Syncope

Overview

Practice Essentials Syncope is defined as a transient, self-limited loss of consciousness [1] with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients. Signs and symptoms History and physical examination are the most specific and sensitive ways of evaluating syncope. These measures, along with 12-lead electrocardiography (ECG), were the only current level A recommendations listed in the 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope. [2] A detailed account of the event must be obtained from the patient, including the following:

• Precipitating factors

• Activity the patient was involved in before the event

• Position the patient was in when the event occurred

The following questions should be asked:

• Was loss of consciousness complete?

• Was loss of consciousness with rapid onset and short duration?

• Was recovery spontaneous, complete, and without sequelae?

• Was postural tone lost?

If the answers are positive, syncope is highly likely; if 1 or more are negative, other forms of loss of consciousness should be considered. [3] Presyncopal symptoms reported may include the following:

• Prior faintness, dizziness, or light-headedness (70% of cases of true syncope)

• Prior vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias

• Red flag symptoms - Exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria

Other information that should be obtained includes the following:

• Detailed account of the event from any available witnesses (eg, whether patient experienced postevent confusion)

• Patient’s medication history

• Patient’s personal or familial medical history of cardiac disease

A complete physical examination is required, with particular attention to the following:

• Analysis of vital signs

• Measurement of the glucose level by rapid fingerstick

• Detailed cardiopulmonary examination

• Detailed neurologic examination

• Assessment for signs of trauma

• Stool guaiac examination (if appropriate, based on the patient's history)

Diagnosis No specific laboratory testing has sufficient power to be absolutely indicated for evaluation of syncope. 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 as follows:

• Serum glucose

• Complete blood count

• Serum electrolytes

• Cardiac enzymes

• Total creatine kinase

• Urinalysis/dipstick

Imaging studies that may be helpful include the following:

• Chest radiography - May serve to identify pneumonia, congestive heart failure (CHF), lung mass, effusion, or widened mediastinum

• Computed tomography (CT) of the head (noncontrast) - Has a low diagnostic yield in syncope but may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope

• CT of the chest and abdomen - Indicated only in select cases (eg, suspected aortic dissection, ruptured abdominal aortic aneurysm, or pulmonary embolism [PE])

• Magnetic resonance imaging (MRI) of the brain and magnetic resonance arteriography (MRA) - May be required in select cases to evaluate vertebrobasilar vasculature

• Ventilation-perfusion (V/Q) scanning - Appropriate for suspected PE

• Echocardiography - The test of choice for evaluating suspected mechanical cardiac causes of syncope

A standard 12-lead ECG is a level A recommendation in the 2007 ACEP consensus guidelines for syncope. [2] The following considerations are relevant:

• Normal ECG findings are a good prognostic sign

• ECG can be diagnostic for acute myocardial infarction or myocardial ischemia and can provide objective evidence of preexisting cardiac disease or dysrhythmia

• Bradycardia, sinus pauses, nonsustained ventricular tachycardia and sustained ventricular tachycardia, and atrioventricular conduction defects are truly diagnostic only when they coincide with symptoms

• Loop recorders have a higher diagnostic yield than Holter monitor evaluation, with a marginal cost savings [4]

• Ambulatory monitoring appears to have a higher negative than positive diagnostic yield [5]

Other diagnostic tests and procedures include the following:

• Head-up tilt-table test - Useful for confirming autonomic dysfunction and can generally be safely arranged on an outpatient basis

• Electroencephalography (EEG) - Can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis

• Stress test - A cardiac stress test is appropriate for patients in whom cardiac syncope is suspected and who have risk factors for coronary atherosclerosis

• Carotid sinus massage (to diagnose carotid sinus syncope)

Management Prehospital management of syncope may require the following:

• Intravenous access

• Oxygen administration

• Advanced airway techniques

• Glucose administration

• Pharmacologic circulatory support

• Pharmacologic or mechanical restraints

• Defibrillation or temporary pacing

Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases. In patients brought to the emergency department with a presumptive diagnosis of syncope, appropriate initial interventions may include the following:

• IV access, oxygen administration, and cardiac monitoring

• ECG and rapid blood glucose evaluation

The treatment choice for syncope depends on the cause or precipitant of the syncope, as follows:

• Situational syncope - Patient education regarding the condition

• Orthostatic syncope - Patient education; additional therapy in the form of thromboembolic disease (TED) stockings, mineralocorticoids, and other drugs (eg, midodrine); elimination of drugs associated with hypotension; intentional oral fluid consumption

• Cardiac arrhythmic syncope - Antiarrhythmic drugs or pacemaker placement

• Cardiac mechanical syncope - Beta blockade; if valvular disease is present, surgical correction
  

