Mahendr S. Kochar, MD, MS

Syncope is responsible for 1% to 6% ofhospital admissions and up to 3% of visitsto the emergency department (ED).

 Thissudden, brief loss of consciousness resultsfrom a decrease in or cessation of cerebralblood flow and is followed by spontaneousrecovery.

 The causes range from benignto life-threatening.

The more common types of syncope can be grouped into the following categories on the basis of the underlying mechanism of cerebral hypoperfusion:

Syncope resulting from orthostatic hypotension.

 the most frequently encountered types of syncope were vasovagal (the most common type of neurally mediated syncope) (21.2%), cardiac (9.5%), and syncope of unknown cause (36%). In another study, which included 650 patients, structural heart disease was identified as the cause of syncope in 11% of patients, arrhythmias in 7%, orthostatic hypotension in 24%, and a vasovagal mechanism in 37%.

 In younger patients without structural heart disease, syncope is most likely to be vasovagal.

 In this type of syncope, transient loss of consciousness results from a temporary failure of the autonomic nervous system to maintain an adequate heart rate and blood pressure. Included in this category are neurocardiogenic syncope (the vasovagal faint); syncope resulting from "situational" triggers, such as emotional stress, micturition, coughing, or anticipation of pain; and syncope caused by carotid sinus syndrome.

Neurocardiogenic, or vasovagal, syncope is characterized by reflexive vasodilatation and bradycardia.

 Patients may experience predominantly vasodilatation (vasodepressor response), predominantly bradycardia (cardioinhibitory response), or both. Neurocar- diogenic syncope may be preceded by fatigue, weakness, diaphoresis, nausea, abdominal discomfort, visual field changes, paresthesias, or feelings of depersonalization.

 This may be associated with organic heart disease (eg, aortic stenosis, hypertrophic cardiomyopathy, myocardial infarction, pulmonary embolism). It also can result from tachyarrhythmias (eg, ventricular tachycardia, torsade de pointes, supraventricular tachycardia) or bradyarrhythmias (eg, sinus node disease, second- or third-degree heart block, drug-induced bradycardia).

Syncope resulting from orthostatic hypotension. 

Orthostatic hypotension is generally defined as a reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg within 3 minutes of standing. Smaller decrements in blood pressure may be significant if they are associated with symptoms. Orthostatic hypotension results when the autonomic nervous system fails to overcome orthostatic stress or when circulating volume is decreased because of volume depletion. Table 1 lists the more common causes of orthostatic hypotension.

Ruling out other causes of transient loss of consciousness.

 Syncope must be distinguished from other conditions (such as seizure, transient ischemic attack, and hypoglycemia) that cause a transient loss of consciousness. These conditions can be excluded on the basis of the history, physical examination, and measurement of blood glucose levels. Table 2 includes clues in the history that suggest conditions other than syncope as the cause of a transient loss of consciousness.

 History taking, physical examination, and electrocardiography are the starting points for establishing the cause of syncope. In a prospective study, the cause was strongly suspected after the initial evaluation in 69% of patients. The history and physical findings alone led to the diagnosis in 38% of patients.

 Extensive laboratory testing has not been shown to provide additional diagnostic benefit.

 Table 2 lists typical elements in the history associated with various types of syncope.

 The physical examination should include cardiac auscultation, palpation and auscultation of carotid arteries for evidence of carotid stenosis, measurement of orthostatic blood pressure, and measurement of blood pressure and pulse in both arms. Cardiac auscultation may identify murmurs consistent with aortic stenosis, mitral stenosis, or hypertrophic cardiomyopathy. Particular attention should be paid to palpation of the carotid arteries and auscultation for bruits. Carotid sinus massage in patients with a history of stroke and in those in whom bruits are detected should be avoided because of the risk of plaque breakage and embolization. Significant differences in the blood pressure or pulse of the 2 arms may indicate  the presence of subclavian steal or aortic dissection.

Measure orthostatic blood pressure in all patients. 

 standardized measurement of orthostatic changes in the ED identified orthostatic hypotension as the probable cause of syncope in 24% of patients. Of those patients, orthostatic hypotension was drug-related in 58%, the result of hypovolemia in 22%, and postprandial in 12%; 28% of patients had idiopathic hypotension.

 This has been shown to reveal the cause of syncope on presentation in 5% of patients.

 Arrhythmias were identified as the cause of syncope in most of these patients. Although electrocardiography has a low yield, the test is relatively inexpensive and can be instrumental in identifying underlying structural heart disease. Detection of such abnormalities as first-degree heart block, bundle-branch block, and sinus bradycardia may point to bradycardia as the cause of syncope. Previous myocardial infarction or pronounced left ventricular hypertrophy in hypertrophic cardiomyopathy may be associated with ventricular tachycardia.

