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Chapter 15


Disclaimer: The opinions or assertions are those of the author and do not necessarily reflect the position of the Army Medical Department or the Department of Defense.


Syncope is the sudden transient loss of consciousness with a loss of postural tone. It is a common presenting complaint in the emergency department (ED). Despite improved understanding of risk and outcomes, consensus on the diagnostic approach and disposition remains elusive. This is in part because of the varied causes of syncope and lack of definitive diagnostic studies, and in part because of confusion and lack of standard terminology to describe the disorder.1 Diagnostic accuracy relies largely on the synthesis of patient risk factors and reported symptoms, with limited reliance on the physical examination and ancillary testing.


The prevalence of syncope in the general population is approximately 19%.2 Patients come to the ED at a rate of 2.8 visits per 1000 population, which accounts for 0.8% of ED visits.2,3 Approximately 32% of these patients are admitted, and syncope accounts for 1 to 6% of all hospitalized patients.2,4 Persons aged 65 years and older account for 80% of such admissions. In the pediatric population, 15% experience at least one episode of syncope.

Risk factors for syncope include cerebrovascular disease, cardiac medications, and hypertension.5 Most causes of syncope are benign and have favorable outcomes. Patients with preexisting cardiovascular disease and syncope from any cause are at the greatest short- and long-term risk of mortality.4,6 Age, congestive heart failure, and coronary artery disease are key predictors of mortality in patients with syncope, but syncope alone does not appear to alter risk.7 In contrast, there is no increased risk of cardiovascular morbidity or mortality associated with neurocardiogenic (vasovagal), orthostatic, and medication-related syncope.6 Recurrence of syncope may be as high as 50% and is not correlated with age or sex.2

Benign causes of syncope predominate in adolescents and young adults. Approximately 30% of athletes who have died during exercise, however, had a prior episode of syncope as a sentinel event.8 Prospective outcome studies in children are lacking, but most reports suggest that mortality rates are extremely low. Significant trauma may result from syncope and can contribute to increased risk of morbidity and mortality, particularly in the elderly.9 The overall U.S. medical cost of syncope is estimated at $2.4 billion annually.10


The final common pathway resulting in syncope is dysfunction of either both cerebral hemispheres or the brainstem (reticular activating system), usually from acute hypoperfusion. Reduced blood flow may be regional (cerebral vasoconstriction) or systemic (hypotension).11 Loss of consciousness results in loss of postural tone, with the resulting syncopal episode. Less severe derangements may result in sensations of presyncope or light-headedness. In this fashion, presyncope and syncope may be considered on a continuum with shared etiologies and mechanisms. By definition, syncope is transient; therefore the cause of central nervous system (CNS) dysfunction should likewise be transient.6,12 Persistent causes of significant CNS dysfunction result in coma or depressed consciousness (see Chapter 16).

Hypoperfusion resulting in approximately 35% or more reduction in cerebral blood flow usually produces unconsciousness, and any mechanism that adversely affects the components of perfusion (cardiac output, systemic vascular resistance, blood volume, regional vascular resistance) can cause or contribute to syncope. Other mechanisms of CNS dysfunction resulting in syncope include hypoglycemia, toxins, metabolic abnormalities, failure of autoregulation, and primary neurologic derangements.

Diagnostic Approach

Differential Considerations

The potential causes of syncope are numerous and can be categorized according to their primary mechanism (Box 15-1). The first differential diagnostic consideration is to distinguish syncope from other causes of an apparent sudden loss of consciousness, especially seizure and uncommon disorders such as cataplexy. When syncope is established as the working diagnosis, the life-threatening causes, primarily cardiovascular in origin, are considered first. The principal serious causes of syncope are dysrhythmias and myocardial ischemia.12 Cerebrovascular disease, principally subarachnoid hemorrhage, is less frequently encountered, but equally serious. Toxic-metabolic abnormalities may induce syncope through alterations in blood pressure or cardiac rhythm. Structural cardiac lesions, such as critical aortic stenosis, and sudden interruption of right ventricular outflow by pulmonary embolism can also cause sudden loss of consciousness.12 Dissection of the thoracic aorta rarely manifests primarily as syncope but is potentially catastrophic.

BOX 15-1   Causes of Syncope

Systemic Hypoperfusion Resulting in CNS Dysfunction

Outflow obstruction

Reduced cardiac output

Vasomotor—neurally mediated (reflex vasodepressor)

Carotid sinus sensitivity

Miscellaneous reflex

Other causes of hypoperfusion

Pivotal Findings

The majority of cases of syncope arise from benign causes, so the evaluation is largely focused on excluding serious pathology. The patient’s history, particularly the setting of the syncope (e.g., postmicturition, venipuncture), patient position (e.g., sitting, standing), prior episodes, and the presence or absence of prodromal symptoms, is central to separating benign from serious causes of the syncopal episode. Young, healthy patients with clearly benign syncope disclosed by a thorough history require little more than a physical examination for anemia or other benign precipitating factors.13–15 The yield of an electrocardiogram (ECG) is generally low; however, it is broadly recommended and has the additional advantages of being noninvasive and relatively inexpensive.1316 The clinical examination (history and physical examination) alone can suggest the diagnosis in 45% of cases.17 For a large portion of the remainder, however, a clear diagnosis for the syncope may not be established in the ED.17


Symptoms can often suggest the diagnosis, although the relative weight of the history diminishes in older patients and in those not able to remember clearly the events leading up to the loss of consciousness.18 The patient is asked to describe the character of the syncopal event.12 Witnesses may be able to supplement and corroborate the patient’s incomplete recall, and that history should be solicited. Key characteristics include the rate of onset (gradual or abrupt), position on symptom onset (e.g., standing, sitting, or supine), and duration and rate of recovery. Abrupt onset, occurrence while sitting or supine, and duration of more than a few seconds are usually ascribed to serious, often cardiac, causes of syncope, but firm data are lacking. Similarly, incomplete or near-syncope may be less serious, but at least one study suggests that onset associated with a prodrome or presyncope may herald cardiac origin, and thus the prognostic value of this aspect of the history is unsettled.18 The diagnostic approach to presyncope, however, is the same as for syncope.

Additional history regarding the events preceding the syncope is helpful.12 Occurrence during significant exertion suggests outflow obstruction, whereas occurrence after exercise or a prolonged exposure to heat stress suggests orthostasis. The myriad mechanisms that may mediate a neurocardiogenic response, including significant emotional events, micturition, eating, bowel movements, emesis, and movement or manipulation of the neck causing stimulation of the carotid sinus, should be addressed. Occurrence in supine position or the presence of acute palpitations is relatively specific for syncope of cardiac origin.18 Seizures may be preceded by an aura and followed by a typical postictal state.

Events during the syncopal episode do not usually clarify the cause.12 Tonic-clonic movements, related to inadequate cerebral perfusion, can occur in any form of syncope, including benign neurocardiogenic syncope, and should be differentiated from the prolonged activity with subsequent postictal depression of consciousness seen in seizure disorders (see Chapter 102). Trauma from a fall or other mechanism may distract the examiner from evaluating for the underlying syncope that caused the injury.9

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