Sleep apnea pathophysiology: Difference between revisions
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{{Sleep apnea}} | {{Sleep apnea}} | ||
{{CMG}} {{AE}} Saarah T. Alkhairy, M.D. | |||
==Overview== | |||
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. | |||
==Pathogenesis== | |||
===Obstructive Sleep Apnea=== | |||
The pathogenesis of obstructive sleep apnea results from a combination of the following components<ref name="pmid18250206">{{cite journal| author=Eckert DJ, Malhotra A| title=Pathophysiology of adult obstructive sleep apnea. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 2 | pages= 144-53 | pmid=18250206 | doi=10.1513/pats.200707-114MG | pmc=PMC2628457 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18250206 }} </ref>: | |||
*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<ref name="pmid17296668">{{cite journal| author=Eckert DJ, Jordan AS, Merchia P, Malhotra A| title=Central sleep apnea: Pathophysiology and treatment. | journal=Chest | year= 2007 | volume= 131 | issue= 2 | pages= 595-607 | pmid=17296668 | doi=10.1378/chest.06.2287 | pmc=PMC2287191 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17296668 }} </ref> | |||
==Genetics== | |||
*The following may have some genetic basis<ref name="pmid18250206">{{cite journal| author=Eckert DJ, Malhotra A| title=Pathophysiology of adult obstructive sleep apnea. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 2 | pages= 144-53 | pmid=18250206 | doi=10.1513/pats.200707-114MG | pmc=PMC2628457 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18250206 }} </ref>: | |||
:*Obesity | |||
:*Craniofacial structure | |||
:*Size of upper airway | |||
:*Ventilatory control abnormalities | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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{{WikiDoc Sources}} | |||
[[Category: | [[Category:Cardiology]] | ||
[[Category:Pulmonology]] | [[Category:Pulmonology]] | ||
Latest revision as of 00:12, 30 July 2020
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Sleep apnea pathophysiology On the Web |
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Risk calculators and risk factors for Sleep apnea pathophysiology |
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 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.
Pathogenesis
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]
Genetics
- The following may have some genetic basis[1]:
- Obesity
- Craniofacial structure
- Size of upper airway
- Ventilatory control abnormalities
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.