Syncope pathophysiology

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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 pathophysiology differs:

• 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	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). 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.

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.

References

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