Hostname: page-component-78c5997874-ndw9j Total loading time: 0 Render date: 2024-11-19T01:50:50.712Z Has data issue: false hasContentIssue false

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

Published online by Cambridge University Press:  16 August 2006

P. H. Tonner
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
J. Scholz
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
T. Krause
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
A. Paris
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
G. von Knobelsdorff
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
J. Schulte am Esch
Affiliation:
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany
Get access

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.

Type
Original Article
Copyright
1997 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)