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Cited by 383Cardiovascular Syncope and Autonomic DisordersHeart Rate Variability and Autonomic ControlTakotsubo Cardiomyopathy and Associated Phenomena

The elusive pathophysiology of neurally mediated syncope

Mosqueda-Garcia, Rogelio, Furlan, Raffaello, MD, Jens Tank, Fernandez-Violante, Roxana·2000·Circulation
DOI 10.1161/01.cir.102.23.2898
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Abstract

yncope is defined as a sudden transient loss of conscious- ness and postural tone due to cerebral hypoperfusion.Although no permanent medical sequelae should result from syncope itself, isolated or recurrent events are often dramatic and disrupt the lifestyle of affected individuals.Syncope is a common clinical problem that affects up to 3.5% of the general population. 1 Strikingly, in close to 40% of cases, the exact cause of syncope remains elusive, and Ϸ30% of affected patients will experience recurrent episodes.1 Neurally mediated syncope (NMS) is a common type of syncope (Figure 1); clinical descriptions of it have been present in the medical literature for Ͼ100 years.Despite its prevalence, significant gaps in our understanding of its pathophysiology and treatment remain.The purpose of this review is to critically evaluate proposed theories that attempt to explain the pathophysiological mechanisms of NMS.

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Crossref · 10.1161/01.cir.102.23.2898

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  • A sudden fall in venous return lowers cardiac output and blood pressure, which baroreceptors sense and which triggers sympathetic vasoconstriction and venoconstriction with a rise in heart rate.

    “This abrupt reduction in venous return decreases cardiac output and blood pressure, which are rapidly sensed by the arterial and cardiopulmonary baroreceptors, thus triggering sympathetic noradrenergic vasoconstriction and venoconstriction accompanied by an increase in heart rate.73”

    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 [73]

    The Pathophysiology section (page unavailable) says that standing reduces venous return, cardiac output, and blood pressure, and that arterial and cardiopulmonary baroreceptors detect these changes. The Ventricular Theory section describes a reflex increase in sympathetic activity, peripheral resistance, and heart rate when blood pressure falls. Our copy does not specify venoconstriction as part of that response or characterize the vasoconstriction as noradrenergic. (LLM, conf=0.85)

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  • During a vasovagal syncope episode, an ineffective reflex response causes venous pooling in peripheral and/or splanchnic regions.

    “During a vasovagal syncope episode, an ineffective reflex response causes venous pooling in the periphery and/or splanchnic regions.73–76”

    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 [73]

    In “Pathophysiological Mechanisms in Postural NMS” (page unavailable), the review describes evidence suggesting increased peripheral pooling in people prone to syncope and reports a failure of reflex venoconstriction during exercise. It also cites evidence against exaggerated pooling. The paper does not establish that an ineffective reflex causes peripheral or splanchnic pooling during a syncope episode; the claim states a proposed, contested mechanism as fact. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The underlying pathophysiology of VVS results from a reflex causing hypotension and bradycardia, triggered by prolonged standing or exposure to emotional stress, pain, or medical procedures.

    “The underlying pathophysiology of VVS results from a reflex causing hypotension and bradycardia, triggered by prolonged standing or exposure to emotional stress, pain, or medical procedures (361–365).”

    From 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope (2017) · cites this paper as [361]

    The Classification section (page unavailable) describes syncope associated with standing or walking and says emotional stimulation can trigger autonomic changes. Pathophysiological Mechanisms in Postural NMS (page unavailable) reports marked hypotension but variable bradycardia, while Pathophysiology says the exact mechanism is not fully elucidated. The copy does not identify pain or medical procedures as triggers, so the claim is more definite and specific than this source supports. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Human studies with different subtypes of serotonin-receptor antagonists demonstrated a decreased tolerance to tilt.

    “Conversely, human studies with different subtypes of serotonin-receptor antagonists demonstrated a decreased tolerance to tilt. 1,282”

    From 2018 ESC Guidelines for the diagnosis and management of syncope (2018) · cites this paper as [1]

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Research works printed but not linked: 4

  1. [4]4. Maloney JD, Jaeger FJ, Fouad-Tarazi FM, et al. Malignant vasovagal syncope: prolonged asystole provoked by head-up tilt. Cleve Clin J Med. 1988;55:542-548.
  2. [14]14. Sharpey-Schafer EP. Emergencies in general practice: syncope. BMJ. 1956;1:506 -509.
  3. [20]20. Fitzpatrick AP, Williams T, Ahmed R, et al. Echocardiographic and endocrine changes during vasovagal syncope induced by prolonged head-up tilt. Eur JCPE. 1992;2:121-128.
  4. [69]69. Grubb BP, Gerard G, Roush K, et al. Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. Circulation. 1991;84: 1157-1164.

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Authors
Mosqueda-Garcia, R., Furlan, R., MD, J. T., & Fernandez-Violante, R.
Affiliations
  • From the Division of Clinical Pharmacology, DuPont Pharmaceuticals, Wilmington, Del (R.M.-G., R.F.-V.); Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale “L. Sacco,” Università di Milano, Italy (R.F.); and Clinic Bavaria Kreischa, Department of Diabetes and Endocrinology, Keischa, Germany (J.T.).
  • University of Milan (IT)
ORCID
Furlan, Raffaello
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2000-12-05
Volume
102
Issue
23
Pages
2898-2906
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.102.23.2898
OpenAlex
W2159580288
Semantic Scholar
23a2006b3e0ca3684e52378547aeb5ed93553960
Cited by
383
References
71
Citations by year
2026: 8 · 2025: 11 · 2024: 11 · 2023: 15 · 2022: 9 · 2021: 15 · 2020: 9 · 2019: 16 · 2018: 18 · 2017: 17 · 2016: 21 · 2015: 13 · 2014: 23 · 2013: 17 · 2012: 20
FWCI
2.08
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
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 › Cardiology and Cardiovascular Medicine › Takotsubo Cardiomyopathy and Associated Phenomena
Keywords
neurally mediated syncope, pathophysiology, cerebral hypoperfusion, recurrent syncope, loss of consciousness, postural tone, autonomic dysfunction
MeSH terms
Blood Volume, Cerebrovascular Circulation, Epinephrine, Heart Ventricles, Humans, Hypotension, Mechanoreceptors, Pressoreceptors, Renin, Serotonin, Vasodilation, Vasopressins, Baroreflex, Syncope, Vasovagal

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