IS THERE STILL A PLACE FOR ROUTINE DEEP H YPOCAPNIA FOR INTRACRANIAL SURGERY

Deliberate hypocapnia during the anaesthetic management of the patient undergoing craniotomy has become an accepted standard of care. Howeve r there has been a resurgence of interest, in how hypocapnia should be applied in intra- and extra-operative settings. There are three possi ble therapeutic effects of hypocapnia, namely, (a) reduction of brain bulk through a reduction in cerebral blood volume, with a decrease cer ebral blood flow; (b) developing an <<inverse steal>> by redistributio n of blood from normal to ischaemic regions and (c) acting to offset c erebral acidosis by increasing pH in the extracellular space. In anaes thetic intraoperative practice, hypocapnia is used as a specific treat ment of, or prophylaxis against, intracranial hypertension during indu ction of anaesthesia and the period before dural exposure. More common ly, hypocapnia is used for intraoperative brain relaxation (intracrani al 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 hea d-injured patients suggest that routine long-term hyperventilation, wi thout an objective index of cerebral flow/metabolism coupling, may pla ce the brain at risk for adverse outcome. The few data available for i ntraoperative management suggest that PaCO2 figures of 30-35 mmHg resu lt in acceptable operating conditions. Unless otherwise specifically i ndicated 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 ne eds reevaluation.