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{{Syncope}}
{{Syncope}}
{{CMG}}; {{AE}} {{KGH}}
{{CMG}}; {{AE}} {{KGH}} {{Sahar}}
==Overview==
==Overview==
[[Blood pressure]] is the main determinant for the presentation of syncope. [[Blood pressure]] is determined by cardiac output and total [[peripheral vascular resistance]], and hence, any disturbances with any of these variables may lead to the presentation of syncope.
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 conscience due to cerebral hipoperfusion presents.  There are several pathways to explain its pathophysiology, depending if it is either reflex syncope, [[orthostatic intolerance]], or cardiovascular syncope.  
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>
===Reflex Syncope===
 
Reflex syncope presents when there is a failure of body's normal compensation of cardiac reflexes in response to a trigger. It can be manifested as 4 categories, whose triggers differ:
 
{{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 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]]
*[[Vasovagal syncope]]
*Situtational syncope
*Situational syncope
*[[Carotid sinus]] syncope
*[[Carotid sinus]] syncope
*Atypical forms
*Atypical forms
Each of these categories has different triggers that lead to the presentation of syncope. Shown below a table for each syncope form and its triggers. Note that in any trigger, different mechanisms may be involved in its presentation, such as in micturition, where different pathways participate.
 
The table below provides information on the triggers of different subtypes of syncope:
{| class="wikitable"
{| class="wikitable"
|-
|-
Line 22: Line 39:


|-bgcolor="LightBlue"
|-bgcolor="LightBlue"
| Vasovagal
|[[Vasovagal syncope|Vasovagal]]
|bgcolor="LightBlue"|
|bgcolor="LightBlue"|
* Emotional distress:
* Emotional distress:
**Fear
**Fear
**Pain
**[[Pain]]
**Blood fear
**Blood fear
*Orthostatic stress
*[[Orthostatic]] stress
|-
|-


Line 34: Line 51:
|Situational
|Situational
|bgcolor="LightBlue"|
|bgcolor="LightBlue"|
* Coughing
*[[Cough|Coughing]]
*Sneezing
*[[Sneezing]]
*Swallowing
*[[Swallowing]]
*Defecation
*[[Defecation]]
*Visceral instrumentation
*Visceral instrumentation
*Micturition
*[[Micturition]]
*Exercise
*[[Exercise]]
|-
|-


|-bgcolor="LightBlue"
|-bgcolor="LightBlue"
|Carotid Sinus
|[[Carotid Sinus Syncope|Carotid Sinus]]
|bgcolor="LightBlue"|
|bgcolor="LightBlue"|
* Due to mechanical manipulation of the [[carotid sinus]]
* Due to mechanical manipulation of the [[carotid sinus]]
Line 54: Line 71:
|bgcolor="LightBlue"|
|bgcolor="LightBlue"|
* Triggers can't be clearly identified.
* Triggers can't be clearly identified.
*Diagnosis is made upon exclusion or by reproduction of symptoms with [[tilt test]]
*[[Diagnosis]] is made upon exclusion or by reproduction of symptoms with [[tilt test]]
|-
|-
|}
|}
===Orthostatic Intolerance===
===Orthostatic Intolerance===
[[Orthostatic intolerance]] is caused by a chronic [[autonomic nervous system]] failure (ANF). This ANF causes a deficient vasoconstriction and ultimately decreased [[blood pressure]], leading to the manifestation of syncope. [[Orthostatic intolerance]] is a syndrome and syncope is one of its symptoms. Among different kinds of [[orthostatic intolerance]] syndromes there are different pathophysiological explantions. Shown below is a table to match each OH syndrome and its mechanism of presentation. Note that reflex syncope whose main trigger is orthostatic stress are also included.
[[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"
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
| '''Classification'''
|'''Classification'''
|bgcolor="LightBlue"|
| bgcolor="LightBlue" |
'''Pathophysiology'''
'''Pathophysiology'''
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
| Initial OH
| Initial OH
|bgcolor="LightBlue"|
| bgcolor="LightBlue" |
Abnormalities among [[cardiac output]] and [[systemic vascular resistance]] (SVR)
* Abnormalities among [[cardiac output]] and [[systemic vascular resistance]] (SVR)
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
|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"
|Delayed/Progressive OH
|Delayed/Progressive OH
|bgcolor="LightBlue"|
| bgcolor="LightBlue" |
Progressive decrease in [[venous return]], causing low [[cardiac output]]. Also failure of adaptation reflex.
* Progressive decrease in [[venous return]], causing low [[cardiac output]]. Also failure of adaptation reflex.
|-
|-
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
|Delayed+Reflex syncope
|Delayed Reflex syncope
|bgcolor="LightBlue"|
| bgcolor="LightBlue" |
Progressive decrease in [[venous return]], with reactive [[vasovagal syncope]] causing vasodilation and bradicardia.
* Progressive decrease in [[venous return]], with reactive [[vasovagal syncope]] causing [[vasodilation]] and [[bradycardia]].
|-
|-
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
|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.
|-
|-
|-
|-
|-bgcolor="LightBlue"
|- bgcolor="LightBlue"
|[[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.
* 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==
==References==
{{reflist|2}}
{{reflist|2}}
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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:

The table below provides information on the triggers of different subtypes of syncope:

Syncope

Triggers:

Vasovagal
Situational
Carotid Sinus
Atypical forms
  • Triggers can't be clearly identified.
  • Diagnosis is made upon exclusion or by reproduction of symptoms with tilt test

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
  • Vasovagal reaction caused by a standing position due to a decrease in venous return, with initial normal adaptation reflex.
POTS (postural orthostatic tachycardia syndrome)
  • Decreased venous flow of uncertain cause.

Cardiovascular Syncope

References

  1. ↑ Hainsworth, Roger (2004). "Pathophysiology of syncope". Clinical Autonomic Research. 14 (S1): i18–i24. doi:10.1007/s10286-004-1004-2. ISSN 0959-9851.
  2. ↑ 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.
  3. ↑ . doi:10.1016/j.pcad.2012.10.01. Missing or empty |title= (help)
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ Goldstein, David S.; Sharabi, Yehonatan (2009). "Neurogenic Orthostatic Hypotension". Circulation. 119 (1): 139–146. doi:10.1161/CIRCULATIONAHA.108.805887. ISSN 0009-7322.
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