[Is there still a place for routine deep hypocapnia in intracranial surgery?]

Deliberate hypocapnia during the anaesthetic management of the patient undergoing craniotomy has become an accepted standard of care. However there has been a resurgence of interest, in how hypocapnia should be applied in intra- and extra-operative settings. There are three possible therapeutic effects of hypocapnia, namely, (a) reduction of brain bulk through a reduction in cerebral blood volume, with a decrease cerebral blood flow; (b) developing an "inverse steal" by redistribution of blood from normal to ischaemic regions and (c) acting to offset cerebral acidosis by increasing pH in the extracellular space. In anaesthetic intraoperative practice, hypocapnia is used as a specific treatment of, or prophylaxis against, intracranial hypertension during induction of anaesthesia and the period before dural exposure. More commonly, hypocapnia is used for intraoperative brain relaxation (intracranial pressure = 0). Severe hypocapnia (< 20 mmHg) may result in cerebral production of lactate; however no studies have shown that a Paco2 in the range of 23-28 mmHg has deleterious effects. Recent studies in head-injured patients suggest that routine long-term hyperventilation, without an objective index of cerebral flow/metabolism coupling, may place the brain at risk for adverse outcome. The few data available for intraoperative management suggest that Paco2 figures of 30-35 mmHg result in acceptable operating conditions. Unless otherwise specifically indicated by surgical conditions or cerebral flow/metabolism coupling (e.g. jugular O2 saturation), routine application of profound (Paco2 < 28-30 mmHg) hyperventilation should probably be avoided and its use needs reevaluation.