Syncope: Evaluation and Differential Diagnosis

 

Am Fam Physician. 2017 Mar 1;95(5):303-312B.

  Patient information: See related handout on fainting.

Author disclosure: No relevant financial affiliations.

Syncope is an abrupt and transient loss of consciousness caused by cerebral hypoperfusion. It accounts for 1% to 1.5% of emergency department visits, resulting in high hospital admission rates and significant medical costs. Syncope is classified as neurally mediated, cardiac, and orthostatic hypotension. Neurally mediated syncope is the most common type and has a benign course, whereas cardiac syncope is associated with increased morbidity and mortality. Patients with presyncope have similar prognoses to those with syncope and should undergo a similar evaluation. A standardized approach to syncope evaluation reduces hospital admissions and medical costs, and increases diagnostic accuracy. The initial assessment for all patients presenting with syncope includes a detailed history, physical examination, and electrocardiography. The initial evaluation may diagnose up to 50% of patients and allows immediate short-term risk stratification. Laboratory testing and neuroimaging have a low diagnostic yield and should be ordered only if clinically indicated. Several comparable clinical decision rules can be used to assess the short-term risk of death and the need for hospital admission. Low-risk patients with a single episode of syncope can often be reassured with no further investigation. High-risk patients with cardiovascular or structural heart disease, history concerning for arrhythmia, abnormal electrocardiographic findings, or severe comorbidities should be admitted to the hospital for further evaluation. In cases of unexplained syncope, provocative testing and prolonged electrocardiographic monitoring strategies can be diagnostic. The treatment of neurally mediated and orthostatic hypotension syncope is largely supportive, although severe cases may require pharmacotherapy. Cardiac syncope may require cardiac device placement or ablation.

Syncope is a sudden, brief, and transient loss of consciousness caused by cerebral hypoperfusion.1 Other nontraumatic loss of consciousness syndromes include seizures, cataplexy, metabolic disorders, acute intoxications, vertebrobasilar insufficiency, transient ischemic attack, cerebrovascular accident, and psychogenic pseudosyncope.2,3

 Enlarge     Print

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Patients who present with presyncope should be evaluated similarly to those who present with syncope.

C

20, 21

Patients with syncope and evidence of congestive heart failure or structural heart disease, abnormal electrocardiographic findings, or a family history of sudden death should be admitted to the hospital for emergent evaluation.

C

1, 25, 27, 29

Patients presenting with syncope should have orthostatic blood pressure measurements and standard 12-lead electrocardiography.

C

1, 2, 25, 27, 29

Laboratory and imaging studies should be ordered for patients with syncope only if clinically indicated by the history and physical examination.

C

1, 27, 39, 40, 42, 43, 50, 51

Implantable loop recorders increase diagnostic yield, reduce time to diagnosis, and are cost-effective for suspected cardiac syncope and unexplained syncope.

C

1, 39, 4448

Patients with syncope who are at low risk of adverse events (e.g., those with symptoms consistent with vasovagal or orthostatic hypotension syncope, no history of heart disease, no family history of sudden cardiac death, and normal electrocardiographic findings) may be safely followed without further intervention or treatment.

C

1, 25, 27, 29


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Patients who present with presyncope should be evaluated similarly to those who present with syncope.

C

20, 21

Patients with syncope and evidence of congestive heart failure or structural heart disease, abnormal electrocardiographic findings, or a family history of sudden death should be admitted to the hospital for emergent evaluation.

C

1, 25, 27, 29

Patients presenting with syncope should have orthostatic blood pressure measurements and standard 12-lead electrocardiography.

C

1, 2, 25, 27, 29

Laboratory and imaging studies should be ordered for patients with syncope only if clinically indicated by the history and physical examination.

C

1, 27, 39, 40, 42, 43, 50, 51

Implantable loop recorders increase diagnostic yield, reduce time to diagnosis, and are cost-effective for suspected cardiac syncope and unexplained syncope.

C

1, 39, 4448

Patients with syncope who are at low risk of adverse events (e.g., those with symptoms consistent with vasovagal or orthostatic hypotension syncope, no history of heart disease, no family history of sudden cardiac death, and normal electrocardiographic findings) may be safely followed without further intervention or treatment.

C

1, 25, 27, 29


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.

 Enlarge     Print

BEST PRACTICES IN NEUROLOGY: RECOMMENDATIONS FROM THE CHOOSING WISELY CAMPAIGN

RecommendationSponsoring organization

Avoid computed tomography of the head in asymptomatic adult patients in the emergency department with syncope, insignificant trauma, and a normal neurologic evaluation.

American College of Emergency Physicians

In the evaluation of simple syncope and a normal neurologic evaluation, do not obtain brain imaging studies (computed tomography or magnetic resonance imaging).

American College of Physicians

Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms.

American Academy of Neurology


Source: For more information on the Choosing Wisely Campaign, see http://www.choosingwisely.org. For supporting citations and to search Choosing Wisely recommendations relevant to primary care, see https://www.aafp.org/afp/recommendations/search.htm.

BEST PRACTICES IN NEUROLOGY: RECOMMENDATIONS FROM THE CHOOSING WISELY CAMPAIGN

RecommendationSponsoring organization

Avoid computed tomography of the head in asymptomatic adult patients in the emergency department with syncope, insignificant trauma, and a normal neurologic evaluation.

American College of Emergency Physicians

In the evaluation of simple syncope and a normal neurologic evaluation, do not obtain brain imaging studies (computed tomography or magnetic resonance imaging).

American College of Physicians

Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms.

American Academy of Neurology


Source: For more information on the Choosing Wisely Campaign, see http://www.choosingwisely.org. For supporting citations and to search Choosing Wisely recommendations relevant to primary care, see https://www.aafp.org/afp/recommendations/search.htm.

Syncope accounts for 1% to 1.5% of all emergency department visits, 250,000 annual hospital admissions, and a median hospital cost of $8,500.4,5 Approximately 40% of the U.S. population will experience a syncopal episode in their lifetimes, and 30% to 50% will be admitted to the hospital for further evaluation.6,7 The etiology is unexplained in up to one-third of cases.8

Although syncope is associated with serious risks, short-term mortality is low (i.e., 0.7% at 10 days and 1.6% at 30 days). At one year, the mortality rate is 8.4%; one-third of these are attributed to cardiovascular causes. Approximately 25% of patients with syncope will experience another event within two years.8,9 Historically, neurally mediated and orthostatic hypotension syncope have not conferred an increased risk of death10; however, in a recent study, healthy adults with a diagnosis of syncope had higher rates of all-cause mortality, recurrent syncope, cardiovascular events, and pacemaker or implantable cardioverter-defibrillator placement compared with matched controls. Patients 44 to 75 years of age had the highest risk.11,12

Management of syncope remains a challenge, particularly in identifying patients with potentially life-threatening etiologies. Lack of physician knowledge, a desire to reassure the patient or clinician, and the fear of medicolegal ramifications result in overuse of diagnostic tests.13 A standardized approach for evaluating patients with syncope reduces admissions, hospital costs, and number of tests performed, and increases accuracy of diagnosis.14 Only 10% to 15% of patients will remain undiagnosed after a comprehensive evaluation using current guidelines.15,16

Classification and Etiology

Syncope is classified as cardiac, neurally mediated (reflex), and orthostatic hypotension (Table 1).1,17 The differential diagnosis should include nontraumatic causes of transient loss of consciousness. Rare causes include subclavian steal syndrome, pulmonary embolism, acute myocardial infarction, acute aortic dissection, leaking aortic aneurysm, subarachnoid hemorrhage, and cardiac tamponade.2,3

 Enlarge     Print

Table 1.

