SLEEP-DEPRIVATION AND THE CONTROL OF VENTILATION

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Abstract
Sleep deprivation is common in acutely ill patients because of their underlying disease and can be compounded by aggressive medical care. While sleep deprivation has been shown to produce a number of psychological and physiologic events, the effects on respiration have been minimally evaluated. Resting ventilation and ventilatory responses to hypoxia and hypercapnia were studied before and after 24 h of sleeplessness in 13 healthy men. Hypoxic ventilatory responses (HVR) were measured during progressive isocapnic hypoxia, and hypercapnic ventilatory responses (HCVR) were measured using a rebreathing technique. Measures of resting ventilation, i.e., minute ventilation, tidal volume, arterial O2 saturation and end-tidal gas concentrations, did not change with short-term sleep deprivation. HVR and HCVR decreased significantly after a single night without sleep. The mean hypoxic response decreased 29% from a slope of 1.20 .+-. 0.22 (SEM [standard error of the mean]) to 0.85 .+-. 0.15 l/min per % saturation (P < 0.02), and the slope of the HCVR decreased 24% from 2.07 .+-. 0.17 to 1.57 .+-. 0.15 l/min per mm Hg PCO2 [partial pressure] (P < 0.01). Ventilatory chemosensitivity may be substantially attenuated by even short-term sleep deprivation. This absence of sleep could contribute to hypoventilation in acutely ill patients.