Posthypoxic jugular venous hyperoxia

Abstract

SUMMARYThe phenomenon of jugular venous hyperoxia following episodes of hypoxic injury has been evaluated. In monkeys respiring 3.5% oxygen in nitrogen for intervals as long as thirty minutes, it was found that the duration of postinsult cerebral venous hyperoxygenation related to the duration of hypoxic exposure as long as the blood pressure was maintained above a mean of 80 mm. Hg. When episodes of hypotension below 80 mm. Hg occurred, the duration of the venous hyperoxic phase was extended in a nonpredictable manner. Recovery of brain electrical activity followed a similar pattern and occurred in approximately one-half of the time required for the normalization of the venous hyperoxia. The hypoxic episodes produced a CSF acidosis which also was more severe in animals whose episodes of hypoxia were complicated by hypotension.

Posthypoxic cerebral venous hyperoxia is indicative of a derangement in the regulatory relationship between cerebral metabolism and cerebral blood flow which normally results in a constant cerebral arteriovenous difference for oxygen. Hypoxia alters this relationship, producing a decrease in the oxygen arteriovenous differential probably due to a diminished cerebral utilization of oxygen or an increased cerebral blood flow or both. A quantitative evaluation of the duration and degree of the cerebral venous hyperoxia phase, particularly with 100% oxygen inhalation, provides a measure of the degree of abnormality in the relation between brain metabolism and cerebral perfusion.