Classification of Syncope

Syncope typeScenarioClinical features

Cardiac syncope

Arrhythmia (e.g., bradyarrhythmias, ventricular tachyarrhythmias, supraventricular tachyarrhythmias), pacemaker dysfunction, channelopathies

Generally abrupt and unprovoked; palpitations may precede symptoms

Abnormal electrocardiographic findings, family history of sudden death, personal history of heart disease, sudden onset of palpitations, symptoms during or after exertion while in supine or prone position

Obstructive cardiomyopathy

Hypertrophic cardiomyopathy or exertional syncope in persons with a family history of sudden cardiac death

Often asymptomatic; may cause arrhythmias, chest pain, shortness of breath, or syncope; dynamic systolic murmur that intensifies from squatting to standing or during Valsalva maneuver

Structural cardiac disease

Acute myocardial infarction or ischemia

Diaphoresis, exertional chest pain, nausea, shortness of breath; rare cause of syncope

Arrhythmogenic right ventricular cardiomyopathy

Asymptomatic, atypical chest pain, dizziness, exertional syncope, family history of sudden cardiac death, palpitations, right ventricular structural abnormalities

Infiltrative (e.g., amyloidosis, hemochromatosis, sarcoidosis)

Arrhythmias, heart block, heart failure

Valvular disease (e.g., aortic stenosis, mitral stenosis, pulmonary stenosis)

Symptoms dependent on severity; severe aortic stenosis can manifest with congestive heart failure, exertional angina, or syncope

Other structural disease

Acute aortic dissection

Hypotension or shock, severe sharp chest pain with or without radiation to the back, history of hypertension

Cardiac masses (e.g., atrial myxoma, cardiac tumors)

Arrhythmia via direct invasion, embolization, heart failure, systemic symptoms, valvular regurgitation

Cardiac tamponade

Elevated jugular venous pressure, hypotension, pulsus paradoxus, sinus tachycardia

Pulmonary hypertension

Often asymptomatic; may cause fatigue and shortness of breath

Saddle pulmonary embolus

Acute shortness of breath, chest pain, hypoxia, right heart strain, sinus tachycardia

Neurally mediated (reflex) syncope

Carotid sinus syndrome/hypersensitivity

Head rotation or pressure on the carotid sinus (e.g., from shaving or tight collar) can reproduce symptoms; consider in patients with unexplained falls

Ventricular pause or decreased systolic blood pressure after carotid sinus massage; may coincide with syncope

Situational

Brought on by coughing, defecation, gastrointestinal stimulation, or urination; may occur after exercise or meals

Absence of heart disease; history of similar syncope; prolonged standing, eating, or voiding

Vasovagal

Mediated by fear, heat exposure, noxious stimuli, pain, or stress

Prodromal symptoms (e.g., diaphoresis, dizziness, nausea), precipitating factors

Orthostatic hypotension syncope

Drug induced

Alcohol, antianginal agents, antidepressants, antidiabetic agents, antihypertensives, antiparkinsonian agents, diuretics, flibanserin (Addyi), insulin

Initiation or change in dosage

Postural tachycardia syndrome

Young adults (predominantly female); associated with chronic fatigue syndrome and mitral valve prolapse

Severe orthostatic intolerance with marked tachycardia

Primary autonomic failure

Multiple sclerosis, multiple system atrophy (e.g., Shy-Drager syndrome), Parkinson disease/parkinsonism, Wernicke encephalopathy

Orthostatic hypotension with postural change

Secondary autonomic failure

Amyloidosis, chronic inflammatory demyelinating polyneuropathy, connective tissue diseases, diabetes mellitus, Lewy body dementia, older age, spinal cord injury, uremia

Orthostatic hypotension with postural change

Volume depletion

Acute blood loss (e.g., gastrointestinal bleeding, ectopic pregnancy), diarrhea, inadequate fluid intake, vomiting

Hypotension, tachycardia, history of volume/blood loss, dehydration on examination


Information from references 1 and 17.

Table 1.

Classification of Syncope

Syncope typeScenarioClinical features

Cardiac syncope

Arrhythmia (e.g., bradyarrhythmias, ventricular tachyarrhythmias, supraventricular tachyarrhythmias), pacemaker dysfunction, channelopathies

Generally abrupt and unprovoked; palpitations may precede symptoms

Abnormal electrocardiographic findings, family history of sudden death, personal history of heart disease, sudden onset of palpitations, symptoms during or after exertion while in supine or prone position

Obstructive cardiomyopathy

Hypertrophic cardiomyopathy or exertional syncope in persons with a family history of sudden cardiac death

Often asymptomatic; may cause arrhythmias, chest pain, shortness of breath, or syncope; dynamic systolic murmur that intensifies from squatting to standing or during Valsalva maneuver

Structural cardiac disease

Acute myocardial infarction or ischemia

Diaphoresis, exertional chest pain, nausea, shortness of breath; rare cause of syncope

Arrhythmogenic right ventricular cardiomyopathy

Asymptomatic, atypical chest pain, dizziness, exertional syncope, family history of sudden cardiac death, palpitations, right ventricular structural abnormalities

Infiltrative (e.g., amyloidosis, hemochromatosis, sarcoidosis)

Arrhythmias, heart block, heart failure

Valvular disease (e.g., aortic stenosis, mitral stenosis, pulmonary stenosis)

Symptoms dependent on severity; severe aortic stenosis can manifest with congestive heart failure, exertional angina, or syncope

Other structural disease

Acute aortic dissection

Hypotension or shock, severe sharp chest pain with or without radiation to the back, history of hypertension

Cardiac masses (e.g., atrial myxoma, cardiac tumors)

Arrhythmia via direct invasion, embolization, heart failure, systemic symptoms, valvular regurgitation

Cardiac tamponade

Elevated jugular venous pressure, hypotension, pulsus paradoxus, sinus tachycardia

Pulmonary hypertension

Often asymptomatic; may cause fatigue and shortness of breath

Saddle pulmonary embolus

Acute shortness of breath, chest pain, hypoxia, right heart strain, sinus tachycardia

Neurally mediated (reflex) syncope

Carotid sinus syndrome/hypersensitivity

Head rotation or pressure on the carotid sinus (e.g., from shaving or tight collar) can reproduce symptoms; consider in patients with unexplained falls

Ventricular pause or decreased systolic blood pressure after carotid sinus massage; may coincide with syncope

Situational

Brought on by coughing, defecation, gastrointestinal stimulation, or urination; may occur after exercise or meals

Absence of heart disease; history of similar syncope; prolonged standing, eating, or voiding

Vasovagal

Mediated by fear, heat exposure, noxious stimuli, pain, or stress

Prodromal symptoms (e.g., diaphoresis, dizziness, nausea), precipitating factors

Orthostatic hypotension syncope

Drug induced

Alcohol, antianginal agents, antidepressants, antidiabetic agents, antihypertensives, antiparkinsonian agents, diuretics, flibanserin (Addyi), insulin

Initiation or change in dosage

Postural tachycardia syndrome

Young adults (predominantly female); associated with chronic fatigue syndrome and mitral valve prolapse

Severe orthostatic intolerance with marked tachycardia

Primary autonomic failure

Multiple sclerosis, multiple system atrophy (e.g., Shy-Drager syndrome), Parkinson disease/parkinsonism, Wernicke encephalopathy

Orthostatic hypotension with postural change

Secondary autonomic failure

Amyloidosis, chronic inflammatory demyelinating polyneuropathy, connective tissue diseases, diabetes mellitus, Lewy body dementia, older age, spinal cord injury, uremia

Orthostatic hypotension with postural change

Volume depletion

Acute blood loss (e.g., gastrointestinal bleeding, ectopic pregnancy), diarrhea, inadequate fluid intake, vomiting

Hypotension, tachycardia, history of volume/blood loss, dehydration on examination


Information from references 1 and 17.

