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J Appl Physiol (July 6, 2006). doi:10.1152/japplphysiol.00173.2006
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Submitted on February 9, 2006
Accepted on June 17, 2006

Dynamic Modulation of Upper Airway Function during Sleep - A Novel Single Breath Method

Jason P Kirkness1*, Alan R. Schwartz2, Susheel P Patil3, Luis E Pichard3, Jason J Marx4, Phillip Lees Smith3, and Hartmut Schneider5

1 Pulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States; School of Anatomy and Human Biology, University of Western Australia, 35 Stirling Highway, CRAWLEY, Western Australia, 6009, Australia
2 Pulmonary & Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States
3 Pulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States
4 Pulmonary and Critcal Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States
5 JPulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States

* To whom correspondence should be addressed. E-mail: jason_kirkness{at}jhmi.edu.

To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the PCRIT within a single breath in tracheostomised 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. Methods: Five apneic subjects (with tracheosomy) were recruit (2 male, 3 female; 18-50 years; 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 (following PCRIT) of the UA during NREM sleep. During each breath, UA function was described by a pressure-flow relationship which defined the collapsibility (PCRIT) and upstream resistance (RUS). UA characteristics were examined in the presence and absence of complete UA occlusion. Results: 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/min) than during inflation (7.5±1.9 cmH2O/L/min) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by ~4 cmH2O. Conclusion: These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle, and subjects that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep




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