Central Neurogenic Hyperventilation in Man

Centrally caused respiratory facilitation was first suggested to us by the unusually heavy breathing of several patients recovering from the effects of transient exposures to acute anoxia. There was no carboxyhemoglobin, persisting anoxemia, cardiac disease, or pulmonary abnormality to stimulate a compensatory hyperpnea; yet several overbreathed themselves into clinical tetany while still in deep coma. Subsequently, the same respiratory pattern was observed in patients with hypoglycemia, severe head injuries, and acute cerebral vascular lesions. Several of these patients were in younger age groups and were completely free of cardiopulmonary disease. Autopsies showed severe brain stem changes, but either the lesions were too diffuse to afford specific conclusions on the neuroanatomy involved or the respiratory changes had not been quantitated adequately. Descriptions of forced, heavy, or stertorous breathing in the case reports of patients with fulminating meningitis,1,2basilar artery thrombosis,3,4pontile hemorrhage,5and encephalitis6supported the impression