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Medical Service, John D. Dingell Veterans Affairs Medical Center, and Division of Pulmonary Critical Care Medicine, Department of Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201
Submitted 15 October 2003 ; accepted in final form 19 February 2004
We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O2 saturation, and end-tidal PCO2. To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 ± 0.5 l/min (83.8 ± 5.7% of room air control) vs. 6.7 ± 0.9 l/min, 69.1 ± 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects (P < 0.05). Nadir tidal volume was 0.55 ± 0.05 liter (80.0 ± 6.6% of room air control) in OSA patients vs. 0.42 ± 0.03 liter, 86.5 ± 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (TE) occurred in the recovery period. There was a significant difference in TE prolongation between normal subjects (2.61 ± 0.3 s, 120 ± 11.2% of C) and OSA patients (5.6 ± 1.5 s, 292 ± 127.6% of C) (P < 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of TE; and 2) posthypoxic ventilatory prolongation of TE was more pronounced in patients with sleep apnea relative to normal subjects.
episodic hypoxia; ventilatory control; obstructive sleep apnea; nonrapid eye movement sleep
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