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Key Points

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  • Place all patients with syncope on a cardiac monitor, obtain a STAT bedside glucose level, and check continuous pulse oximetry.

  • Obtain a detailed history of the events surrounding the episode, including pertinent data from any available bystanders such as family and emergency medical service personnel.

  • All patients with a syncopal episode require an electrocardiogram.

  • Admit all patients with risk factors for a cardiac etiology or alternative life-threatening conditions.

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Introduction

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Syncope is defined as a transient loss of consciousness with an inability to maintain postural tone. The event is classically followed by a spontaneous recovery to normal mentation. Between 12% and 48% of the U.S. population will experience a syncopal episode at some point in their lifetime. It is the presenting complaint in 1–3% of emergency department (ED) visits and accounts for 1–6% of hospital admissions. The etiology of syncope encompasses a wide variety of disorders ranging from the benign to the acutely life-threatening. Often the cause of syncope remains elusive within the ED. That said, a careful history and physical exam combined with the appropriate ancillary testing will help identify high-risk individuals who require hospital admission for further work-up and management.

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Syncope occurs secondary to impaired blood flow to either the reticular activating system or the bilateral cerebral hemispheres. Potential etiologies include transient systemic hypotension or isolated central nervous system (CNS) hypoperfusion (eg, subarachnoid hemorrhage). The reduction in cerebral perfusion produces unconsciousness and a loss of postural tone. A reflexive sympathetic response combined with the recumbent positioning of the patient results in restored cerebral perfusion and a return to a normal level of consciousness. Patients who experience the sensation of nearly “passing out” without an overt loss of consciousness are termed near-syncope or presyncope. From a clinical standpoint, both near-syncope and syncope are approached in the same manner.

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For clinical purposes, syncope is classified by etiology. Examples include neural mediated (reflex), orthostatic, cerebrovascular, and cardiac.

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Neurally mediated (reflex) syncope. Also referred to as “vasovagal syncope,” this occurs because of an excessive parasympathetic output in response to a stressful event. The resulting combination of bradycardia and vasodilation reduces the overall cardiac output and thereby inhibits adequate cerebral perfusion. Prodromal symptoms are common and include subjective feelings such as dizziness, warmth, or lightheadedness. Certain situations involving increased vagal tone such as forceful coughing, micturition, and defecation can also initiate this reflex.

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Orthostatic syncope. This occurs because of transient arterial hypotension after a positional change to either sitting upright or standing. The underlying mechanism depends on either significant volume depletion (bleeding, dehydration) or intrinsic autonomic dysfunction. Elderly patients tend to be the most prone to autonomic dysfunction secondary to blunted sympathetic responses and medication side effects.

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Cerebrovascular syncope. Cerebrovascular disorders are rarely the cause of syncope. That said, loss of consciousness can occur after a subarachnoid hemorrhage when the intracranial pressure rises ...

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