Background and objective We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia.

Methods Forty patients (age: isoflurane 24–62 years; sevoflurane 24–61 years; ASA l–lll) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50–60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspira-tory and end-expiratory concentrations of 0.75, 1.00, nd 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvl). CSvl of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity.

Results Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvl decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 ± 25%/81 ± 23%, 1.0 MAC: 79 ± 19%/74 ± 16%, 1.25 MAC: 71 ± 16%/79 ± 21%; [mean ±SD] P% 0.0001). Conclusions The reduction of the CSvl vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.

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.