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Syncope Workup

  • Author: Rumm Morag, MD, FACEP; Chief Editor: Erik D Schraga, MD  more...
Updated: Dec 07, 2015

Laboratory Studies

Currently, no specific testing has sufficient power to be absolutely indicated for evaluation of syncope. Thus, tests may not be necessary and can be tailored to any signs or symptoms that raise concern for a specific underlying illness. Research-based and consensus guideline recommendations are listed below.

Serum glucose level

In one study, 2 of 170 patients with syncope tested for serum glucose were found to be hypoglycemic.

Despite this low yield, rapid blood glucose assessment is easy, fast, and may be diagnostic, leading to efficient intervention.

Complete blood count (CBC)

If performed empirically, a CBC count has an exceedingly low yield in syncope. Some risk stratification protocols use a low hematocrit level as a poor prognostic indicator.

A prospective evaluation of syncope found that 4 of 170 patients had signs and symptoms of GI hemorrhage with a confirmatory CBC count. No occult bleeding was diagnosed based on an empiric CBC count in this study.

Anemia has been shown in several studies to suggest poor short-term outcomes.

Serum electrolyte levels with renal function

These tests if performed empirically have an exceedingly low yield in syncope. Some risk stratification protocols use electrolyte level abnormalities and renal insufficiency as poor prognostic indicators.

In the study by Martin et al, 134 patients with syncope had electrolytes drawn as part of the routine workup.[27] One patient was unexpectedly found to be hyponatremic secondary to diuretic use.

Serum electrolyte tests are indicated in patients with altered mental status or in patients in whom seizure is being considered.

If arrhythmia is noted, evaluation of electrolytes may be useful.

Cardiac enzymes

These tests are indicated in patients who give a history of chest pain with syncope, dyspnea with syncope, or exertional syncope; those with multiple cardiac risk factors; and those in whom a cardiac origin is highly suspected.

Total creatine kinase (CK)

A rise in CK levels may be associated with prolonged seizure activity or muscle damage secondary to a prolonged period of loss of consciousness.

Levels of B-type natriuretic peptide (BNP) over 300 pg/mL are a predictor of serious outcomes at 30 days.[20]


In elderly and debilitated patients, urinary tract infection (UTI) is common, easily diagnosed, and treatable and may precipitate syncope. UTIs may occur in the absence of fever, leukocytosis, and symptoms in this population.


Imaging Studies

Chest radiography

In elderly patients and in patients who are debilitated, pneumonia is common, easily diagnosed, and treatable and may precipitate syncope. Pneumonia may occur in the absence of fever, leukocytosis, and symptoms in this population.

Evaluation of a select number of etiologies of syncope may be aided by chest radiography. Pneumonia, congestive heart failure (CHF), lung mass, effusion, and widened mediastinum can all be seen if present and may guide therapy.

Head CT scanning (noncontrast)

Head computed tomography (CT) scanning is not indicated in a nonfocal patient after a syncopal event. This test has a low diagnostic yield in syncope.

Of 134 patients prospectively evaluated for syncope using CT scanning, 39 patients had abnormal findings on scans.[27] Only one head CT scan was diagnostic in a patient not expected to have intracranial pathology. Of the remaining scans, 5 showed subdural hematomas thought to be secondary to syncope.

Head CT scanning may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope.

Chest/abdominal CT scanning

This imaging study is indicated only in select cases, such as cases in which aortic dissection, ruptured abdominal aortic aneurysm, or pulmonary embolus is suspected.

Brain magnetic resonance imaging (MRI)/MR arteriography (MRA)

These tests may be required in select cases to evaluate vertebrobasilar vasculature and are more appropriately performed on an inpatient basis in consultation with a neurologist or a neurosurgeon.

Ventilation-perfusion (V/Q) scanning

This test is appropriate for patients in whom pulmonary embolus is suspected.


In patients with known heart disease, left ventricular function and ejection fraction have been shown to have an accurate predictive correlation with death.

Echocardiography is the test of choice for evaluating suspected mechanical cardiac causes of syncope.


