Cardiovascular effects of desflurane in experimental animals and volunteers.

Desflurane (difluoromethyl-1-fluoro-2,2,2-trifluoroethyl ether [I-653]) was introduced into clinical practice in 1992. The present review summarises the current state of knowledge of the cardiovascular effects of desflurane, with emphasis on investigations published in the past 2 years, and compares desflurane's effects with those of isoflurane, and where available, sevoflurane. Desflurane produces two distinct cardiovascular actions. First, desflurane decreases left ventricular systolic and diastolic function to an extent similar to that of isoflurane. It decreases systemic vascular resistance and mean arterial blood pressure in a dose-dependent fashion. Heart rate is unchanged at lower steady-state concentrations, but increases with higher concentrations. Addition of nitrous oxide maintains heart rate unchanged, increases systemic vascular resistance and mean arterial blood pressure, but decreases cardiac output. Secondly, when the end-tidal concentration of desflurane is very rapidly increased to concentrations exceeding 1 MAC, in the absence of premedication, desflurane increases sympathetic activity, heart rate and mean arterial blood pressure. Prior administration of fentanyl, esmolol or clonidine blunts this response. The response and the ability of fentanyl to blunt it probably account for the disparate results in published studies on the use of desflurane in patients undergoing coronary artery bypass graft surgery.