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Abstract

The classic model of obstructive sleep apnea (OSA) pathophysiology involves preferential loss of upper airway muscle activity at sleep onset, leading to upper airway compromise, and a consequent rise in ventilatory drive. Recent work from our team --notably Drs. Laura Gell and Ludovico Messineo-- instead demonstrates that ventilatory drive (diaphragm EMG) typically falls during events, in parallel with upper airway compromise. Reduced drive is strongly associated with reduced flow and dilator muscle activity during sleep, and increased respiratory event risk. Obstructive apneas exhibit a greater loss of ventilatory drive than obstructive hypopneas. Esophageal pressure swings, by contrast, rise during events, which may appear to support the classic model but analysis reveals rising pressures are a product of increased resistance and neuromechanical efficiency. A minority subset of patients with pronounced impairment of pharyngeal muscle function exhibit a more classic form of OSA with rising drive. Lowered drive, rather than preferential loss of dilator muscle activity, also provides an explanation for greater OSA severity in REM. Our work shows that OSA is markedly more central in etiology than we previously appreciated.

Biography

Scott Sands PhD is an early career researcher investigating sleep apnea pathophysiology in Boston Massachusetts (Brigham and Women's Hospital and Harvard Medical School). His laboratory 1) develops translational methods to identify different causes of sleep apnea from routine sleep studies, and 2) performs focused physiology-based trials of novel and existing therapies for sleep apnea in selected patients. He is looking forward to sharing new physiological data on sleep apnea etiology.

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