Pathophysiology of obstructive sleep apnea.

The pharyngeal muscles are essential for effective lung ventilation because they help maintain an open upper airspace for the unhindered passage of air into the lungs. Sleep, especially rapid-eye-movement sleep, however, causes fundamental modifications of pharyngeal muscle tone and reflex responses that in normal individuals lead to airway narrowing and hypoventilation. In individuals with already anatomically narrow upper airways, these effects of sleep predispose them to inspiratory flow limitation (hypopneas), airway closure, and obstructive sleep apnea. Obstructive sleep apnea is a common disorder affecting at least 2% to 4% of North American adults and is associated with serious clinical, social, and economic consequences. This review addresses the physiology and pathophysiology of obstructive sleep apnea, hypopneas, and snoring, that is, the full spectrum of the most common sleep-related breathing events involving the upper airway. Specifically, the anatomical features of the upper airway that are important to its mechanical properties and degree of collapsibility are reviewed. The sites of airway narrowing and closure and the implications for common treatments strategies are also discussed. This article also focuses on the neuromuscular control mechanisms operating in wakefulness and sleep that influence pharyngeal muscle tone and upper airway collapsibility. The effects of sleep on the reflex mechanisms that normally operate to protect the upper airspace from suction collapse during breathing are also addressed. Throughout this review, these mechanisms are discussed with an emphasis on understanding the physiology and pathophysiology of sleep-disordered breathing and obstructive sleep apnea.