Vasovagal syncope is characterized by the common faint, resulting from “vagally” mediated cardioinhibition. The resulting brady-cardia 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 vaso dilatory 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 ofvasovagal syncope include episodes occurringafter a painful or fearful stimulus. Patientsmay 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 andwill provoke a syncopal episode in susceptiblepersons. Most patients with vasovagal syncope can be evaluated in an outpatient setting. When there is a question about the syncope etiology or when immediate evaluationor treatment is needed, hospitalization isappropriate. Some indications for hospitalization include orthostatic hypotension, olderage, structural heart disease, symptoms associated with arrhythmias or ischemia, electro-cardiographic abnormalities or evidence ofnew stroke or focal neurologic findings. (Kapoor WN. Syncope. N Engl J Med December 21, 2000;343:1856–62).—r.s.