Neurally mediated syncope is the most common type, comprising approximately 45% of cases.6,10,18 It can be vasovagal, situational, or secondary to carotid sinus hypersensitivity. The pathophysiology is complex, consisting of an interaction between autonomic systems paradoxically favoring parasympathetic or vagal tone, which causes bradycardia and hypotension.

Cardiac syncope occurs in approximately 20% of syncope presentations. It is most often caused by an arrhythmia, and less often by a structural cardiac abnormality. In a prospective cohort study, patients with cardiac syncope had a twofold increase in mortality over 17 years.10 The presence of cardiovascular disease predicts a cardiac etiology of syncope with 85% to 94% sensitivity and 64% to 83% specificity.16

Orthostatic hypotension syncope has an incidence of approximately 10% and is typically characterized by posturally induced hypotension, most often related to impaired increase in systemic vascular resistance. Associated factors include medication effects, volume depletion, acute hemorrhage, and autonomic dysfunction. Postural tachycardia syndrome is the most prevalent form of orthostatic intolerance, affecting approximately 500,000 persons in the United States. Younger adults, predominantly women who report symptoms of postural presyncope, are more likely to have this condition.19

PRESYNCOPE

Presyncope is poorly studied, and the true incidence is unknown. A study of 881 patients presenting to the emergency department with presyncope showed a 30-day risk of serious outcomes of 5% and a mortality rate of 0.3%.20 Emergency physicians had difficulty stratifying patients at increased risk of adverse outcomes, regardless of presumed etiology. A prospective observational study (n = 244) compared adverse outcomes and hospitalizations in patients who presented with presyncope and syncope.21 Adverse outcomes occurred in 49 of 244 patients (20%) with presyncope compared with 68 of 293 patients (23%) with syncope. Admission rates were 49% and 69%, respectively. Because rates of adverse outcomes are similar in patients with presyncope and syncope, both groups should receive a similar evaluation.

Risk Stratification

The decision to perform an expedited and monitored evaluation of patients presenting with syncope is based on the likelihood of short-term adverse outcomes. Unnecessary admissions for patients meeting low-risk criteria result in high medical costs without improvements in morbidity and mortality, patient safety, or quality of life.22

Several clinical decision rules have been developed to risk stratify patients presenting to the emergency department with syncope. Each has differing variables, and no single rule has proved significantly superior 23,24  (eTable A). The San Francisco Syncope Rule, Evaluation of Guidelines in Syncope Study, and Osservatorio Epidemiologico sulla Sincope nel Lazio are the only rules that have been externally validated. High-risk patients should be admitted for further evaluation (Table 2).1,25

 Enlarge     Print

eTable A.

Major Clinical Decision Rules for Syncope

StudyPopulationPredictor variablesOutcome measuredScore resultsValidationComments

Boston Syncope Rule, 2007 (short-term risk)

Derivation: a priori

Validation: 362 ED patients with syncope

Signs of volume depletion

Persistent abnormal vital signs in the ED

Signs and symptoms of acute coronary syndrome

Signs of conduction disease

Worrisome cardiac history

Family history of sudden death

Primary central nervous system event

Valvular heart disease (from history or physical examination)

Critical intervention or adverse outcome at 30 days

Consider admission for one or more variables

Internal: 97% sensitivity, 62% specificity

External: none

25 variables in eight categories make it less practical

Canadian Syncope Risk Rule, 2016 (short-term risk)

Derivation: 4,030 ED patients with syncope

Validation: pending

Predisposition to vasovagal syncope (prodrome/trigger)

History of heart disease

Systolic blood pressure < 90 mm Hg or > 180 mm Hg

Elevated troponin level

Abnormal QRS axis (< 30 or > 110 degrees)

QRS duration > 130 milliseconds

Corrected QT interval > 480 milliseconds

ED diagnosis of vasovagal syncope

ED diagnosis of cardiac syncope

Serious event at 30 days: death, arrhythmia, MI, PE, aortic dissection, CVA, or procedural intervention for syncope

Estimated risk of serious adverse event at 30 days

Pending

Largest prospective study, outcomes consistent with guidelines, clarifies abnormal ECG findings, pending validation to support use of rule

EGSYS score, 2008 (short- and long-term risk)

Derivation: 260 ED patients with syncope

Validation: 258 ED patients with syncope

Palpitations preceding syncope (4 points)

Abnormal ECG findings* or history of heart disease (3 points)

Syncope during effort (3 points) or when supine (2 points)

Autonomic prodromes (−1 point)

Precipitating and/or predisposing factors (−1 point)

Probability of cardiogenic syncope at two years

Consider admission for score of 3 or higher

Internal: 92% sensitivity, 69% specificity

External: 56% sensitivity, 84% specificity

Mortality at two years was 2% in patients with scores < 3 and 21% for scores = 3

OESIL risk score, 2003 (long-term risk)

Derivation: 270 ED patients with syncope

Validation: 328 ED patients with syncope

Abnormal ECG findings*

Absence of prodromal syndrome

Age > 65 years

History of cardiac disease

Mortality at one year

Consider admission for one or more variables

Internal: 100% sensitivity, 22% specificity

External: 95% sensitivity, 31% specificity

Positive variables:

0: 0% mortality

1: 0.6% mortality

2: 14% mortality

3: 29% mortality

4: 53% mortality

ROSE study, 2010 (short-term risk)

Derivation: 550 ED patients with syncope

Validation: 550 ED patients with syncope

Anemia (hemoglobin = 9 g per dL [90 g per L])

Bradycardia (< 50 beats per minute)

Brain natriuretic peptide = 300 pg per mL (300 ng per L)

Chest pain with syncope

ECG showing Q waves (except in lead III)

Oxygen saturation < 94% on room air

Rectal examination showing occult blood (if gastrointestinal bleeding suspected)

Serious events at one month: death, acute MI, PE, CVA, arrhythmias, hemorrhage requiring transfusion of two or more units, subarachnoid hemorrhage, acute procedure, need for pacemaker in first month

Consider admission for one or more variables

Internal: 87% sensitivity, 66% specificity

One-year outcomes: 72% sensitivity, 71% specificity

External: none

Not useful for predicting outcomes at one year; first study to use a biomarker in risk stratification

San Francisco Syncope Rule, 2004 (short-term risk)

Derivation: 684 ED patients with syncope or near syncope

Validation: 791 ED patients with syncope or near syncope

Abnormal ECG findings*

Congestive heart failure

Hematocrit < 30%

Shortness of breath

Systolic blood pressure < 90 mm Hg

Serious events at seven days: acute MI, PE, CVA, arrhythmias, subarachnoid hemorrhage, return ED visit, readmission

Consider admission for one or more variables

Internal: 98% sensitivity, 56% specificity

External: 87% sensitivity, 52% specificity

First tool for short-term events (seven days); inconsistencies in validation scores, but the most studied decision tool


CVA = cerebrovascular accident; ECG = electrocardiography; ED = emergency department; EGSYS = Evaluation of Guidelines in Syncope Study; MI = myocardial infarction; OESIL = Osservatorio Epidemiologico sulla Sincope nel Lazio; PE = pulmonary embolism; ROSE = Risk Stratification of Syncope in the Emergency Department.

*—Abnormal ECG definitions varied with each study.

Information from: Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M; OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003;24(9):811-819.

Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart. 2008;94(12):1620-1626.

