Reflex syncope
Other namesNeurally mediated syncope, neurocardiogenic syncope[1][2]
Vagus nerve
SpecialtyNeurology, cardiovascular
SymptomsLoss of consciousness before which there may be sweating, decreased ability to see, ringing in the ears[1][2]
TypesVasovagal, situational, carotid sinus syncope[1]
Diagnostic methodBased on symptoms after ruling out other possible causes[3]
Differential diagnosisArrhythmia, orthostatic hypotension, seizure, hypoglycemia[1]
TreatmentAvoiding triggers, drinking sufficient fluids, exercise, cardiac pacemaker[2]
MedicationMidodrine, fludrocortisone[4]
Frequency> 1 per 1,000 people per year[1]

Reflex syncope is a brief loss of consciousness due to a neurologically induced drop in blood pressure and/or a decrease in heart rate.[5][6][7][8][9][10][2] Before an affected person passes out, there may be sweating, a decreased ability to see, or ringing in the ears.[1] Occasionally, the person may twitch while unconscious.[1] Complications of reflex syncope include injury due to a fall.[1]

Reflex syncope is divided into three types: vasovagal, situational, and carotid sinus.[2] Vasovagal syncope is typically triggered by seeing blood, pain, emotional stress, or prolonged standing.[11] Situational syncope is often triggered by urination, swallowing, or coughing.[2] Carotid sinus syncope is due to pressure on the carotid sinus in the neck.[2] The underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels, resulting in low blood pressure and thus not enough blood flow to the brain.[2] Diagnosis is based on the symptoms after ruling out other possible causes.[3]

Recovery from a reflex syncope episode happens without specific treatment.[2] Prevention of episodes involves avoiding a person's triggers.[2] Drinking sufficient fluids, salt, and exercise may also be useful.[2][4] If this is insufficient for treating vasovagal syncope, medications such as midodrine or fludrocortisone may be tried.[4] Occasionally, a cardiac pacemaker may be used as treatment.[2] Reflex syncope affects at least 1 in 1,000 people per year.[1] It is the most common type of syncope, making up more than 50% of all cases.[2]

Signs and symptoms

Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating), ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing.[citation needed]

When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense.[citation needed]

The autonomic nervous system's physiological state (see below) leading to loss of consciousness may persist for several minutes, so


Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows or blood pressure drops, the resulting lack of blood to the brain causes fainting.[12]


Typical triggers include:


Carotid sinus

Pressing upon a certain spot in the neck.[11] This may happen when wearing a tight collar, shaving, or turning the head.[11]


Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. The nucleus tractus solitarii of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.[citation needed]

This results in a spectrum of hemodynamic responses:[citation needed]

  1. On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate (negative chronotropic effect) and in contractility (negative inotropic effect) leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.
  2. On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure (to as low as 80/20) without much change in heart rate. This phenomenon occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone.
  3. The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.

One account for these physiological responses is the Bezold-Jarisch reflex.

Vasovagal syncope may be part of an evolved response, specifically, the fight-or-flight response.[16][17]


In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is difficult. The core of the diagnosis of vasovagal syncope rests upon a clear description of a typical pattern of triggers, symptoms, and time course.[citation needed]

It is pertinent to differentiate lightheadedness, seizures, vertigo, and low blood sugar as other causes.[citation needed]

In people with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:


Treatment for reflex syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the pathophysiologic mechanism described above.[citation needed]

Lifestyle changes


Types of long-term therapy for vasovagal syncope include[18]


Brief periods of unconsciousness usually cause no lasting harm to health. Reflex syncope can occur in otherwise healthy individuals, and has many possible causes, often trivial ones such as prolonged standing with the legs locked.[citation needed]

The main danger of vasovagal syncope (or dizzy spells from vertigo) is the risk of injury by falling while unconscious. Medication therapy could possibly prevent future vasovagal responses; however, for some individuals medication is ineffective and they will continue to have fainting episodes.[29]

