Simultaneous evaluation of left ventricular end-systolic pressure-volume ratio and time constant of isovolumic pressure decline in dogs exposed to equivalent MAC halothane and isoflurane

Abstract

The effects of 1.5, 2.0, and 2.5 MAC halothane (N = 8) and isoflurane (N = 6) upon systolicc performance and isovolumic relaxation were evaluated in open chest dogs. Left ventricular internal volume was determined using piezoelectric crystals. Left ventricular end-systolic pressure-volume points were determined for a series of normal sinus beats during transient venae caval occlusions. The slope of the line formed by those points is a load-independent inotropic index (E(ES)). Left ventricular pressure points during isovolumic relaxation were plotted for computing the time constant of isovolumic pressure decline (T). Both drugs dose-dependently decreased mean arterial blood pressure with no change in heart rate, end-diastolic pressure, or end-diastolic volume. Increasing halothane concentration decreased the values of E(ES), the maximum rate of rise of left ventricular pressure (dP/dt(max)), and systolic ejection fraction (SEF). Total systemic resistance was unchanged by halothane. Increasing isoflurane concentration decreased E(ES) and dP/dt(max). The E(ES) was significantly larger (P < 0.05) with 2.5 MAC isoflurane than 2.5 MAC halothane. The SEF was unchanged by increasing isoflurane. Total systemic vascular resistance was decreased by increasing isoflurane. Isovolumic relaxation was prolonged and became more load-dependent with increasing halothane concentration. Isoflurane did not alter T, but the load-dependency of T was increased by 2.5 MAC isoflurane. There were no differences in T or its load-dependency between drug groups. These results indicate that both anesthetics evoke load-independent negative inotropic effects. Systolic ejection fraction is maintained during isoflurane anesthesia by decreased systemic vascular resistance and less pronounced negative inotropic effects than equivalent MAC halothane. Increasing halothane concentration prolongs left ventricular relaxation rate and alters its load-dependency. The effects of isoflurane upon LV relaxation rate and its load-dependency are not as pronounced as those of halothane.