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The magnitude of the reduction in CBF caused by hypocapnia is more intense when resting CBF is increased (as might occur during anesthesia with volatile agents).
By contrast, with the induction of hypocapnia, CBF is autoregulated over a wider MAP range (Fig 11.6B).9
Acute restoration of a normal Paco2 value will result in a significant CSF acido- sis (after hypocapnia) or alkalosis (after hypercapnia).
Both CO2 responsiveness and autoregulation are pre- served in humans during the administration of propo- fol,87,88 even when administered in doses that produce burst suppression of the EEG.89 The magnitude of the reduc- tion in CBF during hypocapnia is decreased during propofol administration.
Interestingly, CBF in white matter increased by 22%.150 This reduction in CBF is accompanied by a parallel reduction of the cere- bral metabolic rate of glucose (CMRg) by 26%.151 Cerebral autoregulation and CO2 reactivity are preserved during xenon anesthesia in animals.152 Under background pento- barbital anesthesia in an experimental model of increased ICP, the administration of xenon did not increase ICP, and the response to both hypocapnia and hypercapnia was pre- served.153 Diffusion of xenon into air-containing spaces such as the bowel does occur, although the magnitude of air expansion is considerably less than that with N2O.154 Nonetheless, caution will have to be exercised with the use of xenon in patients with intracranial air.
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