Physiology of Arousal in Obstructive Sleep Apnea and Potential Impacts for Sedative Treatment

Obstructive sleep apnea (OSA) is estimated to affect approximately 20% of adults and is associated with numerous adverse health outcomes (1). Several treatments are available for OSA, including continuous positive airway pressure, mandibular advancement splints, and upper airway surgery. However, poor patient tolerance/compliance (2) or partial efficacy (3, 4) leaves many patients without a suitable treatment. This has led to an interest in generating new therapeutic options for patients with OSA. The recent improved understanding of the multiple pathophysiological contributors to OSA has led to the idea of individualized treatments for OSA (5, 6). One such potential treatment involves the use of sedatives to delay arousal from sleep, allowing time for upper airway muscles to recruit and reopen the airway while maintaining sleep. Research regarding the effect of sedatives in individuals with OSA has additional importance because of the widespread use of sedatives in the general population (7, 8), in whom undiagnosed OSA is common (9–11). Sedative use is also common in the perioperative period, when having OSA appears to increase the risk of sedative-related complications (12). Although these are important issues, this Pulmonary Perspective is restricted to an evaluation of the hypothesis that sedatives have a beneficial effect in those patients with OSA who have particular etiological features.