Syncope pathophysiology: Difference between revisions
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===Orthostatic Intolerance=== | ===Orthostatic Intolerance=== | ||
[[Orthostatic intolerance]] is caused by a chronic [[autonomic nervous system]] failure (ANF). | [[Orthostatic intolerance]] is caused by a chronic [[autonomic nervous system]] failure (ANF). ANF causes a deficient [[vasoconstriction]] and ultimately decreased [[blood pressure]], leading to the manifestation of syncope.<ref name="Robertson2008">{{cite journal|last1=Robertson|first1=David|title=The pathophysiology and diagnosis of orthostatic hypotension|journal=Clinical Autonomic Research|volume=18|issue=S1|year=2008|pages=2–7|issn=0959-9851|doi=10.1007/s10286-007-1004-0}}</ref><ref name="MedowStewart2008">{{cite journal|last1=Medow|first1=Marvin S.|last2=Stewart|first2=Julian M.|last3=Sanyal|first3=Sanjukta|last4=Mumtaz|first4=Arif|last5=Sica|first5=Domenic|last6=Frishman|first6=William H.|title=Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope|journal=Cardiology in Review|volume=16|issue=1|year=2008|pages=4–20|issn=1061-5377|doi=10.1097/CRD.0b013e31815c8032}}</ref><ref name="GoldsteinSharabi2009">{{cite journal|last1=Goldstein|first1=David S.|last2=Sharabi|first2=Yehonatan|title=Neurogenic Orthostatic Hypotension|journal=Circulation|volume=119|issue=1|year=2009|pages=139–146|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.108.805887}}</ref> | ||
Table below compares different mechanisms of [[orthostatic hypotension]]. | |||
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|Classic OH | |Classic OH | ||
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* Blood pooling due to [[autonomic nervous system]] failure, and inability to compensate with vasoconstriction, favoring decrease in [[SVR]]. | * Blood pooling due to [[autonomic nervous system]] failure, and inability to compensate with [[vasoconstriction]], favoring decrease in [[SVR]]. | ||
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|Delayed+Reflex syncope | |Delayed+Reflex syncope | ||
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* Progressive decrease in [[venous return]], with reactive [[vasovagal syncope]] causing vasodilation and | * Progressive decrease in [[venous return]], with reactive [[vasovagal syncope]] causing [[vasodilation]] and [[bradycardia]]. | ||
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|Reflex syncope triggered by standing position | |Reflex syncope triggered by standing position | ||
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* Vasovagal reaction caused by standing position due to decrease in venous return, with initial normal adaptation reflex. | *[[Vasovagal syncope|Vasovagal]] reaction caused by a standing position due to a decrease in venous return, with initial normal adaptation reflex. | ||
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|[[POTS]] (postural orthostatic tachycardia syndrome) | |[[POTS]] (postural orthostatic tachycardia syndrome) | ||
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* Decreased venous flow of uncertain cause. | * Decreased venous flow of uncertain [[Causes|cause]]. | ||
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Revision as of 19:23, 21 April 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]
Overview
Syncope is an entity in which loss of conscience due to cerebral hypoperfusion presents. There are several pathways to explain its pathophysiology, depending on if it is either reflex syncope, orthostatic intolerance, or cardiovascular syncope.
Pathophysiology
Syncope is an entity in which loss of conscience due to cerebral hypoperfusion presents. There are several pathways to explain its pathophysiology, depending on if it is either reflex syncope, orthostatic intolerance, or cardiovascular syncope.[1]
Reflex (Neurally-mediated) Syncope
Reflex syncope presents when there is a failure of the body's normal compensation of cardiac reflexes in response to a trigger. It can be manifested as 4 categories, whose triggers differ:
- Vasovagal syncope
- Situational syncope
- Carotid sinus syncope
- Atypical forms
Table below provides information on the triggers of different subtypes of syncope:
| Syncope |
Triggers: |
| Vasovagal |
|
| Situational |
|
| Carotid Sinus |
|
| Atypical forms |
Orthostatic Intolerance
Orthostatic intolerance is caused by a chronic autonomic nervous system failure (ANF). ANF causes a deficient vasoconstriction and ultimately decreased blood pressure, leading to the manifestation of syncope.[2][3][4]
Table below compares different mechanisms of orthostatic hypotension.
