Mechanisms used to restore ventilation after partial upper airway collapse during sleep in humans
- Amy S Jordan1,
- Andrew Wellman1,
- Raphael C Heinzer1,
- Yu-Lun Lo1,
- Karen Schory1,
- Louise Dover1,
- Shiva Gautam2,
- Atul Malhotra1,
- David P White1
- 1Sleep Disorders Research Program, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA
- 2General Clinical Research Center, Beth Israel Deaconess Medical Center, Boston, USA
- Correspondence to:
Dr Amy S Jordan
Sleep Disorders Program @ BIDMC, 75 Francis St, Boston, Massachusetts 02115, USA;
- Received 12 August 2006
- Accepted 28 March 2007
- Published Online First 5 April 2007
Background: Most patients with obstructive sleep apnoea (OSA) can restore airflow after an obstructive respiratory event without arousal at least some of the time. The mechanisms that enable this ventilatory recovery are unclear but probably include increased upper airway dilator muscle activity and/or changes in respiratory timing. The aims of this study were to compare the ability to recover ventilation and the mechanisms of compensation following a sudden reduction of continuous positive airway pressure (CPAP) in subjects with and without OSA.
Methods: Ten obese patients with OSA (mean (SD) apnoea-hypopnoea index 62.6 (12.4) events/h) and 15 healthy non-obese non-snorers were instrumented with intramuscular genioglossus electrodes and a mask/pneumotachograph which was connected to a modified CPAP device that could deliver either continuous positive or negative pressure. During stable non-rapid eye movement sleep the CPAP was repeatedly reduced 2–10 cm H2O below the level required to eliminate flow limitation and was held at this level for 5 min or until arousal from sleep occurred.
Results: During reduced CPAP the increases in genioglossus activity (311.5 (49.4)% of baseline in subjects with OSA and 315.4 (76.2)% of baseline in non-snorers, p = 0.9) and duty cycle (123.8 (3.9)% of baseline in subjects with OSA and 118.2 (2.8)% of baseline in non-snorers, p = 0.4) were similar in both groups, yet patients with OSA could restore ventilation without cortical arousal less often than non-snorers (54.1% vs 65.7% of pressure drops, p = 0.04). When ventilatory recovery did not occur, genioglossus muscle and respiratory timing changes still occurred but these did not yield adequate pharyngeal patency/ventilation.
Conclusions: Compensatory mechanisms (increased genioglossus muscle activity and/or duty cycle) often restore ventilation during sleep but may be less effective in obese patients with OSA than in non-snorers.
- CNAP, continuous negative airway pressure
- CPAP, continuous positive airway pressure
- EMGGG, genioglossal electromyogram
- FB, breathing frequency
- NREM, non-rapid eye movement
- OSA, obstructive sleep apnoea
- Petco2, end-tidal partial pressure of CO2, PCRIT, pharyngeal critical closing pressure
- PEPI, epiglottic pressure
- PIF, peak inspiratory flow
- PMASK, mask pressure
- RUA80, upper airway resistance at 80 ml/s
- TI/TTOT, duty cycle
- V̇i, ventilation
Published Online First 5 April 2007
This study was supported by a grant from the American Heart Association and by the NIH grants P50 HL60292, AG024837–01, HL73146–01 and M01 RR01032.
Competing interests: None.