humans. METHODS: Twenty-eight subjects were studied during either sevoflurane/nitrous oxide or enflurane/nitrous oxide anesthesia. Systolic, diastolic, and mean arterial blood pressure, heart rate, and transesophageal echocardiographic data were determined at 0.9 MAC and 1.35 MAC of sevoflurane or enflurane, both with 60% N2O, and at 1.6 MAC of sevoflurane with 60% N2O. Furthermore, another 28 awake subjects were studied with transthoracic echocardiography to examine the contractile state at awake state, and echocardiograms, heart rate, and arterial blood pressure were recorded. RESULTS: Heart rate did not changed significantly in either group. Enflurane/nitrous oxide produced significantly greater decrease in arterial blood pressure than did sevoflurane/nitrous oxide. The Vcfc at each anesthetic dose in both anesthetic groups was significantly less than that in the awake subjects group. Sevoflurane/nitrous oxide produced no significant change in Vcfc at 1.5 MAC, whereas enflurane/nitrous oxide caused significant dose-related decrease in Vcfc. Vcfc produced by sevoflurane/nitrous oxide was significantly greater than that produced by enflurane/nitrous oxide. There was no significant difference in LVESWS (index of afterload) between the groups. With respect to the LVESWS-Vcfc relationship, myocardial contractility was significantly depressed in both the sevoflurane and the enflurane groups compared to the awake subjects group. However, myocardial contractility produced by enflurane/nitrous oxide was significantly less than that by sevoflurane/nitrous oxide at equiMAC concentration. CONCLUSIONS: The results of the present study suggest that sevoflurane has fewer depressant effects on cardiac function than does enflurane.
BACKGROUND: Few studies have been reported on the direct depressive effects of sevoflurane on myocardial contractility in humans. Direct assessment of contractile state is possible by examining the slope of left ventricular end-systolic wall stress (LVESWS) versus velocity of circumferential fiber shortening with heart rate corrected (Vcfc) relationship with echocardiography. Using this contractile index, the effects of sevoflurane/nitrous oxide were compared with that of enflurane/nitrous oxide on myocardia contractility in humans. METHODS: Twenty-eight subjects were studied during either sevoflurane/nitrous oxide or enflurane/nitrous oxide anesthesia. Systolic, diastolic, and mean arterial blood pressure, heart rate, and transesophageal echocardiographic data were determined at 0.9 MAC and 1.35 MAC of sevoflurane or enflurane, both with 60% N2O, and at 1.6 MAC of sevoflurane with 60% N2O. Furthermore, another 28 awake subjects were studied with transthoracic echocardiography to examine the contractile state at awake state, and echocardiograms, heart rate, and arterial blood pressure were recorded. RESULTS: Heart rate did not changed significantly in either group. Enflurane/nitrous oxide produced significantly greater decrease in arterial blood pressure than did sevoflurane/nitrous oxide. The Vcfc at each anesthetic dose in both anesthetic groups was significantly less than that in the awake subjects group. Sevoflurane/nitrous oxide produced no significant change in Vcfc at 1.5 MAC, whereas enflurane/nitrous oxide caused significant dose-related decrease in Vcfc. Vcfc produced by sevoflurane/nitrous oxide was significantly greater than that produced by enflurane/nitrous oxide. There was no significant difference in LVESWS (index of afterload) between the groups. With respect to the LVESWS-Vcfc relationship, myocardial contractility was significantly depressed in both the sevoflurane and the enflurane groups compared to the awake subjects group. However, myocardial contractility produced by enflurane/nitrous oxide was significantly less than that by sevoflurane/nitrous oxide at equiMAC concentration. CONCLUSIONS: The results of the present study suggest that sevoflurane has fewer depressant effects on cardiac function than does enflurane.