Abstract
Sleep apnea is a common and heterogeneous disorder. Depending on the prevailing level of respiratory effort, three different forms of sleep apnea can manifest: obstructive, central, or mixed. The pathogenesis of sleep apnea is characterized by alteration of one or more of the following physiological traits: (1) anatomical impairment-a collapsible upper airway, which is the key determinant of obstructive apneas, (2) respiratory control or loop gain, which if abnormally high (very sensitive to small changes in CO2), can cause central apneas and contribute to cyclical breathing in obstructive sleep apnea but if too low, can cause sleep hypoventilation, (3) the propensity to arouse from sleep (arousal threshold), and (4) upper airway dilator muscle function during sleep. Because patients with obesity hypoventilation syndrome are obese and frequently have severe sleep apnea, this chapter reviews the latest knowledge on sleep apnea pathogenesis, including highlighting key pathophysiological differences between nonobese versus and obese patients with sleep apnea. Links between sleep apnea phenotypes and severe obstructive sleep apnea (OSA) are also briefly highlighted.
Original language | English |
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Title of host publication | Obesity Hypoventilation Syndrome |
Subtitle of host publication | From Physiologic Principles to Clinical Practice |
Editors | Aiman Tulaimat |
Place of Publication | London, United Kingdom |
Publisher | Elsevier |
Chapter | 6 |
Pages | 55-66 |
Number of pages | 12 |
ISBN (Print) | 9780128152904 |
DOIs | |
Publication status | Published - 2020 |
Keywords
- Arousal threshold
- Critical closing pressure
- Leptin
- Loop gain
- Obesity
- Phenotyping
- Upper airway muscle responsiveness