Syncope pathophysiology
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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
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.
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.
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:
- Vasovagal syncope
- Situtational syncope
- Carotid sinus syncope
- 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.
| Syncope |
Triggers: |
| Vasovagal |
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| Situational |
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| Carotid Sinus |
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| Atypical forms |
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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.
| 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 bradicardia. |
| Reflex syncope triggered by standing position |
Vasovagal reaction caused by standing position due to 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 decrease ability of the heart to pump blood and achieve an 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.
In bradyarrhythmia, such as AV block, the heart decreases the contractions per minute, which leads to a 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 a 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.