See also


  1. ^ a b c d e f g h i j k Aydin MA, Salukhe TV, Wilke I, Willems S (26 October 2010). "Management and therapy of vasovagal syncope: A review". World Journal of Cardiology. 2 (10): 308–15. doi:10.4330/wjc.v2.i10.308. PMC 2998831. PMID 21160608.
  2. ^ a b c d e f g h i j k l m n o p q r Adkisson WO, Benditt DG (September 2017). "Pathophysiology of reflex syncope: A review". Journal of Cardiovascular Electrophysiology. 28 (9): 1088–1097. doi:10.1111/jce.13266. PMID 28776824. S2CID 39638908.
  3. ^ a b Brignole M, Benditt DG (2011). Syncope: An Evidence-Based Approach. Springer Science & Business Media. p. 158. ISBN 9780857292018.
  4. ^ a b c Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD, Grubb BP, Hamdan MH, Krahn AD, Link MS, Olshansky B, Raj SR, Sandhu RK, Sorajja D, Sun BC, Yancy CW (1 August 2017). "2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society". Circulation. 136 (5): e25–e59. doi:10.1161/CIR.0000000000000498. PMID 28280232.
  5. ^ Morillo CA, Eckberg DL, Ellenbogen KA, Beightol LA, Hoag JB, Tahvanainen KU, Kuusela TA, Diedrich AM. Vagal and sympathetic mecha-nisms in patients with orthostatic vasovagal syncope. Circulation. 1997;96: 2509–2513. doi: 10.1161/01.cir.96.8.2509
  6. ^ Abboud FM. Neurocardiogenic syncope. N Engl J Med. 1993: 1117–1120. doi: 10.1056/NEJM199304153281510
  7. ^ Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ.2004;329:336–341. doi: 10.1136/bmj.329.7461.336Abboud FM. Neuro-cardiogenic syncope. N Engl J Med. 1993;328:1117–1120. doi: 10.1056/NEJM199304153281510
  8. ^ Grubb BP. Clinical practice. Neurocardiogenic syncope. N Engl J Med.2005;352:1004–1010. doi: 10.1056/NEJMcp042601
  9. ^ Barón-Esquivias G, Cayuela A, Gómez S, Aguilera A, Campos A, Fernández M, Cabezón S, Morán JE, Valle JI, Martínez A, et al. [Quality of life in patients with vasovagal syncope. Clinical parameters influence]. Med Clin (Barc). 2003;121:245–249. doi: 10.1016/s0025-7753(03)75188-4
  10. ^ Zheng L, Sun W, Liu S, et al. The Diagnostic Value of Cardiac Deceleration Capacity in Vasovagal Syncope. Circ. Arrhythm. electrophysiol.. 2020;13(12):e008659. doi:10.1161/CIRCEP.120.008659, 10.1161/CIRCEP.120.008659
  11. ^ a b c d e f g "Syncope Information Page". National Institute of Neurological Disorders and Stroke. Retrieved 9 November 2017.
  12. ^ "Vasovagal syncope: Causes". 7 August 2010. Retrieved 10 August 2016.
  13. ^ Accurso V, et al. (August 2001). "Predisposition to Vasovagal Syncope in Subjects With Blood/Injury Phobia". Circulation. 104 (8): 903–907. doi:10.1161/hc3301.094910. PMID 11514377. S2CID 11022384. [1]
  14. ^ James G. Hamilton (August 1995). "Needle Phobia - A Neglected Diagnosis". Journal of Family Practice. 41 (2): 169–175 REVIEW. PMID 7636457.
  15. ^ Rossi S, Hallett M, Rossini PM, Pascual-Leone A (2009). "Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research". Clinical Neurophysiology. 120 (12): 2008–2039. doi:10.1016/j.clinph.2009.08.016. hdl:11572/145680. PMC 3260536. PMID 19833552.
