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Mechanisms Used To Restore Ventilation After Partial Upper Airway Collapse During Sleep In Humans.
  1. Amy S Jordan (ajordan{at}rics.bwh.harvard.edu)
  1. Brigham and Women's Hospital and Harvard Medical School, United States
    1. Andrew Wellman (awellman{at}rics.bwh.harvard.edu)
    1. Brigham and Women's Hospital and Harvard Medical School, United States
      1. Raphael C Heinzer (raphael.heinzer{at}chuv.ch)
      1. Centre Hospitalier Universitaire Vaudois, Switzerland
        1. Yu-Lun Lo (lyulun{at}partners.org)
        1. Chang Gang Memorial Hospital and Harvard Medical School, Taiwan
          1. Karen Schory (kschory{at}rics.bwh.harvard.edu)
          1. Brigham and Women's Hospital, United States
            1. Louise Dover (ldover{at}gmail.com)
            1. Brigham and Women's Hospital, United States
              1. Shiva Gautam (sgautam{at}bidmc.harvard.edu)
              1. Beth Israel Deaconess Medical Center, United States
                1. Atul Malhotra (amalhotra1{at}partners.org)
                1. Brigham and Women's Hospital and Harvard Medical School, United States
                  1. David P White (dpwhite{at}rics.bwh.harvard.edu)
                  1. Brigham and Women's Hospital and Harvard Medical School, United States

                    Abstract

                    Objectives: Most obstructive sleep apnoea (OSA) patients 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 likely include increased upper airway dilator muscle activity and/or changes in respiratory timing. The aims of this study were to compare between subjects with and without OSA: 1) the ability to recover ventilation and 2) mechanisms of compensation following sudden reduction of continuous positive airway pressure (CPAP).

                    Methods: 10 obese OSA patients (AHI= 62.6 (12.4) events/hr) 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 both continuous positive or negative pressure. During stable NREM sleep, the CPAP was repeatedly reduced 2-10 cmH2O below the level required to eliminate flow limitation and was held at this level for 5 minutes or until arousal from sleep occurred.

                    Results: During reduced CPAP, the increases in genioglossus activity (311.5 (49.4) in OSA and 315.4 (76.2)% baseline in non-snorers, p=0.9) and duty cycle (123.8 (3.9) in OSA and 118.2 (2.8) % baseline in non-snorers, p=0.4) were similar in both groups, yet OSA patients could restore ventilation without cortical arousal less often than non-snorers (54.1% versus 65.7% of pressure drops respectively, 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 OSA patients than non-snorers.

                    • Genioglossus muscle
                    • Obstructive Sleep Apnea
                    • Respiratory timing
                    • Upper airway patency

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