Syncope pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Syncope}} | {{Syncope}} | ||
{{CMG}}; {{AE}} {{KGH}} | {{CMG}}; {{AE}} {{KGH}} {{Sahar}} | ||
==Overview== | ==Overview== | ||
Syncope is an entity in which loss of | Syncope is an entity in which loss of consciousness 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== | ==Pathophysiology== | ||
Syncope is an entity in which loss of | Syncope is an entity in which loss of consciousness 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.<ref name="Hainsworth2004">{{cite journal|last1=Hainsworth|first1=Roger|title=Pathophysiology of syncope|journal=Clinical Autonomic Research|volume=14|issue=S1|year=2004|pages=i18–i24|issn=0959-9851|doi=10.1007/s10286-004-1004-2}}</ref><ref name="MoyaSutton2009">{{cite journal|last1=Moya|first1=A.|last2=Sutton|first2=R.|last3=Ammirati|first3=F.|last4=Blanc|first4=J.-J.|last5=Brignole|first5=M.|last6=Dahm|first6=J. B.|last7=Deharo|first7=J.-C.|last8=Gajek|first8=J.|last9=Gjesdal|first9=K.|last10=Krahn|first10=A.|last11=Massin|first11=M.|last12=Pepi|first12=M.|last13=Pezawas|first13=T.|last14=Granell|first14=R. R.|last15=Sarasin|first15=F.|last16=Ungar|first16=A.|last17=van Dijk|first17=J. G.|last18=Walma|first18=E. P.|last19=Wieling|first19=W.|last20=Abe|first20=H.|last21=Benditt|first21=D. G.|last22=Decker|first22=W. W.|last23=Grubb|first23=B. P.|last24=Kaufmann|first24=H.|last25=Morillo|first25=C.|last26=Olshansky|first26=B.|last27=Parry|first27=S. W.|last28=Sheldon|first28=R.|last29=Shen|first29=W. K.|last30=Vahanian|first30=A.|last31=Auricchio|first31=A.|last32=Bax|first32=J.|last33=Ceconi|first33=C.|last34=Dean|first34=V.|last35=Filippatos|first35=G.|last36=Funck-Brentano|first36=C.|last37=Hobbs|first37=R.|last38=Kearney|first38=P.|last39=McDonagh|first39=T.|last40=McGregor|first40=K.|last41=Popescu|first41=B. A.|last42=Reiner|first42=Z.|last43=Sechtem|first43=U.|last44=Sirnes|first44=P. A.|last45=Tendera|first45=M.|last46=Vardas|first46=P.|last47=Widimsky|first47=P.|last48=Auricchio|first48=A.|last49=Acarturk|first49=E.|last50=Andreotti|first50=F.|last51=Asteggiano|first51=R.|last52=Bauersfeld|first52=U.|last53=Bellou|first53=A.|last54=Benetos|first54=A.|last55=Brandt|first55=J.|last56=Chung|first56=M. K.|last57=Cortelli|first57=P.|last58=Da Costa|first58=A.|last59=Extramiana|first59=F.|last60=Ferro|first60=J.|last61=Gorenek|first61=B.|last62=Hedman|first62=A.|last63=Hirsch|first63=R.|last64=Kaliska|first64=G.|last65=Kenny|first65=R. A.|last66=Kjeldsen|first66=K. P.|last67=Lampert|first67=R.|last68=Molgard|first68=H.|last69=Paju|first69=R.|last70=Puodziukynas|first70=A.|last71=Raviele|first71=A.|last72=Roman|first72=P.|last73=Scherer|first73=M.|last74=Schondorf|first74=R.|last75=Sicari|first75=R.|last76=Vanbrabant|first76=P.|last77=Wolpert|first77=C.|last78=Zamorano|first78=J. L.|title=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)|journal=European Heart Journal|volume=30|issue=21|year=2009|pages=2631–2671|issn=0195-668X|doi=10.1093/eurheartj/ehp298}}</ref><ref>{{cite journal|doi=10.1016/j.pcad.2012.10.01}}</ref> | ||
{{familytree/start |summary=PE diagnosis Algorithm.}} | |||
{{familytree | E01 | | E02 | | | E05 | | | E03 | | E04 |E01=[[Venous]] depletion/pooling|E02=[[Arrhythmia]] or [[Structural heart disease]]|E05=Vasodepressors/Cardioinhibitors|E03=[[Drugs]]|E04=Autonomic nervous failure}} | |||
{{familytree | |!| | | |!| | | | |!| | | | |!| | | |!| | }} | |||
{{familytree | D01 | | D02 | | | D05 | | | D03 | | D04 |D01=Inadequate [[venous]] return|D02=[[Cardiac]]/[[Pulmonary]] cause|D05=Inappropriate reflex|D03=Normal '''ANS'''|D04=Damaged '''ANS'''}} | |||
{{familytree | |`|-|v|-|'| | | | |!| | | | |`|-|v|-|'| | }} | |||
{{familytree | | | B01 | | | | | B03 | | | | | B02 | | |B01=Low [[cardiac output]]|B03=Low [[cardiac output]]/Low [[peripheral resistance]]|B02=Low [[peripheral resistance]]}} | |||
{{familytree | | | |`|-|-|-|-|-|-|+|-|-|-|-|-|-|'|}} | |||
{{familytree | | | | | | | | | | A02 | | | | | |A02=[[Cerebral]] [[hypoperfusion]]}} | |||
{{familytree | | | | | | | | | | |!| | | | | | | }} | |||
{{familytree | | | | | | | | | | A01 | | | | |A01='''Syncope'''}} | |||
{{familytree/end}} | |||
<small><small> | |||
'''Abbreviations:''' '''ANS''': Autonomic nervous system | |||
</small></small> | |||
===Reflex (Neurally-mediated) Syncope === | ===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: | 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: | ||
