Vasovagal response

Not to be confused with Vagovagal reflex.
Vasovagal episode

Classification and external resources
Specialty Neurologycardiovascular
ICD-10 R55
ICD-9-CM 78Ø.2
OMIM 609289
DiseasesDB 13777
MeSH D019462

A vagal episode or vasovagal response or vasovagal attack[1] (also called neurocardiogenic syncope[2]) is a malaise mediated by the vagus nerve. When it leads to fainting, also known as a "syncope", it is called a vasovagal syncope, which is the most common type of fainting.[3] Vasovagal syncope is most commonly found in adolescents and in younger adults.[4]

There are different syncope syndromes which all fall under the umbrella of vasovagal syncope. The common element among these conditions is the central mechanism which may lead to the loss of consciousness. The differences among them are in the factors that trigger this mechanism.

Signs and symptoms

Episodes of vasovagal response are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Prior to 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 (tinnitus), an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak/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 last for a few seconds before the loss of consciousness (if it is lost), which typically happens when the person is sitting up or standing.

When sufferers pass out, 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. Fainting occurs with a loss of oxygen to the brain.[5]

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

Cause

Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.[6]

Typical triggers for vasovagal episodes include:[7]

Pathophysiology

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.

This results in a spectrum of hemodynamic responses:

  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 vasodilation, 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.

Diagnosis

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 one of the most difficult challenges that a physician can face. The core of the diagnosis of vasovagal syncope rests upon a clear description by the patient of a typical pattern of triggers, symptoms, and time course. It is also pertinent to differentiate lightheadedness, seizures, vertigo, and hypoglycemia as other causes.

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

  1. A tilt table test (results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test)[16]
  2. Implantation of an insertable loop recorder
  3. A Holter monitor or event monitor
  4. An echocardiogram
  5. An electrophysiology study

Treatment

Treatment for vasovagal 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.

Prognosis

Brief periods of unconsciousness do no harm and are seldom symptoms of disease.

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.[25]

See also

References

  1. "vasovagal attack" at Dorland's Medical Dictionary
  2. According to World Journal of Cardiology article (World J Cardiol. 2010 Oct 26; 2(10): 308–315. Published online 2010 Oct 26. doi: 10.4330/wjc.v2.i10.308) "Management and therapy of vasovagal syncope: A review" by Muhammet Ali Aydin, Tushar V Salukhe, [...], and Stephan Willems: the term "neurocardiogenic syncope" is no longer appropriate to use.
  3. "Vasovagal syncope". MayoClinic.com. 2010-08-07. Retrieved 2012-07-06.
  4. "NEURO-CARDIOGENIC SYNCOPE" (PDF). NorthWest Ohio Cardiology Consultants: 1–2. March 2001.
  5. Ajamian, Paul C. "If patient faints, be laid back: what do you do when a patient passes out in your office? Lay the patient back to restore blood and oxygen to the brain." Review of Optometry 143.7 (July 15, 2006): 85(2). Nursing Resource Center. Gale. California State Univ East Bay. 13 Mar. 2013
  6. "Vasovagal syncope: Causes". MayoClinic.com. 2010-08-07. Retrieved 2012-07-06.
  7. "Vasomotor and vasovagal syncope". Heartdisease.about.com. Retrieved 2012-07-06.
  8. Shalev, A., Yehuda, R., & McFarlane, A. (2000). International handbook of human response to trauma. (pp. 263-264). New York: Kluwer Academic/Plenium Publishers.
  9. Hilhorst, John. "Approach to syncope: Is it cardiac or not??". Cardiology. Retrieved 7 October 2012.
  10. Zervou EK, Ziciadis K, Karabini F, Xanthi E, Chrisostomou E, Tzolou A (2005). "Vasovagal reactions in blood donors during or immediately after blood donation". Transfus Med 15 (5): 389–94. doi:10.1111/j.1365-3148.2005.00600.x. PMID 16202053.
  11. Low brain serotonin turnover rate (low CSF 5-HIAA) and impulsive violence. Virkkunen, Matti;Goldman, David;Nielsen, David A.;Linnoila, Markku Journal of Psychiatry & Neuroscience, Vol 20(4), Jul 1995, 271-275.
  12. Farb A, Valenti SA (1999). "Swallow syncope". Md Med J 48 (4): 151–4. PMID 10461434.
  13. fainting. (2005). In The Crystal Reference Encyclopedia. Retrieved from http://www.credoreference.com/entry/cre/fainting
  14. 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. PMC 3260536. PMID 19833552.
  15. Baird D, Dickson J, Jensen M, Talbot M (2012). "Syncope and profound bradycardia associated with intrauterine contraceptive procedures". BMJ 38 (3): 191–193. PMID 22253458.
  16. 1 2 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.
  17. 1 2 Durand, VM, and DH Barlow. 2006. Essentials of Abnormal Psychology 4th Edition. pp. 150.
  18. 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". Clin Physiol Funct Imaging 26 (1): 21–5. doi:10.1111/j.1475-097X.2005.00642.x. PMID 16398666.
  19. 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.
  20. 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.
  21. "The use of methylphenidate in the... [Pacing Clin Electrophysiol. 1996] - PubMed - NCBI". Ncbi.nlm.nih.gov. 2012-05-24. Retrieved 2012-07-06.
  22. Ali Aydin, Muhammet; Salukhe, Tushar; Wilkie, Iris; Willems, Stephan. "Management and therapy of vasovagal syncope: A review". PubMed. World J Cardiol. Retrieved 7 November 2014.
  23. "Vasovagal Syncope: What is it?". Retrieved 7 October 2012.
  24. Vasovagal Syncope Prognosis. MDGuidlines. Retrieved July 25, 2013.

External links

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