Pathophysiology of Upper Airway Collapse

Abstract

Previous pathophysiologic studies have revealed that the upper airway dimension reaches a minimal value at the end of expiration, and pharyngeal negative pressure is not an essential prerequisite for upper airway collapse. Furthermore, pharyngeal collapse occurs in spite of increased activity of upper airway dilator muscles in patients with obstructive sleep apnea (OSA) compared with normal subjects. Pharyngeal sensory threshold is elevated in patients with OSA, which contributes to inadequate activity of upper airway dilator muscles. Pharyngeal narrowing results in several types of airflow limitation, of whom the mechanisms are mainly explained using Starling resistor model and negative effort dependence. Several studies have been conducted over the past years to validate polysomnographic surrogate markers which indicate specific pathophysiologic phenotypes, and such attempts may be able to lead us to personalized treatment for OSA.