Sleep apnea pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.


The pathogenesis of obstructive sleep apnea includes upper airway anatomy defects, the inability of the upper airway dilator muscles to respond to respiratory challenge during sleep, inadequate arousal threshold, loop gain, and potential for state-related changes in lung volume. The pathogenesis of central sleep apnea involves chemoreceptors that modulate ventilation.


Obstructive Sleep Apnea

The pathogenesis of obstructive sleep apnea results from a combination of the following components[1]:

  • Upper airway anatomy
  • The ability of the upper airway dilator muscles to respond to respiratory challenge during sleep
  • Arousal threshold
  • Loop gain
  • Potential for state-related changes in lung volume

Upper Airway Anatomy

  • The airway is composed of numerous muscles and soft tissues
  • It lacks rigid support
  • The collapsible portion is from the hard palate to the larynx
  • The upper airway can momentarily close during speech, swallowing, and during sleep

Upper Airway Dilator Muscles

  • Upper airway dilator muscles, particularly the genioglossus, keeps the airway patent via protective reflexes

Arousal Threshold

  • Low respiratory drive, that causes pleural pressure, induces arousal from sleep (examples are hypoxia and hypercapnia)

Loop Gain

  • Loop gain is stability of the ventilatory control system
  • There is a cyclical breathing pattern that develops between obstructive breathing events during sleep and wakefulness, which makes the ventilatory control system unstable

Changes in Lung Volume

  • Although the exact mechanism is not understood, there is an interaction between pharyngeal patency and lung volume

Central Sleep Apnea

  • Ventilation is modulated with chemoreceptor inputs (medullary neurons that respond to C02)
  • The ventilatory output is given in change in PaO2 or PaCO2
  • If the individual is extremely sensitive to the chemoreceptor inputs, that individual is at a risk for unstable breathing patterns
  • Therefore, individuals with high chemo-responsiveness will hyperventilate, lowering PaCO2 below the ideal level, leading to hypoventilation and potential apnea[2]


  • The following may have some genetic basis[1]:
  • Obesity
  • Craniofacial structure
  • Size of upper airway
  • Ventilatory control abnormalities


  1. 1.0 1.1 Eckert DJ, Malhotra A (2008). "Pathophysiology of adult obstructive sleep apnea". Proc Am Thorac Soc. 5 (2): 144–53. doi:10.1513/pats.200707-114MG. PMC 2628457. PMID 18250206.
  2. Eckert DJ, Jordan AS, Merchia P, Malhotra A (2007). "Central sleep apnea: Pathophysiology and treatment". Chest. 131 (2): 595–607. doi:10.1378/chest.06.2287. PMC 2287191. PMID 17296668.

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