Syncope pathophysiology

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	Emotional distress: Fear Pain Blood fear Orthostatic stress
Situational	Coughing Sneezing Swallowing Defecation Visceral instrumentation Micturition Exercise
Carotid Sinus	Due to mechanical manipulation of the 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	Abnormalities among cardiac output and systemic vascular resistance (SVR)
Classic OH	Blood pooling due to autonomic nervous system failure, and inability to compensate with vasoconstriction, favoring decrease in SVR.
Delayed/Progressive OH	Progressive decrease in venous return, causing low cardiac output. Also failure of adaptation reflex.
Delayed Reflex syncope	Progressive decrease in venous return, with reactive vasovagal syncope causing vasodilation and bradycardia.
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

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.

[Hainsworth2004-1] Hainsworth, Roger (2004). “Pathophysiology of syncope”. Clinical Autonomic Research. 14 (S1): i18–i24. doi:10.1007/s10286-004-1004-2. ISSN 0959-9851.

[MoyaSutton2009-2] 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)

[Robertson2008-4] 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.

[MedowStewart2008-5] 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.

[GoldsteinSharabi2009-6] Goldstein, David S.; Sharabi, Yehonatan (2009). “Neurogenic Orthostatic Hypotension”. Circulation. 119 (1): 139–146. doi:10.1161/CIRCULATIONAHA.108.805887. ISSN 0009-7322.

[1]

[2]

[3]

[4]

[5]

[6]