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INNOVATIVE METHODOLOGY

Dynamic modulation of upper airway function during sleep: a novel single-breath method

¹Johns Hopkins Sleep Disorders Center, Baltimore, Maryland; and ²School of Anatomy and Human Biology, University of Western Australia, Perth, Western Australia, Australia

Submitted 9 February 2006 ; accepted in final form 17 June 2006

To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18–50 yr; 20–35 kg/m²; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH₂O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH₂O). Rus was higher for deflation (18.1 ± 2.4 cmH₂O·l^–1·s) than during inflation (7.5 ± 1.9 cmH₂O·l^–1·s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by 4 cmH₂O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.

sleep apnea; critical pressure; upper airway occlusion; pathophysiology

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