  16. ^ Blanc JJ, Alboni P, Benditt DG (2015). "Vasovagal syncope in humans and protective reactions in animals". Europace. 17 (3): 345–9. doi:10.1093/europace/euu367. PMID 25662986.
  17. ^ Alboni P, Alboni M (2014). "Vasovagal Syncope As A Manifestation Of An Evolutionary Selected Trait". Journal of Atrial Fibrillation. 7 (2): 1035. doi:10.4022/jafib.1035 (inactive 31 January 2024). PMC 5135249. PMID 27957092.((cite journal)): CS1 maint: DOI inactive as of January 2024 (link)
  18. ^ a b Fenton AM, Hammill SC, Rea RF, Low PA, Shen WK (2000). "Vasovagal syncope". Ann. Intern. Med. 133 (9): 714–25. doi:10.7326/0003-4819-133-9-200011070-00014. PMID 11074905. S2CID 45453509.
  19. ^ a b Durand, VM, DH Barlow (2006). Essentials of Abnormal Psychology 4th Edition. Cengage Learning. p. 150. ISBN 978-1111836986. Retrieved 12 August 2016.
  20. ^ Hersen M (2005). Encyclopedia of Behavior Modification and Cognitive Behavior Therapy. SAGE. p. 30. ISBN 9780761927471.
  21. ^ a b Felgoise S, Nezu AM, Nezu CM, Reinecke MA (2006). Encyclopedia of Cognitive Behavior Therapy. Springer Science & Business Media. p. 291. ISBN 9780306485817.
  22. ^ France CR, France JL, Patterson SM (January 2006). "Blood pressure and cerebral oxygenation responses to skeletal muscle tension: a comparison of two physical maneuvers to prevent vasovagal reactions". Clinical Physiology and Functional Imaging. 26 (1): 21–5. doi:10.1111/j.1475-097X.2005.00642.x. PMID 16398666. S2CID 2763372.
  23. ^ Sheldon R, Connolly S, Rose S, Klingenheben T, Krahn A, Morillo C, Talajic M, Ku T, Fouad-Tarazi F, Ritchie D, Koshman ML (March 2006). "Prevention of Syncope (POST): a randomized, placebo-controlled study of metoprolol in the prevention of vasovagal syncope". Circulation. 113 (9): 1164–70. doi:10.1161/CIRCULATIONAHA.105.535161. PMID 16505178. S2CID 12778841.
  24. ^ Madrid AH, Ortega J, Rebollo JG, Manzano JG, Segovia JG, Sánchez A, Peña G, Moro C (February 2001). "Lack of efficacy of atenolol for the prevention of neurally mediated syncope in a highly symptomatic population: a prospective, double-blind, randomized and placebo-controlled study". J. Am. Coll. Cardiol. 37 (2): 554–9. doi:10.1016/S0735-1097(00)01155-4. PMID 11216978.
  25. ^ Grubb BP, Kosinski D, Mouhaffel A, Pothoulakis A (24 May 2012). "The use of methylphenidate in the treatment of refractory neurocardiogenic syncope". Pacing Clin Electrophysiol. 19 (5): 836–40. doi:10.1111/j.1540-8159.1996.tb03367.x. PMID 8734752. S2CID 34197462.
  26. ^ Ali Aydin M, Salukhe T, Wilkie I, Willems S (2010). "Management and therapy of vasovagal syncope: A review". World J Cardiol. 2 (10): 308–15. doi:10.4330/wjc.v2.i10.308. PMC 2998831. PMID 21160608.
  27. ^ Amy M. Karch. "epinephrine (adrenaline)". 2006 Lippincott's Nursing Drug Guide. Archived from the original on 29 June 2017. Retrieved 12 August 2016.
  28. ^ "Vasovagal Syncope: What is it?". Archived from the original on 3 January 2014. Retrieved 11 August 2016.
  29. ^ "Vasovagal Syncope Prognosis". MDGuidelines. Archived from the original on 3 July 2017. Retrieved 11 August 2016.