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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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Evaluation and Management of Vasovagal Syncope
From American Family Physician, 5/15/01 by Richard Sadovsky

Vasovagal syncope is characterized by the common faint, resulting from "vagally" mediated cardioinhibition. The resulting bradycardia reduces cerebral blood flow to a level inadequate to maintain consciousness. Because of the episodic nature of vasovagal syncope and the heterogeneity of the patient population, it is difficult to make specific therapy recommendations. Fenton and associates reviewed the current understanding of vasovagal syncope to provide a diagnostic and therapeutic approach.

The vagus nerve transmits afferent signals from the aortic arch baroreceptors, regulating arterial pressure. Increases in arterial flow stimulate efferent vagal outflow, inhibiting sympathetic drive and decreasing blood pressure. Assumption of an upright position with pooling of blood in the lower extremities activates this autonomic cycle and results in increased sympathetic tone to the vasculature and heart, causing vasoconstriction, increased heart rate and maintenance of blood pressure.

The vasovagal response is caused by excessive venous pooling that paradoxically results in vasodilatation and bradycardia rather than the appropriate physiologic responses of vasoconstriction and tachycardia. Other modulating factors that may be present during syncope include serotonin, adenosine and opioids. Nitric oxide has also been implicated in the vasodilatory response associated with vasovagal syncope.

Vasovagal syncope usually has a gradual onset, although sudden loss of consciousness without warning can occur. Precipitating factors may be the sight of blood, a loss of blood, sudden stress or pain, surgical manipulation or trauma. Before the syncopal event, the patient may report weakness, lightheadedness, yawning, nausea, diaphoresis, hyperventilation, blurred vision or impaired hearing. Sitting or lying down may abort the syncopal episode.

There are no specific physical signs related to vasovagal syncope. Tilt-table testing provokes venous pooling and resultant vasovagal syncope. Pharmacologic agents used to emphasize this effect are not well standardized. Testing is warranted in patients whose syncope is uncertain to be vasovagal and in patients with one or more of the following indications: (1) recurrent syncope, (2) a single syncope episode associated with injury, (3) a single syncope episode associated with a high-risk setting, or (4) syncope of another established cause whose treatment might be affected by vasovagal syncope. Head-up tilt-table testing is contraindicated in patients with critical obstructive cardiac disease (such as critical proximal coronary artery stenosis, critical mitral stenosis or severe left ventricular outflow obstruction) or critical cerebrovascular stenosis.

Treatment is empiric because the specific physiologic triggers of vasovagal syncope are largely unidentified. Infrequent episodes require only counseling and observation. Hydration and salt intake may need to be increased, especially in warm weather. Pharmacologic treatment options include beta-adrenergic blockers, anticholinergic agents, adenosine receptor blockers, selective serotonin reuptake inhibitors, mineralocorticoids and anticonvulsants. The use of compression hose and pacemakers has been recommended.

The authors conclude that beta blockers are probably the appropriate first-line agent in most cases of vasovagal syncope because of their antagonistic actions to catecholamines. Clinical guidelines for can be based on blood pressure and vital signs (see accompanying figure). A conservative nondrug approach should be used in patients with infrequent occurrences and recognizable prodromal symptoms. The role of pacing is unclear at present. Counseling about avoidance of volume depletion is important for all patients with vasovagal syncope.

EDITOR'S NOTE: Common presentations of vasovagal syncope include episodes occurring after a painful or fearful stimulus. Patients may faint after prolonged standing or exertion. A tilt-table test is the best diagnostic test; the hemodynamic and catecholamine response during the test simulates those occurring during a vasovagal syncopal episode and will provoke a syncopal episode in susceptible persons. Most patients with vasovagal syncope can be evaluated in an outpatient setting. When there is a question about the syncope etiology or when immediate evaluation or treatment is needed, hospitalization is appropriate. Some indications for hospitalization include orthostatic hypotension, older age, structural heart disease, symptoms associated with arrhythmias or ischemia, electrocardiographic abnormalities or evidence of new stroke or focal neurologic findings. (Kapoor WN. Syncope. N Engl J Med December 21, 2000;343: 1856-62).--R.S.

COPYRIGHT 2001 American Academy of Family Physicians
COPYRIGHT 2001 Gale Group

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