Ebell MH. Risk stratification of patients presenting with syncope. Am Fam Physician . 2012;85(11):1047-1052.

Ebell MH. Syncope: initial evaluation and prognosis. Am Fam Physician . 2006;74(8):1367-1370.

Grossman SA, Babineau M, Burke L, et al. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012;30(1):203-206. Sun BC, Costantino G, Barbic F, et al. Priorities for emergency department syncope research. Ann Emerg Med. 2014;64(6):649-655.e2.

Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ . 2016;188(12):E289-E298.

eTable A.

Major Clinical Decision Rules for Syncope

StudyPopulationPredictor variablesOutcome measuredScore resultsValidationComments

Boston Syncope Rule, 2007 (short-term risk)

Derivation: a priori

Validation: 362 ED patients with syncope

Signs of volume depletion

Persistent abnormal vital signs in the ED

Signs and symptoms of acute coronary syndrome

Signs of conduction disease

Worrisome cardiac history

Family history of sudden death

Primary central nervous system event

Valvular heart disease (from history or physical examination)

Critical intervention or adverse outcome at 30 days

Consider admission for one or more variables

Internal: 97% sensitivity, 62% specificity

External: none

25 variables in eight categories make it less practical

Canadian Syncope Risk Rule, 2016 (short-term risk)

Derivation: 4,030 ED patients with syncope

Validation: pending

Predisposition to vasovagal syncope (prodrome/trigger)

History of heart disease

Systolic blood pressure < 90 mm Hg or > 180 mm Hg

Elevated troponin level

Abnormal QRS axis (< 30 or > 110 degrees)

QRS duration > 130 milliseconds

Corrected QT interval > 480 milliseconds

ED diagnosis of vasovagal syncope

ED diagnosis of cardiac syncope

Serious event at 30 days: death, arrhythmia, MI, PE, aortic dissection, CVA, or procedural intervention for syncope

Estimated risk of serious adverse event at 30 days

Pending

Largest prospective study, outcomes consistent with guidelines, clarifies abnormal ECG findings, pending validation to support use of rule

EGSYS score, 2008 (short- and long-term risk)

Derivation: 260 ED patients with syncope

Validation: 258 ED patients with syncope

Palpitations preceding syncope (4 points)

Abnormal ECG findings* or history of heart disease (3 points)

Syncope during effort (3 points) or when supine (2 points)

Autonomic prodromes (−1 point)

Precipitating and/or predisposing factors (−1 point)

Probability of cardiogenic syncope at two years

Consider admission for score of 3 or higher

Internal: 92% sensitivity, 69% specificity

External: 56% sensitivity, 84% specificity

Mortality at two years was 2% in patients with scores < 3 and 21% for scores = 3

OESIL risk score, 2003 (long-term risk)

Derivation: 270 ED patients with syncope

Validation: 328 ED patients with syncope

Abnormal ECG findings*

Absence of prodromal syndrome

Age > 65 years

History of cardiac disease

Mortality at one year

Consider admission for one or more variables

Internal: 100% sensitivity, 22% specificity

External: 95% sensitivity, 31% specificity

Positive variables:

0: 0% mortality

1: 0.6% mortality

2: 14% mortality

3: 29% mortality

4: 53% mortality

ROSE study, 2010 (short-term risk)

Derivation: 550 ED patients with syncope

Validation: 550 ED patients with syncope

Anemia (hemoglobin = 9 g per dL [90 g per L])

Bradycardia (< 50 beats per minute)

Brain natriuretic peptide = 300 pg per mL (300 ng per L)

Chest pain with syncope

ECG showing Q waves (except in lead III)

Oxygen saturation < 94% on room air

Rectal examination showing occult blood (if gastrointestinal bleeding suspected)

Serious events at one month: death, acute MI, PE, CVA, arrhythmias, hemorrhage requiring transfusion of two or more units, subarachnoid hemorrhage, acute procedure, need for pacemaker in first month

Consider admission for one or more variables

Internal: 87% sensitivity, 66% specificity

One-year outcomes: 72% sensitivity, 71% specificity

External: none

Not useful for predicting outcomes at one year; first study to use a biomarker in risk stratification

San Francisco Syncope Rule, 2004 (short-term risk)

Derivation: 684 ED patients with syncope or near syncope

Validation: 791 ED patients with syncope or near syncope

Abnormal ECG findings*

Congestive heart failure

Hematocrit < 30%

Shortness of breath

Systolic blood pressure < 90 mm Hg

Serious events at seven days: acute MI, PE, CVA, arrhythmias, subarachnoid hemorrhage, return ED visit, readmission

Consider admission for one or more variables

Internal: 98% sensitivity, 56% specificity

External: 87% sensitivity, 52% specificity

First tool for short-term events (seven days); inconsistencies in validation scores, but the most studied decision tool


CVA = cerebrovascular accident; ECG = electrocardiography; ED = emergency department; EGSYS = Evaluation of Guidelines in Syncope Study; MI = myocardial infarction; OESIL = Osservatorio Epidemiologico sulla Sincope nel Lazio; PE = pulmonary embolism; ROSE = Risk Stratification of Syncope in the Emergency Department.

*—Abnormal ECG definitions varied with each study.

Information from: Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M; OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003;24(9):811-819.

Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart. 2008;94(12):1620-1626.

Ebell MH. Risk stratification of patients presenting with syncope. Am Fam Physician . 2012;85(11):1047-1052.

Ebell MH. Syncope: initial evaluation and prognosis. Am Fam Physician . 2006;74(8):1367-1370.

Grossman SA, Babineau M, Burke L, et al. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012;30(1):203-206. Sun BC, Costantino G, Barbic F, et al. Priorities for emergency department syncope research. Ann Emerg Med. 2014;64(6):649-655.e2.

Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ . 2016;188(12):E289-E298.

 Enlarge     Print

Table 2.

Risk Stratification in Patients with Syncope

High risk (hospital admission recommended)*

Clinical history suggestive of arrhythmic syncope (e.g., syncope during exercise, palpitations, or syncope without warning or prodrome)

Comorbidities (e.g., severe anemia, electrolyte abnormalities)

Electrocardiographic history suggestive of arrhythmic syncope (e.g., bifascicular block, sinus bradycardia < 40 beats per minute in absence of sinoatrial block or medication use, QRS preexcitation, abnormal QT interval, ST segment elevation leads V1 through V3 [Brugada pattern], negative T wave in right precordial leads and epsilon wave [arrhythmogenic right ventricular dysplasia/cardiomyopathy])

Family history of sudden death

Hypotension (systolic blood pressure < 90 mm Hg)

Older age†

Severe structural heart disease, congestive heart failure, or coronary artery disease

Low risk (outpatient evaluation recommended)‡

Age less than 50 years†

No history of cardiovascular disease

Normal electrocardiographic findings

Symptoms consistent with neurally mediated or orthostatic hypotension syncope

Unremarkable cardiovascular findings


*—Patient is at high risk if any of the criteria are met.

†—Different age thresholds have been used in studies for decision making. Older age largely reflects the patient's cardiovascular health.

‡—Patient is at low risk only if all criteria are met.

Information from references 1 and 25.

Table 2.

