Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 96: 2220-2225, 2004. First published February 27, 2004; doi:10.1152/japplphysiol.01120.2003
8750-7587/04 $5.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
96/6/2220    most recent
01120.2003v2
01120.2003v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Omran, A. M.
Right arrow Articles by Badr, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Omran, A. M.
Right arrow Articles by Badr, M. S.

Posthypoxic ventilatory decline during NREM sleep: influence of sleep apnea

Amal M. Omran, Salah E. Aboubakr, Loutfi S. Aboussouan, Lisa Pierchala, and M. Safwan Badr

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


Address for reprint requests and other correspondence: M. S. Badr, Harper Hospital, 3990 John R. 3-Hudson, R-3923, Detroit, MI 48201 (E-mail: sbadr{at}med.wayne.edu).






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.