Submitted on October 15, 2003
Accepted on February 19, 2004
Post-hypoxic Ventilatory Decline During NREM Sleep: influence of sleep apnea
Amal M Omran1, Salah E Aboubakr1, Loutfi S Aboussouan1, Lisa Pierchala1, and M. Safwan Badr1*
1 Pulmonary Critical Care Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA; Pulmonary Critical Care Medicine, John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan, USA
* To whom correspondence should be addressed. E-mail: sbadr{at}med.wayne.edu.
We wished to determine the severity of post-hypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during NREM sleep. Methods: We studied 11 males with sleep apnea/hypopnea syndrome (AHI=27.0 ± 12.5, age=41.0 ±7.7 yr) and 11 normal males (AHI= 1.1 ± 1.0 events per hour of sleep, age+ 34.1 ± 9.6 yr) during stable NREM sleep. We measured EEG, EOG, SaO2 and PETCO2. To maintain upper airway patency in patients with sleep apnea, nasal CPAP was applied at a level sufficient to eliminate apneas and hypopneas. We induced multiple episodes of brief hypoxia for 3 minutes by using a hypoxic mixture (8%); this resulted in oxyhemoglobin desaturation (SaO2 at 80-87%). Hypoxia was abruptly terminated with 1 breath of 100% FIO2 followed by room air. We compared the pre-hypoxic control (C) to post-hypoxic recovery breaths. Results: Nadir VI in normal subjects was 6.3±0.5 L/min, (83.8±5.7% of room air control), versus 6.70±.9 L/min, 69.1±8.5 % of room air control in OSA patients; nadir VI (% of control) was lower in patients with OSA relative to normal subjects (P<0.05). Nadir VT was 0.55±0.05L, (80.0±6.6% of room air control) in OSA patients versus 0.42±0.03L, 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 sec, 120±11.2 % of C) and OSA patients (5.6±1.5 sec, 292±127.6 % of C) (P<0.006). Conclusions: 1. Post-hypoxic ventilatory decline occurred following termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea. 2. Post-hypoxic ventilatory decline manifested as decreased tidal volume and prolongation of expiratory time. 3. Post-hypoxic ventilatory prolongation of expiratory time was more pronounced in patients with sleep apnea relative to normal subjects.
