Figure 1.

Diagram showing the interaction of four endotypic traits on obstructive sleep apnea (OSA) pathogenesis: in the presence of mild-to-moderate collapsibility, indicated by a critical collapsing pressure (Pcrit) between −2 and 2 cmH₂O, other non-anatomical traits play a role in OSA pathophysiology. The inability to recruit the upper airway dilator muscle in response to negative pharyngeal pressure swings during an obstructive event (% activity/cmH₂O close to 0), a low arousal threshold (epiglottic pressure swings before the arousal above −15 cmH₂O) and a high loop gain (close to or above 1) will contribute in different degrees to OSA development. Note that the boundaries between the four traits are intentionally blurred to show that OSA presence and severity is often determined by the interaction of these pathogenic traits. EMG_GG: genioglossus electromyography, V response/V disturbance: ratio between the ventilatory response to a preceding ventilatory disturbance, dimensionless.