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Reflex syncope in adults: Clinical presentation and diagnostic evaluation

Author
David Benditt, MD
Section Editor
Peter Kowey, MD, FACC, FAHA, FHRS
Deputy Editor
Brian C Downey, MD, FACC

INTRODUCTION

Syncope is a clinical syndrome in which transient loss of consciousness (TLOC) is caused by a period of inadequate cerebral nutrient flow, most often the result of an abrupt drop of systemic blood pressure. Reflex syncope (previously termed neurally-mediated syncope) is TLOC due to a reflex response that encompasses vasodilatation and/or bradycardia (rarely tachycardia), leading to systemic hypotension and cerebral hypoperfusion [1,2]. Types of reflex syncope include vasovagal syncope, situational syncope, carotid sinus syncope, and some cases without apparent triggers (table 1).

Vasovagal syncope is the most common cause of syncope [3]. Vasovagal syncope may be suggested or diagnosed by a specific history with well-known triggers, but a classic history is not required. Acute vasovagal reactions leading to syncope or presyncope are common also in a number of stressful settings, such as blood donation. The diagnosis can also be suggested by exclusion of other causes of syncope and by a characteristic response to upright tilt table testing during which the patient may become syncopal. In these cases, the syncope is due to hypotension which may be caused by severe bradycardia, vascular dilation (vasodepressor effect), or both. (See "Blood donor screening: Procedures and processes to enhance safety for the blood recipient and the blood donor", section on 'Vasovagal syncope'.)

The clinical presentation and diagnostic evaluation of patients with vasovagal syncope and situational syncope will be reviewed here. Discussions of the treatment of patients with reflex syncope, as well as the pathogenesis, etiology, evaluation and management of syncope in general, are discussed separately. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies" and "Syncope in adults: Clinical manifestations and diagnostic evaluation" and "Syncope in adults: Management" and "Reflex syncope in adults: Treatment".)

PATHOGENESIS OF REFLEX SYNCOPE

Understanding the pathophysiology involved in reflex syncope is essential to understanding its clinical manifestations and prevention strategies. Both neural (arterial and cardiac baroreceptor, including carotid sinus reflexes) and endogenous chemical pathways are thought to be involved (figure 1) [4].

The most frequent mechanism for reflex syncope is a mixed cardioinhibitory response combining cardioinhibitory and vasodepressor features, although an individual patient may have syncopal events characterized principally by vasodepressor, cardioinhibitory, or mixed responses. Typically the episodes can vary in their presentation for any individual such that asystole may occur at one time and hypotension at another.

                         
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Literature review current through: Oct 2017. | This topic last updated: Jul 31, 2017.
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