Chapter 29: Sleep Apnea

Sleep apnea is characterized by recurrent pauses in breathing during sleep lasting at least ten seconds and occurring five or more times hourly, classified into three primary types based on underlying physiological mechanisms. Obstructive sleep apnea represents the most prevalent form, in which respiratory muscles remain active but airway collapse prevents airflow, typically involving obstruction at the pharyngeal level by soft tissue structures. Central sleep apnea occurs when the brainstem fails to generate respiratory drive signals, eliminating both airflow and breathing effort, accounting for a smaller disease proportion. Mixed apnea combines features of both mechanisms. Severity quantification relies on the Apnea-Hypopnea Index, which correlates with diagnosis thresholds and prognostic outcomes. Epidemiological patterns reveal substantially higher disease prevalence in middle-aged and older males and postmenopausal women, with significant underdiagnosis rates affecting population health. Multiple risk factors contribute to pathogenesis, including obesity with increased pharyngeal soft tissue and elevated neck circumference, substance use such as alcohol and sedatives that reduce airway muscle tone, anatomical variations including tonsillar enlargement and mandibular insufficiency, and genetic predisposition among relatives of affected individuals. The pathophysiological cycle involves progressive hypoxemia and hypercapnia triggering arousal responses that fragment sleep architecture and eliminate restorative sleep stages, creating cumulative cardiovascular and metabolic consequences. Chronic sleep apnea functions as an independent risk factor for systemic and pulmonary hypertension, heart failure, arrhythmias particularly atrial fibrillation, and acute coronary events. Clinical presentation emphasizes excessive daytime somnolence and loud snoring as cardinal symptoms, alongside morning headaches, cognitive impairment, and mood disturbances. Diagnostic evaluation incorporates subjective sleepiness scales and polysomnography as the definitive standard, with home-based testing serving adjunctive but limited roles. Management encompasses lifestyle interventions including weight reduction and positional therapy, positive airway pressure devices with continuous, bilevel, and autotitrating modalities as first-line pharmacological treatment, mandibular advancement oral appliances for mild-to-moderate disease, and surgical airway expansion procedures with moderate success rates. Treatment adherence remains challenging, necessitating comprehensive patient education and psychosocial support to optimize long-term compliance and clinical outcomes.