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Pathophysiology of Upper Airway Collapse
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Previous pathophysiologic studies have revealed that the upper airway dimension reaches aminimal value at the end of expiration, and pharyngeal negative pressure is not an essentialprerequisite for upper airway collapse. Furthermore, pharyngeal collapse occurs in spite of increasedactivity of upper airway dilator muscles in patients with obstructive sleep apnea (OSA)compared with normal subjects. Pharyngeal sensory threshold is elevated in patients withOSA, which contributes to inadequate activity of upper airway dilator muscles. Pharyngeal narrowingresults in several types of airflow limitation, of whom the mechanisms are mainly explainedusing Starling resistor model and negative effort dependence. Several studies have beenconducted over the past years to validate polysomnographic surrogate markers which indicatespecific pathophysiologic phenotypes, and such attempts may be able to lead us to personalizedtreatment for OSA.
Abstract
Previous pathophysiologic studies have revealed that the upper airway dimension reaches aminimal value at the end of expiration, and pharyngeal negative pressure is not an essentialprerequisite for upper airway collapse. Furthermore, pharyngeal collapse occurs in spite of increasedactivity of upper airway dilator muscles in patients with obstructive sleep apnea (OSA)compared with normal subjects. Pharyngeal sensory threshold is elevated in patients withOSA, which contributes to inadequate activity of upper airway dilator muscles. Pharyngeal narrowingresults in several types of airflow limitation, of whom the mechanisms are mainly explainedusing Starling resistor model and negative effort dependence. Several studies have beenconducted over the past years to validate polysomnographic surrogate markers which indicatespecific pathophysiologic phenotypes, and such attempts may be able to lead us to personalizedtreatment for OSA.
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