Risk Stratification in Patients with Syncope

High risk (hospital admission recommended)*

Clinical history suggestive of arrhythmic syncope (e.g., syncope during exercise, palpitations, or syncope without warning or prodrome)

Comorbidities (e.g., severe anemia, electrolyte abnormalities)

Electrocardiographic history suggestive of arrhythmic syncope (e.g., bifascicular block, sinus bradycardia < 40 beats per minute in absence of sinoatrial block or medication use, QRS preexcitation, abnormal QT interval, ST segment elevation leads V1 through V3 [Brugada pattern], negative T wave in right precordial leads and epsilon wave [arrhythmogenic right ventricular dysplasia/cardiomyopathy])

Family history of sudden death

Hypotension (systolic blood pressure < 90 mm Hg)

Older age†

Severe structural heart disease, congestive heart failure, or coronary artery disease

Low risk (outpatient evaluation recommended)‡

Age less than 50 years†

No history of cardiovascular disease

Normal electrocardiographic findings

Symptoms consistent with neurally mediated or orthostatic hypotension syncope

Unremarkable cardiovascular findings


*—Patient is at high risk if any of the criteria are met.

†—Different age thresholds have been used in studies for decision making. Older age largely reflects the patient's cardiovascular health.

‡—Patient is at low risk only if all criteria are met.

Information from references 1 and 25.

Diagnostic Approach

Guidelines from the Canadian Cardiovascular Society, European Society of Cardiology, and the American College of Emergency Physicians recommend obtaining a detailed history and performing a physical examination, standard 12-lead electrocardiography (ECG), and orthostatic blood pressure measurement in patients presenting with syncope.1,2528 Additional testing should be individualized. Figure 1 provides a general framework, emphasizing classification and risk stratification to standardize the evaluation of syncope.2 High-risk patients should be admitted for monitoring and further workup. Low-risk patients with a first episode of syncope may be reassured without further workup.1,25,27,29

 Enlarge     Print

Evaluation of Syncope

Figure 1.

Algorithm for the evaluation of syncope.

Information from reference 2.

Evaluation of Syncope


Figure 1.

Algorithm for the evaluation of syncope.

Information from reference 2.

HISTORY

A detailed history will suggest a diagnosis in up to 50% of patients and is the most important diagnostic tool in the evaluation of syncope.1 The history should focus on three key elements: (1) Is the loss of consciousness attributable to syncope? (2) Is there a history of cardiovascular disease? (3) Are there clinical features to suggest a specific cause of syncope?30  Pertinent historical elements are listed in Table 3.18,3033 Medication reconciliation is relevant because medications are contributory in 5% to 15% of syncope cases, typically causing orthostatic hypotension, sedation, symptomatic bradycardia, or QT interval prolongation.34 The history should also assist in classifying patients as low or high risk.

 Enlarge     Print

Table 3.

Pertinent Historical Information in the Evaluation of Syncope

FeaturesPossible diagnosis

Position before syncope

Prolonged standing

Neurally mediated syncope (vasovagal), orthostatic hypotension syncope

Sudden change in posture*

Orthostatic hypotension syncope

Supine*

Cardiac syncope (arrhythmia, structural heart disease)

Postsyncope

Amnesia regarding loss of consciousness

Seizure or neurally mediated syncope (vasovagal) in older patients

Eyes closed during event*

Pseudoseizure, psychogenic pseudosyncope

Eyes open during event

Seizure or syncope (any cause)

Fatigue, nausea, vomiting*

Neurally mediated syncope (vasovagal)

Focal neurologic deficit

Neurogenic syncope (cerebrovascular accident or transient ischemic attack)

Immediate complete recovery

Cardiac syncope (arrhythmia), psychogenic pseudosyncope

Incontinence

Seizure (uncommon in syncope; vasovagal syncope most likely)

Myoclonic, tonic-clonic movement

Neurally mediated syncope (vasovagal), seizure

Prolonged confusion*

Seizure

Prolonged syncope

Seizure, neurogenic, metabolic, infectious

Slow pulse

Cardiac syncope (bradyarrhythmia)

Tongue biting*

Seizure

Transient disorientation

Neurally mediated syncope (vasovagal)

Precipitating factors

Activities such as coughing, defecation, eating, laughing, urination*

Neurally mediated syncope (situational)

Emotional distress, fear, pain, prolonged standing, warm or crowded area*

Neurally mediated syncope (vasovagal)

Exertion*

Cardiac syncope (arrhythmia, structural heart disease)

Hand or upper extremity exercise

Subclavian steal syndrome

Head movement, shaving, tight collar*

Neurally mediated syncope (carotid sinus)

Medication use

Antiarrhythmics

Cardiac syncope (arrhythmia, prolonged QT interval)

Antihypertensives

Orthostatic hypotension syncope, cardiac syncope (prolonged QT interval)

Macrolides, antiemetics, antipsychotics, tricyclic antidepressants

Cardiac syncope (prolonged QT interval)

Postexertion

Neurally mediated syncope (vasovagal), cardiac syncope (arrhythmia)

Standing after prolonged sitting

Orthostatic hypotension syncope

Unexplained fall

Neurally mediated syncope (carotid sinus), cardiac syncope (arrhythmia, structural heart disease)

Preexisting disease

Alcoholism, diabetes mellitus, Parkinson disease, renal replacement therapy

Orthostatic hypotension syncope

Family history of sudden cardiac death

Cardiac syncope (long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia/cardiomyopathy, structural heart disease)

Heart disease

Cardiac syncope

History of frequent and prolonged syncopal events

Psychogenic pseudosyncope, neurally mediated syncope (vasovagal)

Older age with dementia

Orthostatic hypotension syncope, cardiac syncope

Psychiatric illness

Psychogenic pseudosyncope

Prodrome

Abdominal pain, diaphoresis, nausea*

Neurally mediated syncope (vasovagal)

Aura

Seizure

Blurred vision, dizziness, lightheadedness, vertigo

Neurally mediated syncope (vasovagal), orthostatic hypotension syncope

Chest pain, dyspnea

Cardiac syncope (structural heart disease, pulmonary embolus, acute myocardial infarction)

Fluttering or palpitations*

Cardiac syncope (arrhythmia)

Focal neurologic deficit

Cerebrovascular accident, transient ischemic attack

Headache

Subarachnoid hemorrhage

Slow pulse

Neurally mediated syncope (vasovagal), cardiac syncope (bradyarrhythmia)

Tonic-clonic movement or posture

Seizure

None

Vasovagal or cardiac syncope in older patients, cardiac syncope in younger patients


*—Salient features from history for differentiation.

Adapted with permission from Parry SW, Tan MP. An approach to the evaluation and management of syncope in adults. BMJ. 2010;340:c880, with additional information from references 18, 30, 32 and 33.

Table 3.

Pertinent Historical Information in the Evaluation of Syncope

FeaturesPossible diagnosis

Position before syncope

Prolonged standing

Neurally mediated syncope (vasovagal), orthostatic hypotension syncope

Sudden change in posture*

Orthostatic hypotension syncope

Supine*

Cardiac syncope (arrhythmia, structural heart disease)

Postsyncope

Amnesia regarding loss of consciousness

Seizure or neurally mediated syncope (vasovagal) in older patients

Eyes closed during event*

Pseudoseizure, psychogenic pseudosyncope

Eyes open during event

Seizure or syncope (any cause)

Fatigue, nausea, vomiting*

Neurally mediated syncope (vasovagal)

Focal neurologic deficit

Neurogenic syncope (cerebrovascular accident or transient ischemic attack)

Immediate complete recovery

Cardiac syncope (arrhythmia), psychogenic pseudosyncope

Incontinence

Seizure (uncommon in syncope; vasovagal syncope most likely)

Myoclonic, tonic-clonic movement

Neurally mediated syncope (vasovagal), seizure

Prolonged confusion*

Seizure

Prolonged syncope

Seizure, neurogenic, metabolic, infectious

Slow pulse

Cardiac syncope (bradyarrhythmia)

Tongue biting*

Seizure

Transient disorientation

Neurally mediated syncope (vasovagal)

