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Vasovagal Syncope

Alexis M. Fenton, MD; Stephen C. Hammill, MD; Robert F. Rea, MD; Phillip A. Low, MD; and Win-Kuang Shen, MD
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Copyright ©2004 by the American College of Physicians


Ann Intern Med. 2000;133(9):714-725. doi:10.7326/0003-4819-133-9-200011070-00014
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Background: Vasovagal syncope is the most common type of syncope and is one of the most difficult types to manage.

Purpose: This article reviews the status of mechanisms, diagnosis, and management of vasovagal syncope.

Data Sources: MEDLINE search for English-language and German-language articles on vasovagal syncope published up to June 1999.

Study Selection: Case reports and series, clinical trials, research investigations, and review articles from peer-reviewed journals.

Data Extraction: Findings were summarized and discussed individually. Summaries were made in table format. Statistical analysis of combined data was inappropriate because of differences among studies in patient selection, testing, and follow-up.

Data Synthesis: The population of patients with vasovagal syncope is highly heterogeneous. Triggers of vasovagal syncope are likely to be protean, and many potential central and peripheral triggers have been identified. The specific mechanisms underlying the interactions among decreased preload, sympathetic and parasympathetic modulation, vasodilation, and cardioinhibition remain unknown. Tilt-table testing is a widely used diagnostic tool. The test results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test. Assessment of therapeutic outcomes has been difficult, primarily because of patient heterogeneity, the large number of pharmacologic agents available for therapy, and the sporadic nature of the syndrome complex.

Conclusions: Vasovagal syncope is a common clinical syndrome that has complex and variable mechanisms and is difficult to manage. Advancements are being made in laboratory investigations of its triggering mechanisms. Randomized, controlled trials of pharmacologic and nonpharmacologic interventions are needed. Mechanism-targeted therapeutic trials may improve clinical outcomes.

Figures

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Figure 1.
Autonomic nervous system regulation of cardiovascular hemodynamic responses.
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Figure 2.
Mechanisms of vasovagal response.

The Bezold–Jarisch reflex indicates that the neurocardiogenic reflex is initiated by the cardiac mechanoreceptor activation. The information is transmitted by the vagal afferents to the cardiovascular regulatory center in the medulla. The negative feedback response is transmitted by an activation of the vagal efferents and an inhibition of the sympathetic efferents. Input to the medulla may originate from extracardiac locations as well as directly from the higher central nervous system.

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Figure 3.
A vasovagal response induced by tilt-table testing and isoproterenol infusion in a patient who received a cardiac transplant.BPLeft.Middle.HRRight.(7)

Autonomic denervation and absent Bezold–Jarisch reflex are presumed. The top two tracings are from surface electrocardiogram leads 1 and aVL. The bottom tracing is a beat-to-beat arterial blood pressure ( ) tracing recorded from the radial artery. Hemodynamic responses at baseline in the tilted position. After isoproterenol infusion at 3 µg/min, the patient became hypotensive and syncopal without significant decrease in heart rate ( ). Hemodynamic values during recovery after the patient was returned to the supine position. Reproduced from Shen and Gersh with permission of the Mayo Foundation.

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Figure 4.
Clinical guidelines for vasovagal syncope therapy.

Blood pressure and heart rate values are typical baseline ambulatory values, not the values documented during tilt-table testing.

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