Pathophysiology of adult obstructive sleep apnea

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Pathophysiology of Adult Obstructive Sleep Apnea
Danny J. Eckert1 and Atul Malhotra1,2
1 Division of Sleep Medicine, Sleep Disorders Program, Brigham and Women’s Hospital, and Harvard Medical School; and 2Division of Pulmonary/Critical Care Medicine, Brigham and Women’s Hospital, Boston, Massachusetts

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive narrowing orcollapse of the pharyngeal airway during sleep. The disorder is associated with major comorbidities including excessive daytime sleepiness and increased risk of cardiovascular disease. The underlying pathophysiology is multifactorial and may vary considerably between individuals. Important risk factors include obesity, male sex, and aging. However, the physiological mechanisms underlying theserisk factors are not clearly understood. This brief review summarizes the current understanding of OSA pathophysiology in adults and highlights the potential mechanisms underlying the principal risk factors. In addition, some of the pathophysiological characteristics associated with OSA that may modulate disease severity are illustrated. Finally, the potential for novel treatment strategies, basedon an improved understanding of the underlying pathophysiology, is also discussed with the ultimate aim of stimulating research ideas in areas where knowledge is lacking. Keywords: arousal; genioglossus; lung volume; upper airway; ventilatory control stability

Obstructive sleep apnea (OSA) is characterized by recurrent collapse of the pharyngeal airway during sleep, resulting in substantiallyreduced (hypopnea) or complete cessation (apnea) of airflow despite ongoing breathing efforts. These disruptions to breathing lead to intermittent blood gas disturbances (hypercapnia and hypoxemia) and surges of sympathetic activation. Loud snoring is a typical feature of OSA and in most cases the culmination of a respiratory event is associated with a brief awakening from sleep (arousal). Theseevents result in a cyclical breathing pattern and fragmented sleep as the patient oscillates between wakefulness and sleep. In severe cases respiratory events can occur more than 100 times per hour and typically each event lasts 20–40 seconds (see Figure 1 for an example). OSA is associated with major comorbidities including daytime somnolence, impaired cognition, poor quality of life, and increasedrisk of motor vehicle accidents. There is emerging evidence to suggest that OSA is an independent risk factor for a variety of adverse cardiovascular outcomes (1, 2). The clinical disorder, defined as more than five abnormal breathing disturbances (hypopneas or apneas) per hour of sleep combined with symptoms of daytime sleepiness, affects at least 2–4% of the adult population (3). Although nonobeseindividuals may suffer from OSA, obesity is the main epidemiologic risk factor. Indeed, increases in body mass index, central accumulation of adipose tissue, and neck circumference are strong predictors of

disease (4). Further, the prevalence of OSA is two to three times greater in men than in women (3, 5, 6) and in older individuals (>65 yr) compared with middle-aged individuals (30–64 yr)(7). The pathophysiological causes of OSA likely vary considerably between individuals. Important components likely include upper airway anatomy, the ability of the upper airway dilator muscles to respond to respiratory challenge during sleep, the propensity to wake from increased respiratory drive during sleep (arousal threshold), the stability of the respiratory control system (loop gain), and thepotential for state-related changes in lung volume to influence these factors. These various physiological traits and the potential for each to influence sleep apnea pathophysiology have been described in detail in review articles (8–10). The focus of the current article is to (1) briefly review the key physiological factors, discuss how they may interact with one another, and highlight advances in...