Vasovagal response

From Wikipedia, the free encyclopedia - View original article

Vasovagal episode
Classification and external resources

Vagus nerve
ICD-10R55
ICD-978Ø.2
DiseasesDB13777
MeSHD019462
 
Jump to: navigation, search
Vasovagal episode
Classification and external resources

Vagus nerve
ICD-10R55
ICD-978Ø.2
DiseasesDB13777
MeSHD019462


A vasovagal episode or vasovagal response or vasovagal attack[1] (also called neurocardiogenic syncope) is a malaise mediated by the vagus nerve. When it leads to syncope or "fainting", it is called a vasovagal syncope, which is the most common type of fainting.[2]

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

Contents

Signs and symptoms

Among people with vasovagal episodes, the episodes are typically recurrent, usually happening when the person is exposed to a specific trigger. Prior to losing consciousness, the individual frequently experiences a prodrome of symptoms such as lightheadedness, nausea, the feeling of being extremely hot (accompanied by sweating), ringing in the ears (tinnitus), uncomfortable feeling in the heart, fuzzy thoughts, 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, and sometimes a feeling of nervousness can occur as well. These last for at least a few seconds before consciousness is lost (if it is lost), which typically happens when the person is sitting up or standing. When sufferers pass out, they fall down (unless this is impeded); and when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. Short of fainting a person may experience an almost indescribable weak and tired feeling resulting from a lack of oxygen to the brain due to a sudden drop in blood pressure. Taber's Cyclopedic Medical Dictionary[3] describes this as the "feeling of impending death" caused by expansion of the aorta, drawing blood from the head and upper body.

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.[4]

Typical triggers for vasovagal episodes include:[5]

Pathophysiology

Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. In it, the nucleus tractus solitarius 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
  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. MD Guidelines

See also

References

  1. ^ "vasovagal attack" at Dorland's Medical Dictionary
  2. ^ "Vasovagal syncope". MayoClinic.com. 2010-08-07. http://www.mayoclinic.com/health/vasovagal-syncope/DS00806. Retrieved 2012-07-06. 
  3. ^ Thomas, Clayton L. (1993). Taber's Cyclopedic Medical Dictionary (18 ed.). F.A. Davis. ISBN 0-8036-0194-8. 
  4. ^ "Vasovagal syncope: Causes". MayoClinic.com. 2010-08-07. http://www.mayoclinic.com/health/vasovagal-syncope/DS00806/DSECTION=causes. Retrieved 2012-07-06. 
  5. ^ "Vasomotor and vasovagal syncope". Heartdisease.about.com. http://heartdisease.about.com/cs/arrhythmias/a/Syncope2_2.htm. Retrieved 2012-07-06. 
  6. ^ "Vasovagal Syncope Causes, Symptoms, and Treatment on". Medicinenet.com. 2008-05-16. http://www.medicinenet.com/script/main/art.asp?articlekey=89547. Retrieved 2012-07-06. 
  7. ^ USA (2012-05-24). "Vasovagal reactions in blood donors during or i... [Transfus Med. 2005] - PubMed - NCBI". Ncbi.nlm.nih.gov. http://www.ncbi.nlm.nih.gov/pubmed/16202053. Retrieved 2012-07-06. 
  8. ^ 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.
  9. ^ Swallow syncope. Farb A, Valenti SA. Md Med J. 1999 Jul-Aug;48(4):151-4.
  10. ^ http://www.swallowsyncope.com/
  11. ^ a b Durand, VM, and DH Barlow. 2006. Essentials of Abnormal Psychology 4th Edition. pp. 150.
  12. ^ 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. 
  13. ^ Sheldon R, Connolly S, Rose S et al. (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. 
  14. ^ Madrid AH, Ortega J, Rebollo JG et al. (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. 
  15. ^ USA (2012-05-24). "The use of methylphenidate in the... [Pacing Clin Electrophysiol. 1996] - PubMed - NCBI". Ncbi.nlm.nih.gov. http://www.ncbi.nlm.nih.gov/pubmed/8734752. Retrieved 2012-07-06. 
  16. ^ [1][dead link]

External links