Precipitating factors

Activities such as coughing, defecation, eating, laughing, urination*

Neurally mediated syncope (situational)

Emotional distress, fear, pain, prolonged standing, warm or crowded area*

Neurally mediated syncope (vasovagal)

Exertion*

Cardiac syncope (arrhythmia, structural heart disease)

Hand or upper extremity exercise

Subclavian steal syndrome

Head movement, shaving, tight collar*

Neurally mediated syncope (carotid sinus)

Medication use

Antiarrhythmics

Cardiac syncope (arrhythmia, prolonged QT interval)

Antihypertensives

Orthostatic hypotension syncope, cardiac syncope (prolonged QT interval)

Macrolides, antiemetics, antipsychotics, tricyclic antidepressants

Cardiac syncope (prolonged QT interval)

Postexertion

Neurally mediated syncope (vasovagal), cardiac syncope (arrhythmia)

Standing after prolonged sitting

Orthostatic hypotension syncope

Unexplained fall

Neurally mediated syncope (carotid sinus), cardiac syncope (arrhythmia, structural heart disease)

Preexisting disease

Alcoholism, diabetes mellitus, Parkinson disease, renal replacement therapy

Orthostatic hypotension syncope

Family history of sudden cardiac death

Cardiac syncope (long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia/cardiomyopathy, structural heart disease)

Heart disease

Cardiac syncope

History of frequent and prolonged syncopal events

Psychogenic pseudosyncope, neurally mediated syncope (vasovagal)

Older age with dementia

Orthostatic hypotension syncope, cardiac syncope

Psychiatric illness

Psychogenic pseudosyncope

Prodrome

Abdominal pain, diaphoresis, nausea*

Neurally mediated syncope (vasovagal)

Aura

Seizure

Blurred vision, dizziness, lightheadedness, vertigo

Neurally mediated syncope (vasovagal), orthostatic hypotension syncope

Chest pain, dyspnea

Cardiac syncope (structural heart disease, pulmonary embolus, acute myocardial infarction)

Fluttering or palpitations*

Cardiac syncope (arrhythmia)

Focal neurologic deficit

Cerebrovascular accident, transient ischemic attack

Headache

Subarachnoid hemorrhage

Slow pulse

Neurally mediated syncope (vasovagal), cardiac syncope (bradyarrhythmia)

Tonic-clonic movement or posture

Seizure

None

Vasovagal or cardiac syncope in older patients, cardiac syncope in younger patients


*—Salient features from history for differentiation.

Adapted with permission from Parry SW, Tan MP. An approach to the evaluation and management of syncope in adults. BMJ. 2010;340:c880, with additional information from references 18, 30, 32 and 33.

PHYSICAL EXAMINATION

Most patients with syncope will have normal physical examination findings, with the exception of any trauma incurred from the syncopal event. The examination should focus on initial vital signs; orthostatic blood pressure measurements35; and vascular (pulses and carotid bruits), cardiac, pulmonary (evidence of congestive heart failure), abdominal, rectal, and skin/nail (anemia) signs. Any new focal neurologic findings suggest a primary central nervous system lesion.

DIAGNOSTIC TESTING

Carotid sinus massage can be considered in patients older than 40 years to confirm the diagnosis of carotid sinus hypersensitivity. The maneuver is positive when it produces an asystolic or ventricular pause longer than three seconds or a decrease in systolic blood pressure of at least 50 mm Hg. The test is performed while the patient is supine, with five to 10 seconds of massage consecutively to each carotid sinus. It should be performed initially on the right because the maneuver is more often positive on this side. If results are negative, it should be repeated with the patient upright at approximately 60 to 70 degrees.36 This maneuver should be avoided in patients who have had a stroke or transient ischemic attack in the past three months and in patients with carotid bruits. If a positive carotid hypersensitivity test is associated with patient symptoms, then the patient has carotid sinus syndrome.

Routine laboratory studies have low diagnostic yield and should be ordered only if clinically indicated. Laboratory tests can distinguish syncope from other suspected nontraumatic etiologies of loss of consciousness. Elevated troponin and brain natriuretic peptide levels have been shown to predict a higher likelihood of adverse outcomes but should be used only if cardiovascular disease is clinically suspected.26,37,38

ECG generally has a low diagnostic yield (approximately 3% to 5%) but is recommended for all patients with syncope.39,40 Although arrhythmias are unlikely to be detected on a single ECG, ischemic, structural, or conduction abnormalities may be identified. Any ECG abnormality or change from baseline increases the risk of arrhythmia or death within one year of the syncopal event.41

Echocardiography is essential to evaluate suspected structural abnormalities, but it generally has low diagnostic yield. Two studies (n = more than 310) found echocardiography to be clinically useful in patients with syncope if there is a history of cardiac disease, abnormal ECG findings, or suspected significant valvular disease.42,43

Continuous cardiac monitoring is the diagnostic standard to establish a correlation between symptoms and ECG findings. Devices include Holter monitors (generally up to 72 hours), external loop recorders (typically four to six weeks), and implantable loop recorders (up to three years). The diagnostic yield improves with prolonged monitoring. Up to 50% of patients who present with syncope in the absence of heart disease will have an arrhythmia when an implantable loop recorder is placed.44 These devices may increase diagnostic yield, decrease time to diagnosis, and improve cost-effectiveness. Some guidelines recommend them early in the diagnostic workup of unexplained syncope.4548 Patients most likely to benefit from these devices are those with cardiovascular disease, abnormal baseline ECG findings, cardiac symptoms surrounding the syncopal event, and a family history of sudden cardiac death.39

Provocative testing strategies include head-up tilt testing, exercise testing, and electrophysiologic studies. The head-up tilt test is a safe procedure designed to precipitate hypotension and bradycardia and is used to confirm the diagnosis of neurally mediated syncope in patients with an intermediate pretest probability.11 Persons in high-risk settings with unexplained syncope should also be considered for testing. Protocols using isoproterenol or nitroglycerin have an overall sensitivity of 92% to 94%; however, specificity is low.1,49 Exercise testing is useful in exertional syncope, ischemia, and arrhythmia evaluation. Less than 2% of patients referred to cardiologists for evaluation of unexplained syncope undergo electrophysiologic studies.1 These studies have poor sensitivity and specificity except in the setting of structural heart disease; they have been replaced by noninvasive tools such as prolonged ECG monitoring.1,7 Patients who have an indication for implantable cardioverter-defibrillator placement do not require electrophysiologic studies.

Cranial or cardiac imaging, carotid ultrasonography, electroencephalography, and cardiac enzyme testing are rarely helpful in determining the cause of syncope and should not be ordered routinely. These tests affect diagnosis and management in less than 2% of older patients presenting to the emergency department.40 For most patients with tests results that were significant and affected management, the patient's history indicated the diagnosis.50,51  Table 4 provides an overview of the available testing modalities.1,11

 Enlarge     Print

Table 4.

