Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance
Open accessAbstract
Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the 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.
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In some vasovagal syncope patients, reduced preload is not the main cause of symptoms, and peripheral vasodilation is important instead.
“In some patients, however, decreased preload does not play a dominant role in causing symptoms; instead, peripheral vasodilation plays an important role.”
From 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope (2015) · cites this paper as [81]
The Introduction reports that most presyncopal individuals had a moderate fall in cardiac output with coincident vasodilation, supporting an important role for vasodilation in some cases. The Contribution of cardiac output to syncope section also links reduced venous return to falling stroke volume; it does not establish that decreased preload is not the dominant cause of symptoms in those individuals. Page numbers are unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredBefore presyncope begins, sympathetic vasoconstriction and baroreflex sensitivity are well preserved, and muscle sympathetic nerve activity withdrawal occurs late after hypotension starts.
“Sympathetic vaso-constriction and baroreflex sensitivity prior to the onset of presyncope were well preserved, and muscle sympathetic nerve activity (MSNA) withdrawal occurred late after the onset of hypotension.”
From 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope (2015) · cites this paper as [81]
The section “Role of sympathetic activity and total peripheral resistance in syncope” says sympathetic withdrawal occurs at presyncope, well after the initial blood-pressure decrease. It does not establish that baroreflex sensitivity was preserved, and it reports that total peripheral resistance fell before the obvious MSNA reduction in most presyncopal individuals, rather than establishing preserved vasoconstriction generally. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFu and Levine found a moderate cardiac output decline with vasodilation in most presyncope participants, while a minority had no total peripheral resistance change during presyncope.
“Fu and Levine81 reported a moderate decline in cardiac output with coincident vasodilation in the majority of participants with presyncope and no changes in total peripheral resistance during presyncope in a minority of participants.”
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References 52 · Cited by 39
- Authors
- Fu, Q., & Levine, B. D.
- Affiliations
- Texas Health Dallas (US)
- Venue
- Autonomic Neuroscience
- Publisher
- Elsevier BV
- Published
- 2014-09
- Volume
- 184
- Pages
- 24-26
- ISSN
- 1566-0702 (ISSN-L)
- PMC
- PMC4139450
- OpenAlex
- W2009456931
- Semantic Scholar
- ed14601473ae1616300137361e1ca341d4f58a54
- Cited by
- 39
- References
- 52
- Citations by year
- 2025: 5 · 2023: 3 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 4 · 2014: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Autonomic Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL088184, HL075283, R21HL088184, K23HL075283)
- Topics
- Health Sciences › Medicine › Surgery › Cardiovascular Syncope and Autonomic Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- neurally mediated syncope, cardiac output, systemic vascular resistance, vasodepressor syncope, sympathetic vasoconstriction, sympathetic withdrawal, vasodilation, microneurography
- MeSH terms
- Animals, Cardiac Output, Humans, Syncope, Vascular Resistance
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