Cerebral Oxygen Consumption in Profound Arterial Hypoxemia and Hypocapnia

Abstract

For patients with raised intracranial pressure, respiratory insufficiency always means a threatening complication because of the danger of cerebral hypoxia. Whereas a decrease of arterial PO₂ may directly cause insufficient oxygenation of the brain tissue (“hypoxic hypoxia”), a fall in arterial PCO₂ acts through a decrease of cerebral blood flow due to vasoconstriction of the cerebral vessels and thus may lead to “ischemic hypoxia”. As artificial hyperventilation is advocated in the treatment of raised intracranial pressure, it must be questioned where to set the limit beyond which hypocap-nically induced cerebral tissue hypoxia may occur. In clinical practice, the neurosurgeon has mainly to face the resultant of different pathogenetic factors such as intracranial hypertension, disturbances of respiration and of blood pressure etc. To get better insight into the intrinsic effects of markedly lowered aPO₂ and aPCO₂ on the brain, investigations based on an experimental model are required. The present experimental study contributes to the question to which degree of pure normocapnic normotensive arterial hypoxemia and normoxic normotensive hypocapnia a sufficient oxygen supply to the brain tissue is maintained and which regulatory mechanisms are elicited to keep the cerebral metabolic rate of oxygen (CMRO₂) in the physiological range.