Background Syncope is defined as a transient, self-limited loss of consciousness [1] with an inability to maintain postural tone that is followed by spontaneous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness. Syncope is a prevalent disorder, accounting for 1-3% of emergency department (ED) visits and as many as 6% of hospital admissions each year in the United States. As much as 50% of the population may experience a syncopal event during their lifetime. Although many etiologies for syncope are recognized, categorization into reflex (neurally mediated), orthostatic, and cardiac (cardiovascular) may be helpful during the initial evaluation. Cardiac syncope is associated with increased mortality, whereas noncardiac syncope is not. Syncope may result in significant morbidity and disability due to falls or accidents that occur as a result. [6] In the United States alone, an estimated $2 billion annually is spent on patients hospitalized with syncope. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients. It is unclear whether hospital inpatient admission of asymptomatic patients after syncope affects outcomes. No current criterion standard exists for diagnosing undifferentiated syncope. Many physicians continue to admit patients because of perceived risk. Reviews of the 2001 American College of Emergency Physician (ACEP) clinical policy suggested that evidence-based criteria may decrease admission rates by nearly half by identifying cardiac causes of syncope. Inpatient admission should be reserved for patients in whom identification of specific immediate risk is needed (eg, those with structural heart disease or a history of ventricular arrhythmia). Outpatient management can be used for patients who are at low risk for a cardiac etiology to define a precise cause so that mechanism-specific treatment can be effected.

Pathophysiology Syncope occurs as a consequence of global cerebral hypoperfusion. [1] Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of the high-energy phosphates found elsewhere in the body; consequently, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope. Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output (CO), systemic vascular resistance (SVR), mean arterial pressure (MAP), intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these systems or subclinical defects in several of them may cause syncope. CO can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. SVR can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. MAP decreases with all causes of hypovolemia. Medications can affect CO, SVR, or MAP. Other conditions can mimic syncope. A central nervous system (CNS) event, such as a hemorrhage or an unwitnessed seizure, can present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia, hypercarbia).

Etiology Cardiac (cardiopulmonary) syncope may be due to vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction and predicts a worse short-term and long-term prognosis. Obtaining an initial electrocardiogram (ECG) is mandatory if any of these causes are possible for the differential diagnosis. Low flow states, such as those associated with advanced cardiomyopathy, congestive heart failure (CHF) , and valvular insufficiency, may result in hypotension and cause transient global cerebral hypoperfusion. Often, these patients are on medications that reduce afterload, which may contribute to the cause of syncope. Ventricular arrhythmias, such as ventricular tachycardia and torsade de pointes, tend to occur in older patients with known cardiac disease. These patients tend to have fewer recurrences and have a more sudden onset with few, if any, presyncopal symptoms. Associated chest pain or dyspnea may be present. This type of syncope is generally unrelated to posture and can occur during lying, sitting, or standing. Often, these arrhythmias are not revealed on the initial ECG but may be captured with prolonged monitoring. Supraventricular tachyarrhythmias include supraventricular tachycardia and atrial fibrillation with rapid response. These may be associated with palpitations, chest pain, or dyspnea. Patients typically have prodromal symptoms and may have syncope while attempting to stand or walk because of resultant hypotension. These symptoms may spontaneously resolve prior to evaluation but are often noted during initial triage and assessment. Be sure to scrutinize ECG findings for evidence of Wolff-Parkinson-White syndrome, Brugada syndrome, and long QT syndrome. Bradyarrhythmias include sick sinus syndrome, sinus bradycardia, high-grade atrioventricular blocks, pacemaker malfunction, and adverse medication reactions. Generally, these patients have a history of cardiac problems and are symptomatic. Chest pain, dyspnea, decreased exercise tolerance, and fatigue may all be present. Consider cardiac ischemia and medication side effects as additional causes. Cardiac outflow obstruction may also result in sudden-onset syncope with little or no prodrome. One critical clue is the exertional nature, and the other is the presence of a cardiac murmur. Young athletes may present with this etiology for syncope. Specific pathology includes aortic stenosis, hypertrophic obstructive cardiomyopathy, mitral stenosis, pulmonary stenosis, pulmonary embolus, left atrial myxoma, and pericardial tamponade. Syncope can also result from an acute myocardial infarction (MI), acute aortic dissection, and pulmonary embolus. These conditions can have associated chest pain, neck pain, shoulder pain, dyspnea, epigastric pain, hypotension, alteration of mental status and can result in sudden death. Reflex (neurally mediated) syncope may be due to vasovagal syncope, which is mediated by emotional distress such as fear or physical pain. Situational syncope describes syncope that occurs with a fixed event such as micturition, deglutition, exercise induced, and carotid sinus syncope. These causes tend to be more benign and do not predict poor outcomes. Vasovagal syncope is the most common type in young adults [7] but can occur at any age. It usually occurs in a standing position and is precipitated by fear, emotional stress, or pain (eg, after a needlestick). Autonomic symptoms are predominant. Classically, nausea, diaphoresis, fading or "graying out" of vision, epigastric discomfort, and light-headedness precede syncope by a few minutes. The syncope is thought to occur secondary to efferent vasodepressor reflexes by a number of mechanisms, resulting in decreased peripheral vascular resistance. It is not life-threatening and occurs sporadically. Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defecation, deglutition, tussive, and carotid sinus syncope are types of situational syncope. These stimuli result in autonomic reflexes with a vasodepressor response, ultimately leading to transient cerebral hypotension. These are not life-threatening but can cause morbidity. The treatment involves avoidance of the precipitant when possible and the initiation of counter maneuvers when anticipated. Syncope due to orthostatic hypotension can occur through several mechanisms. Pure autonomic failure can be associated with Parkinson disease or dementia. Secondary autonomic insufficiency can be due to diabetes, uremia, or spinal injury. Drugs such as alcohol cause orthostatic intolerance, and medications such as vasodilators and antidepressants block orthostatic reflexes. Volume depletion due to blood loss, vomiting, diarrhea, poor oral intake, and diuretics also causes orthostatic syncope. Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relation between orthostatic hypotension and syncope. Orthostatic hypotension increases in prevalence with age as a blunted baroreceptor response results in failure of compensatory cardioacceleration. In elderly patients, 45% of these cases are related to medications. Limited evidence suggests that polydipsia may reduce recurrences. Orthostasis is a common cause of syncope and tends to be recurrent. Bedside orthostatics cannot exclude this as an etiology; if it is suspected, patients should be referred to a primary care provider for outpatient tilt-table testing.

