• L Schlünzen, M S Vafaee, N Juul, and G E Cold.
• Department of Neuroanaesthesiology, Aarhus University Hospital, Noerrebrogade 44, 8000 Aarhus C, Denmark. lise.schlunzen@dadlnet.dk
• Acta Anaesthesiol Scand. 2010 May 1;54(5):610-5.

BackgroundArterial carbon dioxide tension (PaCO(2)) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET).MethodsEight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H(2)(15)O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences.ResultsCardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO(2) was decreased from 5.5 + or - 0.7 to 3.8 + or - 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed.ConclusionsThis study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.

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