Adherence Index: sleep depth and nocturnal hypoventilation predict long-term adherence with positive airway pressure therapy in severe obstructive sleep apnea.

STUDY OBJECTIVES: Treatment of obstructive sleep apnea with positive airway pressure (PAP) devices is limited by poor long-term adherence. Early identification of individual patients' probability of long-term PAP adherence would help in their management. We determined whether conventional polysomnogram (PSG) scoring and measures of sleep depth based on the odds ratio product would predict adherence with PAP therapy 12 months after it was started. METHODS: Patients with obstructive sleep apnea referred to an academic sleep center had split-night PSG, arterial blood gases, and a sleep questionnaire. Multiple linear regression analysis of conventional PSG scoring and the odds ratio product both during diagnostic PSG and PAP titration provided an "Adherence Index," which was correlated with PAP use 12 months later. RESULTS: Patients with obstructive sleep apnea (n = 236, apnea-hypopnea index 72.2 ± 34.1 events/h) were prescribed PAP therapy (82% received continuous PAP, 18% received bilevel PAP). Each patient's adherence with PAP therapy 12 months later was categorized as "never used," "quit using," "poor adherence," and "good adherence." PSG measures that were most strongly correlated with PAP adherence were apnea-hypopnea index and odds ratio product during nonrapid eye movement sleep; the additional contribution of nocturnal hypoxemia to this correlation was confined to those with chronic hypoventilation treated with bilevel PAP. The Adherence Index derived from these measures, during both diagnostic PSG and PAP titration, was strongly correlated with PAP adherence 12 months later. CONCLUSIONS: Long-term adherence with PAP therapy can be predicted from diagnostic PSG in patients with severe obstructive sleep apnea, which may facilitate a precision-based approach to PAP management. CITATION: Younes MK, Beaudin AE, Raneri JK, Gerardy BJ, Hanly PJ. Adherence Index: sleep depth and nocturnal hypoventilation predict long-term adherence with positive airway pressure therapy in severe obstructive sleep apnea. J Clin Sleep Med. 2022:18(8):1933-1944.

Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment.

Historically, brief awakenings from sleep (cortical arousals) have been assumed to be vitally important in restoring airflow and blood-gas disturbances at the end of obstructive sleep apnea (OSA) breathing events. Indeed, in patients with blunted chemical drive (e.g., obesity hypoventilation syndrome) and in instances when other defensive mechanisms fail, cortical arousal likely serves an important protective role. However, recent insight into the pathogenesis of OSA indicates that a substantial proportion of respiratory events do not terminate with a cortical arousal from sleep. In many cases, cortical arousals may actually perpetuate blood-gas disturbances, breathing instability, and subsequent upper airway closure during sleep. This brief review summarizes the current understanding of the mechanisms mediating respiratory-induced cortical arousal, the physiological factors that influence the propensity for cortical arousal, and the potential dual roles that cortical arousal may play in OSA pathogenesis. Finally, the extent to which existing sedative agents decrease the propensity for cortical arousal and their potential to be therapeutically beneficial for certain OSA patients are highlighted.

Obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive collapse of the pharyngeal airway during sleep. Control of pharyngeal patency is a complex process relating primarily to basic anatomy and the activity of many pharyngeal dilator muscles. The control of these muscles is regulated by a number of processes including respiratory drive, negative pressure reflexes, and state (sleep) effects. In general, patients with OSA have an anatomically small airway the patency of which is maintained during wakefulness by reflex-driven augmented dilator muscle activation. At sleep onset, muscle activity falls, thereby compromising the upper airway. However, recent data suggest that the mechanism of OSA differs substantially among patients, with variable contributions from several physiologic characteristics including, among others: level of upper airway dilator muscle activation required to open the airway, increase in chemical drive required to recruit the pharyngeal muscles, chemical control loop gain, and arousal threshold. Thus, the cause of sleep apnea likely varies substantially between patients. Other physiologic mechanisms likely contributing to OSA pathogenesis include falling lung volume during sleep, shifts in blood volume from peripheral tissues to the neck, and airway edema. Apnea severity may progress over time, likely due to weight gain, muscle/nerve injury, aging effects on airway anatomy/collapsibility, and changes in ventilatory control stability.