Obstructive sleep apnea (OSA) is characterized by repetitive partial (hypopnea) or complete (apnea) upper airway obstruction during sleep, resulting in intermittent hypoxia, hypercapnia, sleep fragmentation, and sustained cardiovascular injury. The pharynx is the only segment of the airway lacking rigid cartilaginous or bony support, relying instead on the tonic activity of pharyngeal dilator muscles — primarily the genioglossus — to maintain patency. During wakefulness, neural drive from the hypoglossal motor nucleus maintains sufficient dilator muscle tone to keep the airway open. During sleep, this neuromuscular drive decreases physiologically, narrowing the airway. In OSA, anatomical factors (obesity with parapharyngeal fat deposition, retrognathia, macroglossia, enlarged tonsils, thick neck circumference) reduce the pharyngeal cross-sectional area below the critical closing pressure (Pcrit), and the loss of sleep-related dilator tone causes airway collapse at the retropalatal and/or retroglossal regions. Each obstructive event produces progressive hypoxemia and hypercapnia until the rising PaCO2 and falling PaO2 trigger a cortical arousal, activating the sympathetic nervous system and restoring dilator muscle tone to reopen the airway — producing the characteristic gasping, snoring, and sleep fragmentation. The cardiovascular consequences of...