Neurocardiogenic syncope pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Neurocardiogenic syncope is defined as a syndrome in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral vasodilation.
It is caused by an abnormal or exaggerated autonomic response to various stimuli, commonly standing and emotion.[1][2] The underlying mechanism for this exaggerate autonomic response remains unclear; however, the activation of cardiac C fibres has shown to play role which subsequently causes reflex-mediated changes in the vascular tone and heart rate.[3]
On the contrary, failure of autonomic reflex response results in orthostatic hypotension.
Pathophysiology
References
- ↑ Krediet CT, van Dijk N, Linzer M, van Lieshout JJ, Wieling W (2002). "Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing". Circulation. 106 (13): 1684–9. PMID 12270863. Retrieved 2012-05-17. Unknown parameter
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ignored (help) - ↑ Lu CC, Diedrich A, Tung CS, Paranjape SY, Harris PA, Byrne DW, Jordan J, Robertson D (2003). "Water ingestion as prophylaxis against syncope". Circulation. 108 (21): 2660–5. doi:10.1161/01.CIR.0000101966.24899.CB. PMID 14623807. Retrieved 2012-05-17. Unknown parameter
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ignored (help) - ↑ Kapoor WN (2000). "Syncope". The New England Journal of Medicine. 343 (25): 1856–62. doi:10.1056/NEJM200012213432507. PMID 11117979. Retrieved 2012-05-17. Unknown parameter
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ignored (help)