Epidemiology Data from Europe and Japan suggest an occurrence rates similar to that in the United States, accounting for 1-3.5% of ED visits. Race-, sex-, and age-related demographics No significant differences regarding race are observed with respect to syncope risk. Larger prospective studies fail to show clinically significant differences between men and women. National Hospital Ambulatory Medical Care Survey (NHAMCS) data show that syncope occurs in all age groups but is most common in adult populations. Noncardiac causes tend to be more common in young adults, whereas cardiac syncope becomes increasingly more frequent with advancing age. Syncope is relatively uncommon in pediatric populations. One small retrospective study by Pratt and Fleisher reported a prevalence of less than 0.1% in children. [10] Pediatric syncope warrants prompt detailed evaluation. Advancing age is an independent risk factor for both syncope and death. Various studies suggest categorizing patients older than 45 years, 65 years, and 80 years as being at higher risk. Advancing age correlates with increasing frequency of coronary artery and myocardial disease, arrhythmia, vasomotor instability, autonomic failure, polyneuropathy, and use of polypharmacy.

Prognosis Cardiac syncope has a poorer prognosis than other forms of syncope. The 1-year endpoint mortality has been shown to be as high as 18-33%. Studies evaluating mortality within 4 weeks of presentation and 1 year after presentation both report statistically significant increases in this patient group. Patients with cardiac syncope may be significantly restricted in their daily activities, and the occurrence of syncope may be a symptom of their underlying disease progression. Syncope of any etiology in a patient with cardiac conditions (to be differentiated from cardiac syncope) has also been shown to imply a poor prognosis. Patients with New York Heart Association (NYHA) functional class III or IV who have any type of syncope have a mortality as high as 25% within 1 year. However, some patients do well after definitive surgical treatment or pacemaker placement. Evaluation by a cardiologist for pacemaker placement should be considered in select patients older than 40 years who have recurrent syncope that is confirmed to be neurally mediated syncope (NMS) with a documented period of asystole. Preliminary data suggests that although syncope may recur in this subset of patients, the frequency is reduced by more than 50%. [11] Noncardiac syncope seems to have no effect on overall mortality and includes syncope due to vasovagal response, autonomic insufficiency, situations, and orthostatic positions. Vasovagal syncope has a uniformly excellent prognosis. This condition does not increase the mortality, and recurrences are infrequent. Situational syncope and orthostatic syncope also have an excellent prognosis. They do not increase the risk of death; however, recurrences do occur and are sometimes a source of significant morbidity in terms of quality of life and secondary injury. Syncope of unknown etiology generally has a favorable prognosis, with 1-year follow-up data showing a low incidence of sudden death (2%), a 20% chance of recurrent syncope, and a 78% remission rate. Recurrent falls due to syncope can result in lacerations, orthopedic injuries, and intracranial trauma. Morbidity/mortality Data suggest that patients with cardiac syncope are more likely to experience a poor outcome. Patients who have a significant cardiac history and those who seem to have a cardiac syncope (because of associated chest pain, dyspnea, cardiac murmur, signs of CHF, or ECG abnormalities) should be considered to be at increased risk. Most published methods of risk stratification take into account cardiac symptoms and risk factors. [12] Morbidity from syncope includes recurrent syncope, which occurs in 20% of patients within 1 year of the initial episode. Lacerations, extremity fractures, head injuries, and motor vehicle accidents can occur secondary to syncope. Syncope in a patient with poor baseline cardiac function portends a poor prognosis, irrespective of etiology. Middlekauff et al studied 491 patients with NYHA functional class III or IV disease and noted that, regardless of the cause, 45% of those with syncope died