Obstructive Sleep Apnea occurs due to repetitive episodes of upper airway collapse during sleep, which leads to apneic (cessation of airflow) or hypopneic (reduced airflow) events. These interruptions in breathing cause a drop in oxygen saturation, leading to hypoxemia and hypercapnia, and subsequently trigger arousal from sleep to reestablish airway patency. This pattern of apnea and arousal severely disrupts the normal sleep cycle and causes non-restorative sleep and excessive daytime sleepiness.
The pathophysiology of obstructive sleep apnea involves several factors, including:
- Anatomical features: A narrow upper airway due to large tonsils, a thick neck, or excess tissue around the airway (as seen in obesity) can predispose patients to obstructive sleep apnea.
- Neuromuscular control: A reduction in the tone of the pharyngeal muscles during sleep further exacerbates airway collapse, particularly during the deeper stages of sleep when muscle tone is lowest.
- Systemic impacts: obstructive sleep apnea is linked to systemic complications such as hypertension, cardiovascular disease, and metabolic syndrome due to the repeated surges of sympathetic activity caused by arousal from sleep and hypoxia.