If the initial evaluation fails to yield the cause of syncope, it can be used to guide further diagnostic testing. Neurological imaging is generally not indicated unless focal neurological signs are present.

 By the time patients present to the ED after an episode of syncope, they are often asymptomatic. Some of these patients are nonetheless at increased risk for morbidity and mortality.	

Cardiac syncope is associated with significantly greater mortality than other types of syncope. In one study, mortality rates in patients with syncope that resulted from underlying arrhythmia or ischemia were double those in patients with syncope from any cause.

 Multivariate-adjusted hazard ratios among patients with syncope from any cause were 1.31 for death from any cause, 1.27 for myocardial infarction or death from coronary heart disease, and 1.06 for fatal and nonfatal stroke. The corresponding hazard ratios among patients with cardiac syncope were 2.01, 2.66, and 2.01, respectively.

Syncope of unknown cause was associated with an increased risk of death from any cause. Patients with vasovagal, orthostatic, or medication-induced syncope were at no higher risk for death from any cause, myocardial infarction, or coronary heart disease than were patients without syncope.

Thus, a main goal is to identify patients at higher risk for arrhythmias and sudden cardiac death who require hospital admission for evaluation and management. Significant risk factors for arrhythmia or sudden cardiac death at 1 year include an abnormal ECG (defined as ventricular tachycardia of 3 beats or more, sinus pause of 2 seconds or longer, symptomatic sinus bradycardia or supraventricular tachycardia, atrial fibrillation, third-degree heart block, or Mobitz type II heart block); age greater than 45 years;  and a history of ventricular arrhythmia; history of congestive heart failure.

In patients with no risk factors, the incidence of major arrhythmia ranged from 3.3% to 5.5%. In patients with 3 or 4 risk factors, the incidence ranged from 45.5% to 63.0%. One-year mortality rates ranged from 1.1% to 1.8% in patients with no risk factors to 27.3% to 37% in patients with 3 or 4 risk factors. Table 3 lists additional indications for hospitalization.

 In patients in whom the initial evaluation fails to definitively identify the cause of syncope, further evaluation may be indicated.

 Suspect arrhythmias in older patients and in those with heart disease. Ambulatory ECG monitoring using an event recorder or mobile outpatient telemetry is indicated in such patients. In patients at high risk for ventricular arrhythmia, consultation with a cardiologist is indicated. The cardiologist can perform an electrophysiologic study to detect ventricular tachycardia, sinus node dysfunction, atrioventricular block, or other arrhythmia.

Order an ECG to assess patients with heart murmurs consistent with obstructive lesions. Echocardiographic findings that may be diagnostic of the cause of syncope include:

Mean aortic gradient greater than 50 mm Hg or valve area of less than 0.9 cm (indicative of severe aortic stenosis).

Evidence of hypertrophic cardiomyopathy with outflow tract obstruction.

Mean pulmonary arterial pressure greater than 30 mm Hg (severe pulmonary hypertension).

Even if echocardiography in patients with unexplained syncope does not reveal any unsuspected cardiac abnormalities that might be the cause of the syncope, it can help identify those patients with documented or suspected cardiovascular disease who have systolic dysfunction (left ventricular ejection fraction, 40% or greater) and are thus at higher risk for ventricular arrhythmia.

 In patients at high risk for the development of coronary artery disease, order cardiac stress testing to rule out ischemia.

 A tilt-table test is used to detect neurocardiogenic syncope.

 Such tests have a sensitivity of 67% to 83% and a specificity of 75% to 100%. Tilt-table testing need not be performed in most patients whose symptoms suggest vasovagal syncope. Indications for testing include:

Presence of structural heart disease in conjunction with exclusion of cardiac causes of syncope.

Single episode of syncope in a patient with a high-risk occupation or hobby (eg, flying an airplane, operating heavy machinery, driving a commercial vehicle).

Syncope associated with significant injury.

When neurocardiogenic syncope occurs infrequently and in a patient who does not have a high-risk occupation or hobby, nonpharmacological treatment is usually sufficient. This includes instructing the patient to avoid predisposing conditions and to lie down at the onset of any prodromal symptoms. Isometric contractions of the extremities to augment venous return may be helpful. Increasing sodium and fluid intake may decrease the risk of syncope recurrence.

Patients who experience debilitating symptoms or significant injury and those who are involved in high-risk occupations need prophylactic therapy. Numerous interventions for syncope are available (Table 4); however, the data from randomized controlled trials (RCTs) are limited and sometimes conflicting.

