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Auton Neurosci. 2014 Sep;184:24-6. doi: 10.1016/j.autneu.2014.07.004. Epub 2014 Jul 16.

Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance.

Author information

1
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: QiFu@TexasHealth.org.
2
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, The University of Texas Southwestern Medical Center, Dallas, TX, USA.

Abstract

Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the most common cause of syncope in individuals without any structural heart disease. Based on traditional wisdom, loss of sympathetic tone with relaxation of vascular smooth muscle is the key mechanism underlying the pathophysiology of syncope, especially in patients without an acute decrease in heart rate. However, this concept has recently been challenged. Some microneurographic studies indicate that sympathetic withdrawal may not always be a prerequisite even for the development of classic "vasodepressor" forms of syncope. Conversely, a decrease in cardiac output appears to be a determinant factor for syncope in most circumstances. This article reviews the relative contribution of cardiac output versus sympathetic vasoconstriction in neurally mediated syncope in otherwise healthy individuals. It is suggested that a moderate to severe fall in cardiac output with or without vasodilatation may contribute to syncope.

KEYWORDS:

Heart rate; Hemodynamics; Stroke volume; Sympathetic activity; The autonomic nervous system; Vasovagal syncope

PMID:
25081417
PMCID:
PMC4139450
DOI:
10.1016/j.autneu.2014.07.004
[Indexed for MEDLINE]
Free PMC Article

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