This Article Full Text Full Text (PDF) Online Supplement All Versions of this Article: 200805-741OCv1 179/4/313    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sankri-Tarbichi, A. G. Articles by Badr, M. S. Search for Related Content PubMed PubMed Citation Articles by Sankri-Tarbichi, A. G. Articles by Badr, M. S.

Expiratory Pharyngeal Narrowing during Central Hypocapnic Hypopnea

¹ Wayne State University Sleep Research Laboratory, John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan

Correspondence and requests for reprints should be addressed to Abdul Ghani Sankri-Tarbichi, M.D., Division of Pulmonary, Critical Care and Sleep Medicine, 3990 John R, 3-Hudson, Detroit, MI 48201. E-mail: atarbich{at}med.wayne.edu

Rationale: Ventilatory motor output is an important determinant of upper airway patency during sleep.

Objectives: We hypothesized that central hypocapnic hypopnea would lead to increased expiratory upper airway resistance and pharyngeal narrowing during non-REM sleep.

Methods: Noninvasive positive pressure ventilation was used to induce hypocapnic hypopnea in 20 healthy subjects. Expiratory pressure was set at the lowest pressure (2 cm H₂O), and inspiratory pressure was increased gradually during each 3-minute noninvasive positive pressure ventilation trial by increments of 2 cm H₂O. Analysis 1 (n = 9) included measured retropalatal cross-sectional area (CSA) using nasopharyngoscope to compare CSA at five points of the respiratory cycle between control (eupneic) and hypopneic breaths. The pharyngeal pressure (P_ph) was measured using a catheter positioned at the palatal rim. Analysis 2 (n = 11) included measured supraglottic pressure and airflow to compare inspiratory and expiratory upper airway resistance (R_UA) at peak flow between eupneic and hypopneic breaths.

Measurements and Main Results: Expiratory CSA during hypopneic breaths was decreased relative to eupnea (CSA at beginning of expiration [BI]: 101.5 ± 6.3 vs. 121.6 ± 8.9%; P < 0.05); P_ph-BI was lower than that generated during eupnea (1.5 ± 0.3 vs. 3.3 ± 0.9 cm H₂O; P < 0.05). Body mass index was an independent predictor of retropalatal narrowing during hypopnea. Hypopnea-R_UA increased during expiration relative to eupnea (14.0 ± 5.7 vs. 10.6 ± 2.5 cm H₂O/L/s; P = 0.01), with no change in inspiratory resistance.

Conclusions: Expiratory pharyngeal narrowing occurs during central hypocapnic hypopnea. Reduced ventilatory drive leads to increased expiratory, but not inspiratory, upper airway resistance. Central hypopneas are obstructive events because they cause pharyngeal narrowing.

Key Words: ventilatory motor output • expiratory • upper airway resistance

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Pharyngeal narrowing/obstruction during sleep is often described as an inspiratory phenomenon resulting from obstructive hypopnea/apnea. It is unknown, however, whether central hypopnea can lead to airway narrowing. What This Study Adds to the Field Central hypopnea results in pharyngeal narrowing during the expiratory phase, indicating a possible role in the pathogenesis of upper airway obstruction during sleep.

 

This article has been cited by other articles:

				S. Chowdhuri, I. Shanidze, L. Pierchala, D. Belen, J. H. Mateika, and M. S. Badr Effect of episodic hypoxia on the susceptibility to hypocapnic central apnea during NREM sleep J Appl Physiol, February 1, 2010; 108(2): 369 - 377. [Abstract] [Full Text] [PDF]