Diagnostic Evaluation of Syncope

TestIndicationComments

Basic laboratory testing

As clinically indicated

Rarely helpful; complete blood count, brain natriuretic peptide testing, fecal occult blood testing, human chorionic gonadotropin testing in women of childbearing age; troponin testing may be beneficial to identify cardiac etiology

Carotid sinus massage

Syncope of unknown etiology in patients older than 40 years1

Diagnostic if ventricular pause is more than three seconds or if systolic blood pressure decreases by more than 50 mm Hg; contraindicated in patients with bruits or a history of transient ischemic attack/cerebrovascular accident within the past three months

ECG

All patients with syncope

Diagnostic yield is 3% to 5%, but can aid in diagnosing arrhythmia, ischemia, pulmonary embolus (increased pulmonary pressures or right ventricular enlargement), hypertrophic cardiomyopathy, and Brugada syndrome; findings suggestive of arrhythmia include bundle branch block, intraventricular conduction delay, sinus bradycardia (less than 50 beats per minute), prolonged QT interval, QRS preexcitation, Q waves

Recurrent syncope with unremarkable initial evaluation; clinical or ECG features suggestive of arrhythmic syncope; unexplained falls

Holter monitoring for 24 to 48 hours, external loop recorders for four to six weeks, implantable loop recorders for up to three years; consider testing in patients with suspected epilepsy not responsive to therapy; implantable loop recorders have high diagnostic yield in recurrent unexplained syncope1

Echocardiography

Suspected structural cardiac disease or when history, examination, and ECG are not diagnostic

Diagnostic in aortic stenosis, pericardial tamponade, obstructive cardiac tumors or thrombi, aortic dissection, hypertrophic cardiomyopathy, congenital anomalies of the coronary arteries, acute right ventricular strain (in pulmonary embolism)

Electrophysiology

Arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, high-risk occupations, suspected intermittent bradycardia, syncope in patients with bundle branch block,1 syncope preceded by palpitations suspicious for sinus tachycardia

Not recommended in patients without underlying heart disease; consider in high-risk patients with recurrent unexplained syncope

Exercise testing

Hemodynamic and ECG abnormalities with syncope during exercise, syncope reproduced with exercise, polymorphic ventricular tachycardia, prolonged QT interval, to precipitate a Mobitz type 2 second- or third-degree block during exercise1

Inadequate blood pressure increase in younger patients suggests hypertrophic cardiomyopathy or ischemia; similar findings in older persons may suggest autonomic dysfunction; may unmask ECG changes of channelopathies

Head-up tilt test

Neurally mediated syncope, recurrent unexplained falls, frequent syncopal episodes, psychiatric disease, to distinguish between neurally mediated and orthostatic hypotension syncope, to differentiate syncope with jerking movements from seizure1

Used in patients with negative initial findings, normal cardiac structure, and no evidence of ischemia; contraindicated in patients with ischemic heart disease, uncontrolled hypertension, left ventricular outflow tract obstruction, or aortic stenosis

Neurologic testing*

Suspected seizures, cerebrovascular event, neurodegenerative disorder, increased intracranial pressure

Seizure can be confirmed with electroencephalography; cranial imaging studies as clinically indicated; 20% to 30% of seizures with transient loss of consciousness could be the result of syncope; tonic-clonic limb movements and muscle twitching may occur in cardiac and neurally mediated syncope

Orthostatic blood pressure measurement

Neurally mediated syncope, postural tachycardia syndrome, orthostatic hypotension syncope1

Diagnostic if systolic blood pressure is less than 90 mm Hg or decreases by 20 mm Hg or more (10 mm Hg or more in symptomatic patients); increase of 30 beats per minute suggests postural tachycardia syndrome; up to 40% of asymptomatic adults older than 70 years and 23% of patients younger than 60 years will have positive orthostatic blood pressure measurements

Psychiatric evaluation

Suspected psychogenic pseudosyncope1

Consider with concurrent electroencephalography and video monitoring


ECG = electrocardiography.

*—Includes electroencephalography, computed tomography, magnetic resonance imaging, or carotid ultrasonography. Information from references 1 and 11.

Table 4.

Diagnostic Evaluation of Syncope

TestIndicationComments

Basic laboratory testing

As clinically indicated

Rarely helpful; complete blood count, brain natriuretic peptide testing, fecal occult blood testing, human chorionic gonadotropin testing in women of childbearing age; troponin testing may be beneficial to identify cardiac etiology

Carotid sinus massage

Syncope of unknown etiology in patients older than 40 years1

Diagnostic if ventricular pause is more than three seconds or if systolic blood pressure decreases by more than 50 mm Hg; contraindicated in patients with bruits or a history of transient ischemic attack/cerebrovascular accident within the past three months

ECG

All patients with syncope

Diagnostic yield is 3% to 5%, but can aid in diagnosing arrhythmia, ischemia, pulmonary embolus (increased pulmonary pressures or right ventricular enlargement), hypertrophic cardiomyopathy, and Brugada syndrome; findings suggestive of arrhythmia include bundle branch block, intraventricular conduction delay, sinus bradycardia (less than 50 beats per minute), prolonged QT interval, QRS preexcitation, Q waves

Recurrent syncope with unremarkable initial evaluation; clinical or ECG features suggestive of arrhythmic syncope; unexplained falls

Holter monitoring for 24 to 48 hours, external loop recorders for four to six weeks, implantable loop recorders for up to three years; consider testing in patients with suspected epilepsy not responsive to therapy; implantable loop recorders have high diagnostic yield in recurrent unexplained syncope1

Echocardiography

Suspected structural cardiac disease or when history, examination, and ECG are not diagnostic

Diagnostic in aortic stenosis, pericardial tamponade, obstructive cardiac tumors or thrombi, aortic dissection, hypertrophic cardiomyopathy, congenital anomalies of the coronary arteries, acute right ventricular strain (in pulmonary embolism)

Electrophysiology

Arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, high-risk occupations, suspected intermittent bradycardia, syncope in patients with bundle branch block,1 syncope preceded by palpitations suspicious for sinus tachycardia

Not recommended in patients without underlying heart disease; consider in high-risk patients with recurrent unexplained syncope

Exercise testing

Hemodynamic and ECG abnormalities with syncope during exercise, syncope reproduced with exercise, polymorphic ventricular tachycardia, prolonged QT interval, to precipitate a Mobitz type 2 second- or third-degree block during exercise1

Inadequate blood pressure increase in younger patients suggests hypertrophic cardiomyopathy or ischemia; similar findings in older persons may suggest autonomic dysfunction; may unmask ECG changes of channelopathies

Head-up tilt test

Neurally mediated syncope, recurrent unexplained falls, frequent syncopal episodes, psychiatric disease, to distinguish between neurally mediated and orthostatic hypotension syncope, to differentiate syncope with jerking movements from seizure1

Used in patients with negative initial findings, normal cardiac structure, and no evidence of ischemia; contraindicated in patients with ischemic heart disease, uncontrolled hypertension, left ventricular outflow tract obstruction, or aortic stenosis

Neurologic testing*

Suspected seizures, cerebrovascular event, neurodegenerative disorder, increased intracranial pressure

Seizure can be confirmed with electroencephalography; cranial imaging studies as clinically indicated; 20% to 30% of seizures with transient loss of consciousness could be the result of syncope; tonic-clonic limb movements and muscle twitching may occur in cardiac and neurally mediated syncope

Orthostatic blood pressure measurement

Neurally mediated syncope, postural tachycardia syndrome, orthostatic hypotension syncope1

Diagnostic if systolic blood pressure is less than 90 mm Hg or decreases by 20 mm Hg or more (10 mm Hg or more in symptomatic patients); increase of 30 beats per minute suggests postural tachycardia syndrome; up to 40% of asymptomatic adults older than 70 years and 23% of patients younger than 60 years will have positive orthostatic blood pressure measurements

Psychiatric evaluation

Suspected psychogenic pseudosyncope1

Consider with concurrent electroencephalography and video monitoring


ECG = electrocardiography.

*—Includes electroencephalography, computed tomography, magnetic resonance imaging, or carotid ultrasonography. Information from references 1 and 11.

Treatment

The treatment of syncope is directed at the underlying cause. Morbidity and mortality are generally low except in cardiac syncope; therefore, patient reassurance is an important part of treatment.