| Classification |
Pathophysiology |
| Initial OH |
|
| Classic OH |
|
| Delayed/Progressive OH |
|
| Delayed+Reflex syncope |
|
| Reflex syncope triggered by standing position |
|
| POTS (postural orthostatic tachycardia syndrome) |
|
Cardiovascular Syncope
Cardiovascular syncope is the consequence of a decreased ability of the heart to pump blood and achieve adequate perfusion to all tissues; The brain is the main organ affected, causing cerebral hypoperfusion that leads to syncope. The main causes of cardiovascular syncope is due to arrhythmias and structural heart disease. In arrhythmia, the inadequate heart rate would cause a decrease in the synchronicity of the heart, consequently decreasing the perfusion of peripheral organs.[5]
In bradyarrhythmia, such as AV block, the heart decreases the contractions per minute, which leads to decrease perfusion of peripheral tissues. On the other hand, in tachyarrhythmia, the heart has not enough time to fill completely the ventricle and the ejection volume decreases, which leads also to decrease perfusion.
In structural heart disease, an obstruction of the outflow (ex: aortic stenosis) would decrease the amount of blood reaching peripheral tissues and decrease the blood pressure. A myocardial infarction could also be the cause of syncope, an ischemic cardiac muscle could lead to an acute left ventricle dysfunction and decrease cerebral perfusion which causes loss of consciousness.
References
- ↑ Hainsworth, Roger (2004). "Pathophysiology of syncope". Clinical Autonomic Research. 14 (S1): i18–i24. doi:10.1007/s10286-004-1004-2. ISSN 0959-9851.
- ↑ Robertson, David (2008). "The pathophysiology and diagnosis of orthostatic hypotension". Clinical Autonomic Research. 18 (S1): 2–7. doi:10.1007/s10286-007-1004-0. ISSN 0959-9851.
- ↑ Medow, Marvin S.; Stewart, Julian M.; Sanyal, Sanjukta; Mumtaz, Arif; Sica, Domenic; Frishman, William H. (2008). "Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope". Cardiology in Review. 16 (1): 4–20. doi:10.1097/CRD.0b013e31815c8032. ISSN 1061-5377.
- ↑ Goldstein, David S.; Sharabi, Yehonatan (2009). "Neurogenic Orthostatic Hypotension". Circulation. 119 (1): 139–146. doi:10.1161/CIRCULATIONAHA.108.805887. ISSN 0009-7322.
- ↑ Moya, A.; Sutton, R.; Ammirati, F.; Blanc, J.-J.; Brignole, M.; Dahm, J. B.; Deharo, J.-C.; Gajek, J.; Gjesdal, K.; Krahn, A.; Massin, M.; Pepi, M.; Pezawas, T.; Granell, R. R.; Sarasin, F.; Ungar, A.; van Dijk, J. G.; Walma, E. P.; Wieling, W.; Abe, H.; Benditt, D. G.; Decker, W. W.; Grubb, B. P.; Kaufmann, H.; Morillo, C.; Olshansky, B.; Parry, S. W.; Sheldon, R.; Shen, W. K.; Vahanian, A.; Auricchio, A.; Bax, J.; Ceconi, C.; Dean, V.; Filippatos, G.; Funck-Brentano, C.; Hobbs, R.; Kearney, P.; McDonagh, T.; McGregor, K.; Popescu, B. A.; Reiner, Z.; Sechtem, U.; Sirnes, P. A.; Tendera, M.; Vardas, P.; Widimsky, P.; Auricchio, A.; Acarturk, E.; Andreotti, F.; Asteggiano, R.; Bauersfeld, U.; Bellou, A.; Benetos, A.; Brandt, J.; Chung, M. K.; Cortelli, P.; Da Costa, A.; Extramiana, F.; Ferro, J.; Gorenek, B.; Hedman, A.; Hirsch, R.; Kaliska, G.; Kenny, R. A.; Kjeldsen, K. P.; Lampert, R.; Molgard, H.; Paju, R.; Puodziukynas, A.; Raviele, A.; Roman, P.; Scherer, M.; Schondorf, R.; Sicari, R.; Vanbrabant, P.; Wolpert, C.; Zamorano, J. L. (2009). "Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)". European Heart Journal. 30 (21): 2631–2671. doi:10.1093/eurheartj/ehp298. ISSN 0195-668X.