within 1 year, whereas 12% of those without syncope died during the same interval. [13] Patients with cardiac syncope appear to do worse than patients with noncardiac syncope. Soteriades et al followed 7814 patients with syncope for 17 years and found a higher mortality for patients with cardiac syncope than for those with noncardiac syncope. [14] Suzuki et al studied 912 patients with syncope for an average of 3 years and found the same result. [15] Risk of serious outcome and death in patients with syncope increases with higher peak troponin concentrations, according to a prospective cohort study of 338 patients who had plasma troponin I levels measured with a sensitive assay 12 hours after syncope. [16] The percentage of patients with a serious outcome increased across patients divided into quintiles on the basis of peak troponin concentration at 1 month (0%, 9%, 13%, 26%, 70%) and at 1 year (10%, 22%, 26%, 52%, 85%). [16] Decision rules may assist in identifying patients who are at risk. Martin et al described a risk stratification system that predicted an increased incidence of death at 1 year on the basis of abnormal ECG findings, a history of ventricular arrhythmia, a history of CHF, and age older than 45 years. [17] Sarasin et al demonstrated a risk of arrhythmia that is proportional to the number of cardiac risk factors, including abnormal ECG findings, history of CHF, and age older than 65 years. [18] The San Francisco Syncope Rule (SFSR) was determined to have a 96% sensitivity for identifying patients at immediate risk for serious outcomes within 7 days, on the basis of the presence of abnormal ECG findings, a history of CHF, dyspnea, a hematocrit level lower than 0.30, and hypotension. [19] The presence of these findings should prompt serious consideration for hospital admission. In an external retrospective review, validation of the SFSR in a Canadian ED was undertaken. The rule performed with a sensitivity of 90% (44/49 outcomes; 95% confidence interval [CI] 79-96%) and a specificity of 33%, which was much lower than previously reported. The results of this study suggested that implementation of the rule would have significantly increased admission rates. The authors concluded that further study was needed. [20] Another study was also unable to validate the rule, with a sensitivity of 74% and a specificity of 57% reported. [21] The ROSE (Risk stratification Of Syncope in the Emergency department) criteria suggested that an elevated B-type natriuretic peptide (BNP), Hemoccult-positive stool, anemia, low oxygen saturation, and presence of Q waves on ECG predict serious outcomes at 30 days. [22] These rules had a 87% sensitivity and a 98.5% negative predictive value to help risk-stratify patients. In this study, the isolated finding of BNP greater than 300 pg/mL was a major predictor of serious outcomes and was present in 89% of patients who died within 30 days. Constantino et al discovered that 6.1% of patients had severe outcomes within 10 days of syncope evaluation. [23] The mortality was 0.7%, and 5.4% of patients were readmitted or experienced major therapeutic intervention. Risk factors associated with severe short-term outcomes included abnormal ECG, history of CHF, age older than 65 years, male gender, history of chronic obstructive pulmonary disease (COPD), structural heart disease, presence of trauma, and lack of prodromal symptoms. The Evaluation of Guidelines in SYncope Study 2 (EGSYS 2) prospectively followed nearly 400 patients at 1 month and 2 years. The death rate was 2% at 1 month and 9% at 2 years. Patients with advancing age, presence of structural heart disease, and/or abnormal ECG had higher risk. [24] Clinical judgment, Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score, [25] and SFSR criteria all have relatively low sensitivities individually for predicting severe short-term outcomes. Some evidence suggests that combining various risk stratification tools may increase sensitivity and reduce unnecessary admissions. [26] A review and meta-analysis by Serrano et al assessed the methodologic quality and prognostic accuracy of the SFSR and the OESIL risk score. [27] The analysis of 18 eligible studies determined that the quality and accuracy of both sets of clinical decision rules are limited.

