OSA pathophysiology: a contemporary update

Abstract Defined as an elevated frequency of obstructive respiratory events in sleep, obstructive sleep apnoea (OSA) is driven by a combination of four pathophysiologic mechanisms: elevated upper airway collapsibility, unstable ventilatory control, impaired upper airway dilator muscle responsiveness and decreased arousal threshold. Established therapies such as continuous positive airway pressure (CPAP) and oral appliance therapy (OAT) work chiefly through targeting elevated collapsibility, which affects the majority of OSA patients. However, many patients respond poorly or do not tolerate these ‘anatomic’ therapies. The emerging field of ‘precision sleep medicine’ seeks to determine if novel treatment approaches specifically targeting the other, ‘non‐anatomic’ mechanisms will improve treatment efficacy and acceptance. In this review, we consider the concepts underlying each pathophysiologic mechanism, the predisposing factors, and the potential implications for established and future OSA treatments.