| Line 13: | Line 29: | ||
*Atypical forms | *Atypical forms | ||
The table below provides information on the triggers of different subtypes of syncope: | |||
{| class="wikitable" | {| class="wikitable" | ||
|- | |- | ||
| Line 59: | Line 75: | ||
|} | |} | ||
===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> | ||
The table below compares different mechanisms of [[orthostatic hypotension]]. | |||
{| class="wikitable" | {| class="wikitable" | ||
|- | |- | ||
| Line 77: | Line 93: | ||
|Classic OH | |Classic OH | ||
| bgcolor="LightBlue" | | | bgcolor="LightBlue" | | ||
* 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]]. | ||
|- | |- | ||
|- bgcolor="LightBlue" | |- bgcolor="LightBlue" | ||
| Line 86: | Line 102: | ||
|- | |- | ||
|- bgcolor="LightBlue" | |- bgcolor="LightBlue" | ||
|Delayed | |Delayed Reflex syncope | ||
| bgcolor="LightBlue" | | | bgcolor="LightBlue" | | ||
* 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]]. | ||
|- | |- | ||
|- | |- | ||
| Line 94: | Line 110: | ||
|Reflex syncope triggered by standing position | |Reflex syncope triggered by standing position | ||
| bgcolor="LightBlue" | | | bgcolor="LightBlue" | | ||
* 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. | ||
|- | |- | ||
|- | |- | ||
| Line 100: | Line 116: | ||
|[[POTS]] (postural orthostatic tachycardia syndrome) | |[[POTS]] (postural orthostatic tachycardia syndrome) | ||
| bgcolor="LightBlue" | | | bgcolor="LightBlue" | | ||
* Decreased venous flow of uncertain cause. | * Decreased venous flow of uncertain [[Causes|cause]]. | ||
|- | |- | ||
|} | |} | ||
===Cardiovascular Syncope=== | ===Cardiovascular Syncope=== | ||
Cardiovascular syncope is the consequence of a decreased ability of the heart to pump blood and achieve adequate perfusion to all tissues | * [[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]]. | |||
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 | * The main causes of cardiovascular syncope is due to [[arrhythmias]] and [[structural heart disease]]. | ||
* [[Arrhythmia]], the inadequate [[heart rate]] would cause a decrease in the synchronicity of the [[heart]], consequently decreasing the perfusion of peripheral organs. | |||
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]]. | * 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 completely fill the [[ventricle]] and the [[ejection volume]] decreases, which also leads 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== | ==References== | ||
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[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Neurology]] | [[Category:Neurology]] | ||
[[Category: | [[Category:Up-To-Date]] | ||
Latest revision as of 20:30, 21 January 2021
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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] Sahar Memar Montazerin, M.D.[3]
Overview
Syncope is an entity in which loss of consciousness 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 consciousness 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][2][3]
| Venous depletion/pooling | Arrhythmia or Structural heart disease | Vasodepressors/Cardioinhibitors | Drugs | Autonomic nervous failure | |||||||||||||||||||||||||||||||||||||||
| Inadequate venous return | Cardiac/Pulmonary cause | Inappropriate reflex | Normal ANS | Damaged ANS | |||||||||||||||||||||||||||||||||||||||
| Low cardiac output | Low cardiac output/Low peripheral resistance | Low peripheral resistance | |||||||||||||||||||||||||||||||||||||||||
| Cerebral hypoperfusion | |||||||||||||||||||||||||||||||||||||||||||
| Syncope | |||||||||||||||||||||||||||||||||||||||||||
Abbreviations: ANS: Autonomic nervous system
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
The 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.[4][5][6]
The 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.
- Arrhythmia, the inadequate heart rate would cause a decrease in the synchronicity of the heart, consequently decreasing the perfusion of peripheral organs.
- 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 completely fill the ventricle and the ejection volume decreases, which also leads 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.
- ↑ 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.
- ↑ . doi:10.1016/j.pcad.2012.10.01. Missing or empty
|title=(help) - ↑ 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.