IT HAS BEEN demonstrated that the appearance of EEG slowing, light-headedness and confusion during hyperventilation is closely related to the rapid reduction of alveolar Pco₂or arterial Pco₂(Paco₂)⁶,⁸,¹⁵,²⁹,³⁰,³⁸and not to rise of arterial blood pH (aph).⁴,²⁸However, the mechanism of action of the fall of Paco₂in producing EEG slowing in man still remains in dispute. Theoretically, EEG slowing during active hyperventilation could be due to (1) cerebral ischemic anoxia resulting from hypocapnic cerebral vasoconstriction, (2) lack of some specific property of CO₂per se on nerve cells and membranes, or (3) some effect of cerebral alkalosis. In 1942 Davis and Wallace⁴offered the hypothesis that EEG slowing during hyperventilation was due to vasoconstriction with resultant ischemic anoxia. On the other hand, Gibbs et al⁸denied Davis' hypothesis showing that subjects who reacted to overventilation by EEG slowing
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Gotoh et al. (1965) studied this question.
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