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Vasovagal syncope

Vasovagal syncope (also vasodepressor syncope, neurally mediated syncope or neurocardiogenic syncope), a form of dysautonomia, is the most common cause of fainting ("syncope" in medical terminology). Although it is particularly common (both historically and stereotypically) among young women, it is seen across all ages and genders and in otherwise completely healthy people. It is triggered by a number of factors, including prolonged standing, alcohol, fatigue, hunger, and anxiety. more...

VACTERL association
Van der Woude syndrome
Van Goethem syndrome
Varicella Zoster
Variegate porphyria
Vasovagal syncope
VATER association
Velocardiofacial syndrome
Ventricular septal defect
Viral hemorrhagic fever
Vitamin B12 Deficiency
VLCAD deficiency
Von Gierke disease
Von Hippel-Lindau disease
Von Recklinghausen disease
Von Willebrand disease

Vasovagal syncope is caused by low heart rate and blood pressure, leading to inadequate circulation. The reduced oxygen supply to the brain results in syncope, or temporary loss of consciousness. Individuals usually regain consciousness within a few minutes and their prognosis is good, although the syncope has a tendency to recur.


Prior to losing consciousness, the individual usually experiences symptoms such as nausea, inability to hear properly, difficulty speaking, exhaustion, tightness in the throat and blurry vision. Sweatiness and dizziness are also very common. These symptoms may last anywhere from seconds to minutes. This is followed by an episode of fainting; the individual regains consciousness within seconds to minutes. It is uncommon for vasovagal syncope to occur while the individual is lying down (supine); it normally occurs while standing or sitting.

During the episode, the individual will be unresponsive, and the pulse and blood pressure will be low. In some cases the individual may react violently while unconscious, this may be due to a fear response and increased adrenaline. The reaction may have the appearance of a seizure. Upon regaining consciousness, the individual may appear flushed and feel generally lethargic. The heart rate may still be slow, although it soon returns to normal.


In addition to vasovagal syncope, a number of other medical conditions may cause fainting. It is essential to perform a thorough history (interview of the patient) and physical examination. If there is no sign of other medical problems or causes of fainting, and the patient's description is consistent with or suggestive of vasovagal syncope, no diagnostic testing may be necessary. However, if the fainting is recurrent, a tilt table test is usually performed. In this test, the patient lies flat on a table and is then tilted upright so that blood pressure and heart rate may be observed and measured to identify any severe changes. This test is particularly effective in identifying patients suffering from sensitive nervous systems. Depending on the physician's level of suspicion, other tests, including an electrocardiogram, may be performed.


Vasovagal syncope is due to a disorder of autonomic control of the cardiovascular system. It commonly occurs in normal people of all ages. Precipitating factors include alcohol consumption, fatigue, pain, hunger, and prolonged standing. It can also be triggered by situations causing anxiety, such as having blood drawn, as well as by hot or crowded situations.

The initial responses appear to be venous pooling and increased activity of the sympathetic nervous system. This causes the heart to contract forcefully while relatively empty, triggering ventricular mechanoreceptors and vagal nerve fibers. This has the effect of reducing sympathetic activity while stimulating parasympathetic activity, resulting in bradycardia and vasodilation, followed by syncope.


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Vasovagal Syncope and Related Disorders
From American Family Physician, 4/1/00 by Richard Sadovsky

The management of patients in whom a primary abnormality in blood pressure regulation results in hypotension and loss of consciousness presents clinical challenges. The hypotension may be primary, or it may be secondary to a condition such as tachyarrhythmia or bradyarrhythmia. Vasovagal syncope describes this condition, as well as other conditions that are considered to be dysautonomic responses to upright posture, such as orthostatic hypotension and postural orthostatic tachycardia syndrome (POTS). Bloomfield and associates reviewed the pathophysiology of these two causes of syncope and developed an algorithm to guide diagnosis and treatment.

In patients with vasovagal syncope, the initial cardiovascular response to an upright posture appears to be relatively normal. Syncope occurs after an abrupt decrease in blood pressure, sometimes accompanied by a marked decrease in heart rate after a delayed period of head-up tilt, which triggers blood pooling in the lower extremities. The mean time to syncope in patients undergoing a tilt-table test is 25 minutes. The dysautonomic response occurs in the presence of a failing autonomic system. Patients with this condition are unable to compensate for the acute decrease in venous return that occurs with upright position, causing orthostatic hypotension. This failure to compensate can occur immediately or be delayed because of blood pooling in the lower extremities. The difference in mechanisms causing vasovagal syncope and the dysautonomic response result in different treatment considerations. For an algorithm detailing diagnosis and treatment of vasovagal syncope and related disorders, see the accompanying figure on page 2212.

Approaches to treatment must take into account the patient's quality of life and the extent of risk factors present. Patients who have experienced only one or two episodes may require only education and counseling. Factors associated with increased risk of recurrent syncope include the absolute number of prior episodes, a shorter length of time between recurrences and recurrence after a tilt-table test. Other at-risk factors include syncope that develops without warning or prodromal symptoms, especially in persons who work as truck drivers or pilots.

The initial approach to treatment involves education about ways to avoid syncopal episodes. Adjusting potentiating medications, including peripherally active alpha antagonists and nitrates, can be useful in preventing recurrences when clinically possible. An assessment of volume status and an increase in

dietary salt may also reduce syncopal episodes. Empiric therapy with beta blockers or fludrocortisone can be initiated without a tilt-table test in patients with vasovagal syncope, and therapy with fludrocortisone or midodrine is indicated in patients with suspected orthostatic intolerance. Assessment of treatment efficacy should emphasize reducing symptoms and assessing side effects. Treatment for 12 months is reasonable, at which time medication is stopped or tapered.

The authors conclude that a patient's hemodynamic response to standing should be part of all routine examinations and that tilt-table testing may be useful in establishing a diagnosis and guiding treatment of vasovagal syncope. Two abnormalities may occur with standing: (1) POTS, defined as an excessive increase in heart rate (greater than 30 beats per minute or a heart rate of greater than 120 beats per minute) with or without syncope and (2) orthostatic hypotension, defined as a decrease in systolic pressure of 20 mm Hg or a decrease in diastolic pressure of 10 mm Hg within three minutes of standing. Education, reassurance and an increase in dietary salt may be sufficient treatment in many patients. POTS can be treated empirically with beta blockers, salt and fludrocortisone. Orthostatic hypotension can be treated with volume expansion therapy with salt and fludrocortisone and vasoconstrictor therapy with midodrine. Evidence of a dysautonomic response, in which the patient's blood pressure decreases without a significant increase in heart rate, suggests autonomic failure and is treated with fludrocortisone or midodrine.


Bloomfield DM, et al. Putting it together: a new treatment algorithm for vasovagal syncope and related disorders. Am J Cardiol October 21, 1999;84:33Q-9Q.

COPYRIGHT 2000 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group

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