Clinical Presentation

History History and physical examination are the most specific and sensitive ways to evaluate syncope. [1] The diagnosis is achieved with a thorough history and physical examination in 50-85% of patients. No single laboratory test has greater diagnostic efficacy. The 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope listed history, physical examination, and 12-lead electrocardiography (ECG) as their only current level A recommendations. [2] A detailed account of the event must be obtained from the patient. The account must include the circumstances surrounding the episode: the precipitant factors, the activity the patient was involved with prior to the event, and the patient's position when it occurred. Precipitating factors can include fatigue, sleep or food deprivation, warm ambient environment, alcohol consumption, pain, and strong emotions such as fear or apprehension. Activity prior to syncope may give a clue as to the etiology of symptoms. Syncope may occur at rest; with change of posture; on exertion; after exertion; or with specific situations such as shaving, coughing, voiding, or prolonged standing. Syncope occurring within 2 minutes of standing suggests orthostatic hypotension. [28] Assess whether the patient was standing, sitting, or lying when the syncope occurred. Syncope while seated or lying is more likely to be cardiac. [29] The following questions should be answered:

• Was loss of consciousness complete?

• Was loss of consciousness with rapid onset and short duration?

• Was recovery spontaneous, complete, and without sequelae?

• Was postural tone lost?

If the answers to these questions are positive, the episode has a high likelihood of being syncope. If one or more answers are negative, consider other forms of loss of consciousness prior to proceeding with syncope evaluation. [3] The clinician should attempt to gather all information with respect to symptoms preceding the syncope. Prior faintness, dizziness, or light-headedness occurs in 70% of patients experiencing true syncope. Other symptoms, such as vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias, may also occur in the presyncopal period. Symptoms of nausea or diaphoresis prior to the event may suggest syncope rather than seizure when the episode was not witnessed, whereas an aura may suggest seizure. Patients with true syncope do not remember actually falling to the ground. Presyncope involves the same symptoms and pathophysiology but terminates prior to loss of consciousness and can occasionally include loss of postural tone. The duration of symptoms preceding a syncopal episode has been reported to be an average of 2.5 minutes in vasovagal syncope and an average of only 3 seconds in arrhythmia-related cardiac syncope. Clinicians should specifically inquire as to red-flag symptoms, such as exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event. Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma, incontinence, or myalgias. A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, and seizure. Convulsive activity, automatisms, or attempts to elicit focality can indicate seizure. Witnesses may be able to estimate the duration of unconsciousness and to assist in ascertaining whether the patient experienced postevent confusion. Postevent confusion is the most powerful tool for discriminating between syncope and seizure. A postictal phase suggests that a seizure has occurred. Postevent confusion has been described with syncope, but the confusion should not last more than 30 seconds. Seizurelike activity can occur with syncope if the patient is held in an upright posture. A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:

• Agents that reduce blood pressure (eg, antihypertensive drugs, diuretics, nitrates)

• Agents that affect cardiac output (eg, beta blockers, digitalis, antiarrhythmics)

• Agents that prolong the QT interval (eg, tricyclic antidepressants, phenothiazines, quinidine, amiodarone)

• Agents that alter sensorium (including alcohol, cocaine, analgesics with sedative properties)

• Agents that alter serum electrolytes (especially diuretics)

Inquiry must be made into any personal or familial past medical history of cardiac disease. Patients with a history of myocardial infarction (MI), arrhythmia, structural cardiac defects, cardiomyopathies, or congestive heart failure (CHF) have a uniformly worse prognosis than other patient groups. Remember to consider the broad differential diagnosis of syncope. Assess whether the patient has a history of seizure disorder, diabetes, stroke (cerebrovascular accident [CVA]), deep vein thrombosis (DVT), or abdominal aortic aneurysm (AAA) or if pregnancy is a possibility.

