What is the pathophysiology of obstructive sleep apnea?

• A. Central brainstem hyperactivity
• B. Increased nasal resistance only during waking
• C. Allergic rhinitis causing obstruction
• D. Recurrent pharyngeal airway collapse during sleep causing intermittent hypoxia and arousals.

Answer: (D)

Recurrent collapse of the upper airway during sleep is the key idea. When you fall asleep, the pharyngeal dilator muscles relax, especially in REM, allowing the soft tissues of the throat to narrow or obstruct the airway. Even though the person may still try to breathe, airflow stops or is markedly reduced, creating an apnea or hypopnea. This obstruction triggers brief arousals that restore muscle tone and reopen the airway, and the cycle repeats throughout the night. The result is intermittent hypoxemia and sleep fragmentation, with downstream effects like daytime sleepiness and cardiovascular stress from repeated sympathetic activation and inflammatory processes. This mechanism is what distinguishes obstructive sleep apnea from central sleep apnea, where breathing stops because the brain fails to send the drive to breathe rather than due to airway collapse. Nasal congestion or allergic rhinitis can worsen symptoms but are not the primary cause of the obstructive process.