Sleep apnea pathophysiology: Difference between revisions
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Revision as of 16:04, 2 July 2015
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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.
Overview
The pathogenesis of obstructive sleep apnea is a combination of upper airway anatomy, the ability of the upper airway dilator muscles to respond to respiratory challenge during sleep, arousal threshold,loop gain, and potential for state-related changes in lung volume. The pathogenesis central sleep apnea involves chemoreceptors modulating ventilation. There may be some genetic basis with sleep apnea, although further studies should be performed. Central sleep apnea is associated with congestive heart failure.
Pathogenesis
Obstructive Sleep Apnea[1]
The pathogenesis of obstructive sleep apnea results from a combination of the following components:
- 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
- Collapsible portion from the hard palate to the larnyx
- The upper airway can momentarily close during speech, swallowing, and inopportune times during sleep
Upper Airway Dilator Muscles
- Evidence suggests that upper airway dilator muscles, particularly the genioglossus, keeps the airway patent via protective reflexes
Arousal Threshold
- Evidence suggests that low respiratory drive that causes pleural pressure induces arousal from sleep
- Examples of low respiratory drive 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
- This makes the ventilatory control unstable
Changes in Lung Volume
- Although the exact mechanism is not defined, there is an interaction between pharyngeal patency and lung volume
Central Sleep Apnea[2]
- 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
Genetics[1]
- The following may have some genetic basis:
- Obesity
- Craniofacial structure
- Size of upper airway
- Ventilatory control abnormalites
Associated Conditions[3]
- Patients that have congestive heart failure are at a risk for a type of central sleep apnea called Cheyne-Stokes respiration
- This is periodic breathing with recurrent episodes of apnea alternating with episodes of rapid breathing
- Respirations occur while both awake and asleep
References
- ↑ 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.
- ↑ 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.
- ↑ Leung RS, Huber MA, Rogge T, Maimon N, Chiu KL, Bradley TD (2005). "Association between atrial fibrillation and central sleep apnea". Sleep. 28 (12): 1543–6. PMID 16408413.