ADMINISTRATION OF SUFENTANIL AND NITROUS-OXIDE BLUNTS CARDIOVASCULAR EFFECTS OF DESFLURANE BUT DOES NOT PREVENT AN INCREASE IN MIDDLE CEREBRAL-ARTERY BLOOD-FLOW VELOCITY

Desflurane has been reported to cause tachycardia and hypertension dur ing induction of anaesthesia. The aim of this study was to determine t he effects of desflurane on cerebral blood flow (CBF) velocity using t ranscranial Doppler ultrasonography in a setting that closely resemble d usual clinical practice. In two groups (n = 9 in each) ASA Grade I o r II patients, anaesthesia was induced with etomidate and vecuronium i ntravenously (i.v.), sufentanil (0.3 mu g kg(-1) i.v.) was added in th e second group. Patients were ventilated by facemask for 2 min before desflurane was administered in steps of 0.5 MAC min(-1) until 1.5 MAC was reached and maintained for 7 min. Haemodynamic variables and CBF v elocity in the middle cerebral artery (MCA) were monitored throughout the study period. In group 1 heart rate increased to 108 +/- 2 b.p.m. (37% increase) whereas MAP increased to 114 +/- 6 mmHg after administr ation of desflurane (33% increase). CBF velocity increased to 86 +/- 7 cm s(-1) (69% increase). In group 2 no significant changes in systemi c haemodynamic responses were measured after desflurane administration ; however, CBF velocity increased to 73 +/- 5 cm s(-1) (59% increase). The results indicate that desflurane increases CBF velocity concurren tly with induction of tachycardia and hypertension. Although sufentani l and N2O attenuate the systemic haemodynamic alterations caused by de sflurane, the CBF velocity increases. These data suggest that the abru pt addition of desflurane may have adverse consequences in patients at risk for intracranial hypertension.