Fludrocortisone (a mineralocorticoid that promotes sodium retention and raises blood pressure) and midodrine (an alpha sympathomimetic agent that causes vasoconstriction) are the 2 mainstays of drug treatment. Some experts use ß-blockers as first-line agents to treat neurocardiogenic syncope. These agents are purported to act by blocking the initial increase in adrenergic tone and its negative inotropic effects, thereby inhibiting the activation of left ventricular mechanoreceptors. Few randomized, double-blind, placebo-controlled studies support their use, however.

In one RCT, etilefrine, an α-agonist and potent vasoconstrictor, was not shown to be effective in preventing episodes of vasovagal syncope.

 In another RCT, the response to paroxetine was significant after 1 month of follow-up.

Dual-chamber pacemaker implantation may be an option for select patients with refractory vasovagal syncope of the predominantly cardioinhibitory type. In the North American Vasovagal Pacemaker Study, 54 patients with a lifetime history of 6 or more episodes of syncope and tilt-table- induced syncope or presyncope were randomly assigned to receive a dual-chamber pacemaker or no intervention. The risk of syncope was 85.4% lower in the pacemaker group than in the group that did not receive pacemakers.

These results were later corroborated by a prospective, controlled, multicenter study of 42 patients with a history of recurrent syncope and a positive cardioinhibitory response to tilt-table testing. The patients were randomly assigned to receive a device-device interaction pacemaker or no intervention and were observed for a minimum of 1 year. Syncope recurred in 1 patient (5%) in the pacemaker group after 15 months and in 14 patients (61%) in the group that did not receive pacemakers after 5 months (

Because these studies were not blind, their power was limited. A blind, placebo-controlled study by Connolly and colleagues

 found that pacemakers were not helpful as first-line therapy in patients with vasovagal syncope. However, pacemakers continue to be used in patients with refractory syncope.

. Patients with acute orthostatic hypotension require intravascular volume replacement. Medications known to cause or exacerbate orthostatic hypotension should be avoided. Patients with autonomic dysfunction may benefit from salt supplementation and elastic support stockings. Fludrocortisone has been used as a first-line agent; midodrine is also usually beneficial.

 Management of structural heart disease and refractory arrhythmias is the province of the cardiologist. Patients with significant arrhythmias who are unresponsive to antiarrhythmic medications require an implantable cardioverter defibrillator, a pacemaker, or both.   

 Goldschlager N, Epstein A, Grubb B, et al. Etiologic considerations in the patient with syncope and an apparently normal heart. 

 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. 

 Sarasin FP, Louis-Simonet M, Carballo D, et al. Prospective evaluation of patients with syncope: a population-based study. 

 Linzer M, Yang E, Estes M III, et al. Diagnosing syncope, part 1. 

 Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with syncope. 

 Krahn AD, Klein GJ, Raymond Y, Skanes A. Randomized assessment of syncope trial: conventional diagnostic testing versus a prolonged monitoring strategy. 

 Sarasin FP, Junod AF, Carballo D, et al. Role of echocardiography in the evaluation of syncope: a prospective study. 

 Benditt D, Ferguson D, Grubb B, et al. Tilt table for assessing syncope. American College of Cardiology. 

 Kapoor W. Using a tilt-table to evaluate syncope. 

 Madrid AH, Ortega J, Rebollo JG, et al. Lack of efficacy of atenolol for the prevention of neurally mediated syncope in a highly symptomatic population: a prospective, double-blind, randomized, and placebo-controlled study. 

 Raviele A, Brignole M, Sutton R, et al. Effect of etilefrine in preventing syncopal recurrence in patients with vasovagal syncope. 

 Di Girolamo E, Di Iorio C, Sabatini P, et al. Effects of paroxetine hydrochloride, a selective serotonin reuptake inhibitor, on refractory vasovagal syncope: a randomized, double-blind, placebo-controlled study.

 Connolly S, Sheldon R, Roberts R, Gent M. The North American Vasovagal Pacemaker Study (VPS). 

 Sutton R, Brignole M, Menozzi C, et al. Dual chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope. 

 Connolly SJ, Sheldon R, Thorpe KE, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope: Second Vasovagal Pacemaker Study (VPS II): a randomized trial.

 Linzer M, Yang E, Estes M III, et al. Diagnosing syncope, part 2: unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. 

Articles

Syncope is responsible for 1% to 6% ofhospital admissions and up to 3% of visitsto the emergency department (ED). Thissudden, brief loss of consciousness resultsfrom a decrease in or cessation of cerebralblood flow and is followed by spontaneousrecovery. The causes range from benignto life-threatening.

Author | Mahendr S. Kochar, MD, MS

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