Physical Examination A complete physical examination is requisite for all patients who present to the emergency department (ED). Special attention must be paid to certain aspects of the physical examination in patients who present with syncope. Always analyze the vital signs. Fever may point to a precipitant of syncope, such as a urinary tract infection (UTI) or pneumonia. Postural changes in blood pressure (BP) and heart rate may point toward an orthostatic cause of syncope but are generally unreliable. Tachycardia may be an indicator of pulmonary embolism, hypovolemia, tachyarrhythmia, or acute coronary syndrome. Bradycardia may point toward a vasodepressor cause of syncope, a cardiac conduction defect, or acute coronary syndrome. A glucose level, checked by rapid fingerstick (eg, Accu-Chek), should be evaluated in any patient with syncope. Hypoglycemia can produce a clinical picture identical to syncope, including the prodromal symptoms, absence of memory for the event, and spontaneous resolution. A detailed cardiopulmonary examination is essential. Irregular rhythms, ectopy, bradyarrhythmias, and tachyarrhythmias should be detected. Auscultation of heart sounds may reveal murmurs indicating high-grade valvular defects. Search for objective evidence of congestive heart failure, including jugular venous distension, lung rales, hepatomegaly, and pitting-dependent edema. Examine the abdomen for the presence of a pulsatile abdominal mass. A detailed neurologic examination assists in establishing a baseline as well as defining new or worsening deficits. Patients with syncope should have a normal baseline mental status. Confusion, abnormal behavior, headache, fatigue, and somnolence must not be attributed to syncope; a toxic, metabolic, or central nervous system cause must be considered. The patient should have a detailed neurologic examination, including evaluation for carotid bruits, cranial nerve deficits, motor deficits, deep tendon reflex lateralization, and sensory deficits. Severe neuropathies may correlate with vasodepressor syncope. The patient must be examined for signs of trauma. Trauma may be sustained secondary to syncope with resultant head injury, lacerations, and extremity fractures. Tongue trauma is thought to be more specific for seizures. Remember to consider antecedent head trauma resulting in loss of consciousness as opposed to syncope with resultant trauma if the history or findings are unclear. Patients with syncope may require a stool guaiac examination, as appropriate based on their history. In one study, all patients with anemia contributing to syncope were guaiac-positive. A few bedside examinations may help to elucidate the origin of a patient's syncope. The Hallpike maneuver may be performed in patients who describe short, intermittent prodromes with primarily vertiginous components to assess for benign paroxysmal positional vertigo. Orthostatic changes marked by a decrease in systolic BP by 20 mm Hg, a decrease in diastolic BP by 10 mm Hg, or an increase in heart rate by 20 beats/min (bpm) with positional changes or systolic BP less than 90 mm Hg with the presence of symptoms may indicate postural hypotension. Bradycardia coinciding with the examination indicates vasodepressor syncope. Be aware that this examination is notoriously insensitive and has limited use. Carotid sinus massage has been used with some success to diagnose carotid sinus syncope but can prompt prolonged sinus pauses and hypotension.

Diagnostic Considerations

There are well-publicized implications of patients with syncope returning to activities such as sports, driving, and operating machinery. Consultation with a subspecialist and/or a hospital attorney may be prudent prior to making definitive recommendations.

Elderly patients with dementia and episodes of suspected sycope may have an atypical clinical presentation and render it difficult to use a standard diagnostic protocol for syncope. [6] These patients also suffer frequent unexplained falls.

Note the following:

• Consider and diagnose life-threatening etiologies of syncope

• Scrutinize the initial electrocardiogram (ECG) and seek comparison to a prior ECG

• Provide adequate subspecialty and/or primary care follow-up

• Educate patients adequately about the etiology of the syncope and preventive measures to avoid recurrence

• Adequately address short-term recurrence probability and ensure low risk of subsequent morbidity

• Consider and diagnose life-threatening conditions that occur as a result of the syncopal episode

Vasomotor/vascular conditions to consider in patients with suspected syncope include the following:

• Dehydration

• Diabetic neuropathy

• Diuresis

• Drug-induced orthostasis

• Dysautonomia

• Ectopic pregnancy

• Hemorrhage

• Hypotension

• Hypovolemia

• Multisystem atrophy

• Peripheral polyneuropathy

• Postural hypotension

• Subclavian steal

• Vasodepressor/vasovagal response

• Vasomotor insufficiency

Cardiac conditions to consider in patients with suspected syncope include the following:

• Bradydysrhythmias

• Cardiac myxoma

• Cardiac outflow obstruction

• Dysrhythmias

• Hypertrophic subaortic stenosis

• Paroxysmal supraventricular tachycardia

• Paroxysmal ventricular tachycardia

• Primary pulmonary hypertension

• Prolonged QT syndrome

• Sick sinus syndrome

• Sinoatrial block

• Sinus pause (>3 s)

• Tachydysrhythmias

• Tricuspid stenosis

Situational conditions to consider in patients with suspected syncope include the following:

• Carotid sinus syncope

• Cough (posttussive) syncope

• Defecation syncope

• Micturition syncope

• Postprandial syncope

• Swallow syncope

Metabolic/endocrine conditions to consider in patients with suspected syncope include the following:

• Hypothyroidism

• Hypoxemia

• Pheochromocytoma

Central nervous system conditions to consider in patients with suspected syncope include the following:

