Neurologic Significance of Posthyperventilation Apnea
Fred Plum, M.D., Harold W. Brown, M.D., and Else Snoep, SeattleSINCE HERING (1867)1 noted that anesthetized animals showed brief respiratory arrest following hyperventilation, many physicians and physiologists have viewed posthyperventilation apnea as a normal hypocarbic response. Haldane and Priestly2 extensively investigated the phenomenon, and Henderson3 devised experiments to take advantage of the presumed abeyance of respiratory drives which accompanied hypocarbia in well-oxygenated subjects. These early observations were made mostly on laboratory personnel or on medical students familiar with the theory that respiration ceased when blood carbon dioxide was lowered. Boothby's4 inability to elicit acapnic apnea was generally regarded as a unique failure. However, Mills5 supported Boothby's findings, and was able to elicit posthyperventilation apnea in less than one-third of normal subjects. Indeed, among Mills' subjects, hyperpnea followed voluntary hyperventilation more often than did apnea. Recently, Fink6 reaffirmed Mills'