Other Tests


Obtain a standard 12-lead electrocardiogram (ECG) in patients with syncope. This is a level A recommendation by 2007 ACEP consensus guidelines for syncope. ECG is used in most every clinical decision rule for risk stratification.

Normal ECG findings are a good prognostic sign.

ECG can be diagnostic for acute myocardial infarction (MI) or myocardial ischemia and can provide objective evidence of preexisting cardiac disease or dysrhythmia such as Wolff-Parkinson-White syndrome, Brugada syndrome, atrial flutter, or atrioventricular (AV) blocks.

Bradycardia, sinus pauses, nonsustained ventricular tachycardia and sustained ventricular tachycardia, and atrioventricular conduction defects occur with increasing frequency with age and are truly diagnostic only when they coincide with symptoms.

Holter monitor/loop event recorder

This is an outpatient test. In the past, all patients with syncope were monitored for 24 hours in a hospital. Later, loop recorders and signal-averaged event recorders allowed for monitoring over longer time periods, which increased the yield of detecting an arrhythmia.

Recent studies show that age-matched asymptomatic populations have an equivalent number of arrhythmic events recorded by ambulatory monitoring. Loop recorders have a higher diagnostic yield than Holter monitor evaluation with a marginal cost savings.[4]

A study completed through an ECG outpatient registry in Vermont by Gibson and Heitzman involving 1512 patients referred for syncope, showed that symptomatic arrhythmias were found in just 0.5% of patients.[5] In fact, patients had symptoms without arrhythmias more often than symptoms with arrhythmias, advancing the notion that ambulatory monitoring has a higher negative than positive diagnostic yield.

Head-up tilt-table test

This test is useful for confirming autonomic dysfunction and can generally be safely arranged on an outpatient basis.[1]

The test involves using a tilt table to stand a patient at 70 degrees for 45 minutes. Various modified protocols with concomitant medications, fasting, and maneuvers exist. Normally, norepinephrine (NE) levels initially rise, and they are maintained to hold blood pressure (BP) constant.

A positive result occurs when NE levels fatigue with time and a falling BP and pulse rate produce symptoms.

In the pediatric population, in conjunction with a detailed history and physical evaluation, the head-up tilt-table test may differentiate between presyncopal and syncopal episodes in children who present with seizurelike events.[28]

The head-up tilt-table test is less sensitive than electrophysiologic stress testing, and a negative result does not exclude the diagnosis of neurogenic syncope. In a study to evaluate whether a statistical model could be used for an early prediction of head-up tilt-table test outcome from heart rate variability and baroreflex sensitivity parameters in 105 Italian patients with a previous history of vasovagal syncope, investigators did not find any syncopal predictions that were of practical value.[29]


Electroencephalography (EEG) can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis.

Stress test

Stress test/electrophysiologic studies (EPS) have a higher diagnostic yield than the Holter monitor and should be obtained for any patient with a suspected arrhythmia as a cause of syncope.

A cardiac stress test is appropriate for patients in whom cardiac syncope is suspected and in whom have risk factors for coronary atherosclerosis. This test can assist with cardiac risk stratification and can guide future therapy.



Carotid sinus massage has been used with some success to diagnose carotid sinus syncope. Patients are placed on a cardiac monitor and beat-to-beat BP monitoring device. Atropine is kept at the bedside.

Longitudinal massage lasting 5 seconds is initiated at the point of greatest carotid pulse intensity at the level of the thyroid cartilage on one side at a time.

The maximal response occurs after approximately 18 seconds, and a positive result is one that produces 3 seconds of asystole or syncope. If the result is negative, the process is repeated on the other carotid sinus.

Carotid sinus massage may theoretically precipitate an embolic stroke in persons with preexisting carotid artery disease.

Contributor Information and Disclosures

Rumm Morag, MD, FACEP Member of Salem Emergency Physician Services, PC (SEPS), Salem Hospital

Rumm Morag, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

David A Peak, MD Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, American Medical Association

Disclosure: Partner received salary from Pfizer for employment.

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