• Hyperventilation syndrome

• Hydrocephalus

• Migraine headache

• Narcolepsy

• Panic attacks

• Seizure disorder

Differential Diagnoses

• Acute Aortic Dissection

• Acute Hypoglycemia

• Adrenal Crisis in Emergency Medicine

• Amphetamine Toxicity

• Antidepressant Toxicity

• Antidysrhythmic Toxicity

• Aortic Stenosis Imaging

• Asystole

• Atrial Fibrillation

• Beta-Blocker Toxicity

• Brugada Syndrome

• Calcium Channel Blocker Toxicity

• Cocaine Toxicity

• Emergent Management of Subarachnoid Hemorrhage

• Hyponatremia in Emergency Medicine

• Mitral Stenosis Imaging and Diagnosis

• Restrictive Cardiomyopathy Imaging and Diagnosis

• Tetralogy of Fallot Imaging

• Long QT Syndrome

• Multifocal Atrial Tachycardia

• Myocardial Infarction

• Pacemakers and Implantable Cardioverter-Defibrillators

• Pulmonary Embolism (PE)

• Pulmonic Valvular Stenosis

• Second-Degree Atrioventricular Block

• Sinus Bradycardia

• Third-Degree Atrioventricular Block (Complete Heart Block)

• Torsade de Pointes

• Tricyclic Antidepressant Toxicity

• Wolff-Parkinson-White Syndrome

Workup

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. [30] Research-based and consensus guideline recommendations are listed below. Serum glucose level In one study, two 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 If performed empirically, a complete blood count (CBC) 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 four of 170 patients had signs and symptoms of gastrointestinal (GI) hemorrhage with a confirmatory CBC. No occult bleeding was diagnosed on the basis of an empiric CBC in this study. Anemia has been shown in several studies to suggest poor short-term outcomes. Serum electrolyte levels with renal function tests These tests have an exceedingly low yield in syncope if performed empirically. Some risk stratification protocols use electrolyte level abnormalities and renal insufficiency as poor prognostic indicators. In a study by Martin et al, 134 patients with syncope had electrolytes drawn as part of the routine workup. [31] 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 strongly suspected. Total creatine kinase A rise in creatine kinase (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. [22] Urinalysis/dipstick 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 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. Computed tomography Head (noncontrast) Noncontrast computed tomography (CT) of the head 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. [31] Only one head CT scan was diagnostic in a patient not expected to have intracranial pathology. Of the remaining scans, five showed subdural hematomas thought to be secondary to syncope. Head CT may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope. Chest and abdomen CT of the chest and abdomen is indicated only in select cases, such as cases in which aortic dissection, ruptured abdominal aortic aneurysm (AAA), or pulmonary embolism (PE) is suspected. Magnetic resonance imaging Magnetic resonance imaging (MRI) of the brain and magnetic resonance arteriography (MRA) may be required in select cases to evaluate the vertebrobasilar vasculature and are more appropriately performed on an inpatient basis in consultation with a neurologist or a neurosurgeon. Ventilation-perfusion scanning Ventilation-perfusion (V/Q) scanning is appropriate for patients in whom PE is suspected. Echocardiography 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 Electrocardiography Obtain a standard 12-lead electrocardiogram (ECG) in patients with syncope. This is a level A recommendation in the 2007 American College of Emergency Physicians (ACEP) consensus guidelines for syncope. [2] ECG is used in virtually 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. [32] 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. Studies showed 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] In a prospective, randomized, controlled study, Sulke et al evaluated the first-line use of a remotely monitored implantable loop recorder (ILR) in the initial investigation of unexplained syncope, in comparison with conventional therapy and a dedicated Syncope Clinic (SC). [33] A total of 246 patients were randomly allocated to conventional management, SC alone, ILR alone, or SC + ILR, with a median follow-up of 20 months. ILRs offered rapid diagnosis, increased the likelihood of syncope being reported, showed a high rate of intermittent bradycardia that required pacing, and reduced recurrent syncope. 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 the negative diagnostic yield of ambulatory monitoring is a higher than its positive 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, 34] It involves using a tilt table to stand a patient at 70º 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. [35] 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 aimed at determining 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 found no syncopal predictions that were of practical value. [36] Electroencephalography Electroencephalography (EEG) can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis. Stress testing Stress testing/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 who have risk factors for coronary atherosclerosis. This test can assist with cardiac risk stratification and can guide future therapy.

Procedures 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.

Treatment & Management

Prehospital Care Prehospital management of syncope covers a wide spectrum of acute care and includes rapid assessment of airway, breathing, circulation, and neurologic status. Treatment may require the following:

• Intravenous (IV) access

• Oxygen administration

• Advanced airway techniques

• Glucose administration

• Pharmacologic circulatory support

• Pharmacologic or mechanical restraints

• Defibrillation or temporary pacing

Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.

