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Published on: December 6, 2016
The pathogenesis of obstructive sleep apnea
1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins Sleep Disorders Center, Johns Hopkins University, Baltimore, Maryland, USA.
Obstructive sleep apnea (OSA) involves upper airway collapse during sleep, disrupting breathing. Pathogenic models explain how this collapse destabilizes respiratory patterns, impacting cardiovascular health.
Area of Science:
- Sleep Medicine
- Cardiovascular Health
- Respiratory Physiology
Background:
- Obstructive sleep apnea (OSA) significantly contributes to cardiovascular morbidity and mortality.
- OSA presents a growing challenge to healthcare systems globally.
- Understanding OSA pathogenesis is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To review current concepts regarding the pathogenesis of obstructive sleep apnea (OSA).
- To present a framework for modeling the biomechanical properties and collapse propensity of the upper airway during sleep.
- To discuss anatomical and neuromuscular factors influencing upper airway obstruction in OSA.
Main Methods:
- Review of current scientific literature on OSA pathogenesis.
- Development of a conceptual model for upper airway biomechanics and collapse.
- Analysis of periodic breathing models and their relation to upper airway obstruction.
- Elaboration of mechanisms linking upper airway obstruction to respiratory pattern destabilization.
Main Results:
- The upper airway plays a primary role in OSA pathogenesis.
- Upper airway obstruction triggers a mismatch between ventilatory supply and demand.
- Trade-offs between sleep stability and ventilation explain OSA severity.
- Recurrent arousals and altered neuromuscular responses modulate OSA expression.
Conclusions:
- Upper airway obstruction is a key driver of OSA.
- Models of respiratory control during sleep can elucidate OSA mechanisms.
- The interplay between sleep stability and ventilation explains the spectrum of OSA.
- Therapeutic strategies may target upper airway patency and respiratory control mechanisms.
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