British Journal of Anaesthesia, Vol 81, Issue 2 155-160, Copyright © 1998 by The Board of Management and Trustees of the British Journal of Anaesthesia
F. Mielck, H. Stephan, W. Buhre, A. Weyland and H. Sonntag
We investigated the cerebral haemodynamic effects of 1 MAC desflurane
anaesthesia in nine male patients scheduled for elective coronary bypass
grafting. For the measurement of cerebral blood flow (CBF) a modified
Kety-Schmidt saturation technique with argon as inert tracer gas was used.
Measurements of CBF were made before induction of anaesthesia and 30 min
after induction under normocapnic, hypocapnic and hypercapnic conditions in
sequence. Changes in mean arterial pressure after induction of anaesthesia
and during the course of the study were minimized using norepinephrine
infusion. In comparison with the awake state under normocapnic conditions,
desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51%
and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly,
CBF was significantly reduced by 22%; jugular venous oxygen saturation
(SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22%
decrease and a 178% increase in CBF, respectively. These findings may be
interpreted as the result of two opposing mechanisms: cerebral
vasoconstriction induced by a reduction of cerebral metabolism and a direct
vasodilator effect of desflurane. CBF alterations under variation of PaCO2
indicate that cerebrovascular carbon dioxide reactivity is not impaired by
application of 1 MAC desflurane.
CLINICAL INVESTIGATIONS
Effects of 1 MAC desflurane on cerebral metabolism, blood flow and carbon dioxide reactivity in humans
Department of Anaesthesiology, Emergency, and Intensive Care Medicine, Georg-August-University Gottingen, Germany
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