Emergency Department Care In patients brought to the emergency department (ED) with a presumptive diagnosis of syncope, appropriate initial interventions include the following:

• IV access

• Oxygen administration

• Cardiac monitoring

Electrocardiography (ECG) and rapid blood glucose evaluation should be promptly performed. A study to determine the sensitivity and specificity of the San Francisco Syncope Rule (SFSR) ECG criteria for determining cardiac outcomes found that when used correctly, the criteria can help predict which syncope patients are at risk of cardiac outcomes. [37] The SFSR ECG criteria predicted 36 of 42 patients with cardiac outcomes, with a sensitivity of 86%, a specificity of 70%, and a negative predictive value of 99%. Syncope may be the manifestation of an acute life-threatening process but is generally not an emergency. Clinically ruling out certain processes is important. The treatment choice for syncope depends on the cause or precipitant of the syncope. Patients in whom a cause cannot be ascertained in the ED, especially if they have experienced significant trauma, should receive supportive care and monitoring. Situational syncope treatment focuses on educating patients about the condition. For example, in carotid sinus syncope, patients should be instructed to avoid wearing tight collars, to use a razor rather than electric shaver, and to maintain good hydration status; they should also be informed of the possibility of pacemaker placement in the future. Orthostatic syncope treatment also focuses on educating the patient. Inform patients about avoiding postprandial dips in blood pressure (BP), teach them to elevate the head of their bed to prevent rapid BP fluctuations on arising from bed, and emphasize the importance of assuming an upright posture slowly. Additional therapy may include thromboembolic disease (TED) stockings, mineralocorticoids (eg, fludrocortisone for volume expansion), and other drugs such as midodrine (an alpha1-agonist with vasopressor activity). Patients' medications must be reviewed carefully to eliminate drugs associated with hypotension. Intentional oral fluid consumption is useful in decreasing frequency and severity of symptoms in these patients. [38] The Syncope Evaluation in the Emergency Department Study (SEEDS) data suggested that specialized syncope units with protocoled approaches to ruling out cardiac causes of syncope reduce hospital costs and length of stay without compromising quality of care. [39] Data from subsequent studies confirmed these findings. [1] Cardiac arrhythmic syncope is treated with antiarrhythmic drugs or pacemaker placement. Consider cardiologist evaluation or inpatient management, in that this is more commonly associated with poor outcomes. [2] Trials assessing beta-blockade to prevent syncope have conflicting results, [40] but no clear effect has been demonstrated. In the prospective, multicenter Syncope Unit Project 2 (SUP 2) study, Brignole et al investigated the long-term effects and determinants of success of cardiac pacing in patients with severe unpredictable recurrent reflex syncope. Patients underwent carotid sinus massage (CSM), followed by tilt testing (TT) if CSM was negative, followed by implantation of an implantable loop recorder (ILR) if TT was negative; patients with an asystolic response to one of these tests received a dual-chamber pacemaker. The benefit of cardiac pacing was maintained at 3 years and was greatest in patients with negative TT. [41] Cardiac mechanical syncope may be treated with beta-blockade to decrease outflow obstruction and myocardial workload. Valvular disease may require surgical correction. This, too, is associated with increased future morbidity and mortality. Patients with select etiologies of syncope may require transfer for specialty evaluation or procedures.

Consultations The etiology of syncope dictates the need, if any, for specialty consultation. Select cases may require consultation with a neurosurgeon, a neurologist, a cardiologist, a vascular surgeon, a cardiothoracic surgeon, an endocrinologist, or a toxicologist.

Medication

Medication Summary The goals of pharmacotherapy are to prevent complications and to reduce morbidity.

Anticholinergics Class Summary These agents improve conduction through the atrioventricular node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective. Atropine (Atropair, Isopto Atropine, Atropisol)

Anticholinergic (or parasympatholytic) drug that exerts its action by competitively inhibiting acetylcholine at muscarinic receptors on postganglionic smooth muscle. Can counteract rapidly heightened vagal tone in response to pathologic carotid sinus syndrome. Additionally, can reverse bradycardia and lessen degree of heart block when vagal activity is etiologic factor. Usual doses are used to reduce severe bradycardia and syncope associated with hyperactive carotid sinus reflex.

Nutrient Supplements Class Summary Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations. Dextrose (D-Glucose)

Nutrient replenisher, serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose, whereas each 100 mL of 10% dextrose contains 10 g of dextrose. Should be given only after demonstrated hypoglycemia.

Benzodiazepines Class Summary CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis. Alprazolam (Xanax)

Indicated for treatment of anxiety and management of panic attacks. Following PO administration, absorbed readily. Peak concentrations in plasma occur 1-2 h following administration.

Vasopressor Class Summary Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist that acts on receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of BP. This drug has minimal beta effects and diffuses poorly across the blood-brain barrier. Midodrine HCl (ProAmatine)

Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect persisting for 2-3 h. Has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.

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