TY - JOUR
T1 - Pathophysiology of neurally mediated syncope
T2 - Role of cardiac output and total peripheral resistance
AU - Fu, Qi
AU - Levine, Benjamin D
N1 - Funding Information:
Some of the work included in this review was supported by grants from the National Institutes of Health ( HL075283 and HL088184 ).
PY - 2014/9
Y1 - 2014/9
N2 - 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.
AB - 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.
KW - Heart rate
KW - Hemodynamics
KW - Stroke volume
KW - Sympathetic activity
KW - The autonomic nervous system
KW - Vasovagal syncope
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U2 - 10.1016/j.autneu.2014.07.004
DO - 10.1016/j.autneu.2014.07.004
M3 - Article
C2 - 25081417
AN - SCOPUS:84906088456
SN - 1566-0702
VL - 184
SP - 24
EP - 26
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
ER -