Sleep Apnea

Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep caused by pharyngeal collapse, resulting in apnea (complete cessation of airflow ≥10 seconds) or hypopnea (≥30% reduction in airflow with ≥3% oxygen desaturation or arousal). The pathophysiology involves loss of pharyngeal dilator muscle tone during sleep (especially genioglossus), combined with anatomic narrowing from obesity (fat deposition in the parapharyngeal space), retrognathia, tonsillar hypertrophy, macroglossia, or craniofacial abnormalities. Severity is quantified by the apnea-hypopnea index (AHI) on polysomnography: mild (5-14 events/hour), moderate (15-29), severe (≥30). Each obstructive event causes intermittent hypoxemia and hypercapnia, triggering sympathetic surges (catecholamine release, hypertension, tachycardia), cortical arousals (fragmenting sleep architecture), and intrathoracic pressure swings (increasing cardiac afterload). Chronic consequences include: resistant hypertension (OSA is the leading identifiable cause of secondary hypertension — present in >80% of resistant HTN), atrial fibrillation (4x increased risk), heart failure (both HFrEF and HFpEF), stroke, type 2 diabetes (intermittent hypoxia impairs insulin sensitivity), pulmonary hypertension, nocturnal arrhythmias, and cognitive impairment. Central sleep apnea (CSA) involves loss of central respiratory drive (no airway obstruction) — seen in heart failure...