Neurocardiogenic syncope pathophysiology

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Neurocardiogenic Syncope Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]


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.[1][2]

It is caused by an abnormal or exaggerated autonomic response to various stimuli, commonly standing and emotion.[3][4] 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.[5] On the contrary, failure of autonomic reflex response results in orthostatic hypotension.

The pathogenesis for syncope in patients with hypersensitive carotid sinus and neurocardiogenic syncope remain the same with the only difference being the receptor involved to stimulate the brainstem nucleus.


The underlying mechanism of exaggerated autonomic response to various stimuli in patients with neurocardiogenic stimuli remains unclear. However, the activation of cardiac C-fibres has been implicated in the pathogenesis of neurocardiogenic syncope.[6]

Regardless of the triggers, the mechanism of syncope is similar among various vasovagal syncope syndromes.

Multiple triggering stimuli activate the nucleus tractus solitarius of the brainstem via the cardiac C fibres, which then results in the simultaneous enhancement of the parasympathetic nervous system (vagal) tone and withdrawal of the sympathetic nervous system tone.[7][5][8]

This results in a spectrum of hemodynamic responses:

  • On one end of the spectrum is the cardioinhibitory response caused by an increased vagal tone that is characterized by bradycardia and consequent hypotension that is significant enough to result in loss of consciousness.

As a result of increased vagal tone and vasodilation, subsequent decrease in venous return and cardiac output is observed which is significant enough to cause syncope or loss of consciousness.[9][10]

Neurocardiogenic Syncope

Triggers such as pain, post-exercise stimulate the sympathetic nervous system causing an increase in the sympathetic tone (tachycardia and increased cardiac contractility) which then causes reflex-mediated activation of the cardiac C fibres and brainstem nucleus to counterbalance these effects and results in an increased vagal tone and bradycardia.

Hypersensitive Carotid Sinus

Triggers such as carotid massage, rapid head turning cause stimulation of the carotid sinus and cardiopulmonary receptors which subsequently activate the brainstem nucleus to follow the common pathway of increased vagal tone and bradycardia.


  1. Grubb BP (2005). "Neurocardiogenic syncope and related disorders of orthostatic intolerance". Circulation. 111 (22): 2997–3006. doi:10.1161/CIRCULATIONAHA.104.482018. PMID 15939833. Retrieved 2012-05-17. Unknown parameter |month= ignored (help)
  2. Benditt DG, Ferguson DW, Grubb BP, Kapoor WN, Kugler J, Lerman BB, Maloney JD, Raviele A, Ross B, Sutton R, Wolk MJ, Wood DL (1996). "Tilt table testing for assessing syncope. American College of Cardiology". Journal of the American College of Cardiology. 28 (1): 263–75. PMID 8752825. Retrieved 2012-05-17. Unknown parameter |month= ignored (help)
  3. 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 |month= ignored (help)
  4. 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 |month= ignored (help)
  5. 5.0 5.1 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 |month= ignored (help)
  6. Fogoros RN. Practical cardiac diagnosis: electrophysiologic testing. 3 rd ed. Malden, MA: Blackwell Publishing, 1999
  7. Fogoros RN. Practical cardiac diagnosis: electrophysiologic testing. 3 rd ed. Malden, MA: Blackwell Publishing, 1999
  8. Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, van Dijk JG, Fitzpatrick A, Hohnloser S, Janousek J, Kapoor W, Kenny RA, Kulakowski P, Moya A, Raviele A, Sutton R, Theodorakis G, Wieling W (2001). "Guidelines on management (diagnosis and treatment) of syncope". European Heart Journal. 22 (15): 1256–306. doi:10.1053/euhj.2001.2739. PMID 11465961. Retrieved 2012-05-17. Unknown parameter |month= ignored (help)
  9. White CM, Tsikouris JP (2000). "A review of pathophysiology and therapy of patients with vasovagal syncope". Pharmacotherapy. 20 (2): 158–65. PMID 10678294. Retrieved 2012-05-17. Unknown parameter |month= ignored (help)
  10. Zaqqa M, Massumi A. Neurally mediated syncope. Tex Heart Institute J 2000;27: 268-72.

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