Hyperventilation in Awake and Anesthetized Man

Abstract

THE EFFECTS of hyperventilation on cerebral blood flow are well known, but the changes in cerebral metabolism associated with hypocapnia are in some dispute. Kety and Schmidt,^1,2 using the nitrous oxide technique, originally showed that there was a diminution of cerebral blood flow but no change in cerebral oxygen consumption with passive hyperventilation. The measurement of cerebral cortical oxygen tension with the oxygen electrode, however, has given different results. Sugioka and Davis³ reported "a marked drop in cerebral oxygen tension as the result of hyperventilation" and postulated that cerebral hypoxia may be caused by hyperventilation and that the use of hyperventilation in anesthesia and resuscitation may be dangerous. In another study based on polarographic oxygen electrode, Meyer and Gotoh⁴ showed that hyperventilation caused vasoconstriction up to 50% and a marked reduction in cortical pO₂. Meyer concluded that hyperventilation causes progressive vasoconstriction of small cerebral arterioles and