Administration of sufentanil and nitrous oxide blunts cardiovascular effects of desflurane but does not prevent an increase in middle cerebral artery blood flow velocity

Abstract

Desflurane has been reported to cause tachycardia and hypertension during induction of anaesthesia. The aim of this study was to determine the effects of desflurane on cerebral blood flow (CBF) velocity using transcranial Doppler ultrasonography in a setting that closely resembled usual clinical practice. In two groups (n = 9 in each) ASA Grade I or II patients, anaesthesia was induced with etomidate and vecuronium intravenously (i.v.), sufentanil (0.3 μg kg⁻¹ i.v.) was added in the 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 velocity 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 administration of desflurane (33% increase). CBF velocity increased to 86 ± 7 cm s⁻¹ (69% increase). In group 2 no significant changes in systemic 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 concurrently with induction of tachycardia and hypertension. Although sufentanil and N₂O attenuate the systemic haemodynamic alterations caused by desflurane, the CBF velocity increases. These data suggest that the abrupt addition of desflurane may have adverse consequences in patients at risk for intracranial hypertension.