NEURALLY MEDIATED SYNCOPE

Treatment of neurally mediated syncope includes reassurance, education, and physical therapy.1 In situational syncope, it is important to avoid potential triggers. Physical counterpressure maneuvers such as leg crossing, squatting, and tensing the lower extremities are effective at the onset of prodromal symptoms.7 One randomized trial showed that these maneuvers reduce syncope by 39%.52 Tilt training involves standing for prolonged periods, and compliance is generally poor.7

Pharmacologic therapy with beta blockers, alpha agonists, and fludrocortisone has shown no effectiveness or conflicting results in reducing vasovagal syncope.1 In one small randomized trial of patients with a history of recurrent vasovagal syncope, paroxetine (Paxil) prevented additional episodes in 82.4% compared with 47.1% in the placebo group over two years (P < .001), although guidelines recommend its use only in patients with concurrent psychiatric disease.53 In patients with severe asystole from neurally mediated syncope, a double-blind, randomized, placebo-controlled trial showed that the use of permanent dual chamber pacing reduced the risk of recurrent syncope.54

ORTHOSTATIC HYPOTENSION

Treatment of orthostatic hypotension includes education and lifestyle modifications, such as slowly transitioning from a supine or sitting position to standing and increasing fluid and sodium intake.1 Contributing medications should be discontinued or decreased, if possible. Other treatment modalities include elevating the head of the bed by 10 degrees, compression stockings/abdominal binders, and counterpressure maneuvers.1 If these do not mitigate symptoms, midodrine and fludrocortisone are effective treatments.55

CARDIAC SYNCOPE

Management of cardiac syncope is directed at the underlying etiology. Options include antiarrhythmic drugs, cardiac pacing, catheter-directed ablation, and, rarely, implantable cardioverter-defibrillator placement.1

This article updates previous articles on this topic by Gauer,56 and by Miller and Kruse.57

Data Sources: We searched OvidSP, Essential Evidence Plus, the National Guideline Clearinghouse, Cochrane Library, and UpToDate using combinations of the following key words: syncope, transient loss of consciousness, presyncope, clinical decision rules, risk stratification, mortality, morbidity, etiology, incidence, electrocardiographic monitoring, electrophysiologic studies, diagnostic evaluation, hospitalization, brain natriuretic peptide, troponin, cardiac enzymes, implantable loop recorders, cost, quality of life, carotid sinus massage, head-up tilt table, implantable cardioverter defibrillator, guidelines, orthostatic hypotension, diagnostic evaluation, medical cost, postural tachycardia syndrome. Search dates: June 22 to August 6, 2015, and October 15, 2016.

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Defense.

The Authors

show all author info

LLOYD A. RUNSER, MD, MPH, FAAFP, is associate program director and research coordinator at the Womack Army Medical Center Family Medicine Residency Program, Fort Bragg, N.C., and assistant professor in the Department of Family Medicine at the Uniformed Services University of the Health Sciences, Bethesda, Md....

ROBERT L. GAUER, MD, is assistant professor of family medicine at the Uniformed Services University of the Health Sciences and a hospitalist at Womack Army Medical Center.

ALEX HOUSER, DO, is a second-year resident at the Womack Army Medical Center Family Medicine Residency Program.

Address correspondence to Lloyd A. Runser, MD, MPH, at lloyd.a.runser2.mil@mail.mil. Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations.

REFERENCES

show all references

1. The European Society of Cardiology guidelines for the diagnosis and management of syncope. Eur Heart J. 2009;30(21):2539–2540....

2. Mereu R, Sau A, Lim PB. Diagnostic algorithm for syncope. Auton Neurosci. 2014;184:10–16.

3. Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol. 2014;63(3):171–177.

4. Alshekhlee A, Shen WK, Mackall J, Chelimsky TC. Incidence and mortality rates of syncope in the United States. Am J Med. 2009;122(2):181–188.

5. Sun BC, Emond JA, Camargo CA Jr. Direct medical costs of syncope-related hospitalizations in the United States. Am J Cardiol. 2005;95(5):668–671.

6. Hatoum T, Sheldon R. A practical approach to investigation of syncope. Can J Cardiol. 2014;30(6):671–674.

7. Saklani P, Krahn A, Klein G. Syncope. Circulation. 2013;127(12):1330–1339.

8. D'Ascenzo F, Biondi-Zoccai G, Reed MJ, et al. Incidence, etiology and predictors of adverse outcomes in 43,315 patients presenting to the emergency department with syncope: an international meta-analysis. Int J Cardiol. 2013;167(1):57–62.

9. Solbiati M, Casazza G, Dipaola F, et al. Syncope recurrence and mortality: a systematic review. Europace. 2015;17(2):300–308.

10. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878–885.

11. Ray JC, Kusumoto F, Goldschlager N. Syncope. J Intensive Care Med. 2016;31(2):79–93.

12. Ruwald MH, Hansen ML, Lamberts M, et al. Prognosis among healthy individuals discharged with a primary diagnosis of syncope. J Am Coll Cardiol. 2013;61(3):325–332.

13. Kachalia A, Berg A, Fagerlin A, et al. Overuse of testing in preoperative evaluation and syncope: a survey of hospitalists. Ann Intern Med. 2015;162(2):100–108.

14. Sun BC, McCreath H, Liang LJ, et al. Randomized clinical trial of an emergency department observation syncope protocol versus routine inpatient admission. Ann Emerg Med. 2014;64(2):167–175.

15. Brignole M, Ungar A, Casagranda I, et al.; Syncope Unit Project (SUP) investigators. Prospective multicentre systematic guideline-based management of patients referred to the syncope units of general hospitals. Europace. 2010;12(1):109–118.

16. Mitro P, Kirsch P, Valočik G, Murín P. A prospective study of the standardized diagnostic evaluation of syncope. Europace. 2011;13(4):566–571.

17. Saal DP, van Dijk JG. Classifying syncope. Auton Neurosci. 2014;184:3–9.

18. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol. 2001;37(7):1921–1928.

19. Robertson D. The epidemic of orthostatic tachycardia and orthostatic intolerance. Am J Med Sci. 1999;317(2):75–77.

20. Thiruganasambandamoorthy V, Stiell IG, Wells GA, Vaidyanathan A, Mukarram M, Taljaard M. Outcomes in presyncope patients: a prospective cohort study. Ann Emerg Med. 2015;65(3):268–276.e6.

21. Grossman SA, Babineau M, Burke L, et al. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012;30(1):203–206.

22. Sun BC, Costantino G, Barbic F, et al. Priorities for emergency department syncope research. Ann Emerg Med. 2014;64(6):649–655.e2

23. Ebell MH. Syncope: initial evaluation and prognosis. Am Fam Physician. 2006;74(8):1367–1370.

24. Ebell MH. Risk stratification of patients presenting with syncope. Am Fam Physician. 2012;85(11):1047–1052.

25. Sheldon RS, Morillo CA, Krahn AD, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol. 2011;27(2):246–253.

26. Reed MJ, Newby DE, Coull AJ, Prescott RJ, Jacques KG, Gray AJ. The ROSE (Risk Stratification of Syncope in the Emergency Department) study. J Am Coll Cardiol. 2010;55(8):713–721.

27. Huff JS, Decker WW, Quinn JV, et al.; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007;49(4):431–444.

28. van Dijk N, Boer KR, Colman N, et al. High diagnostic yield and accuracy of history, physical examination, and ECG in patients with transient loss of consciousness in FAST: the Fainting Assessment study. J Cardiovasc Electrophysiol. 2008;19(1):48–55.

29. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF scientific statement on the evaluation of syncope. J Am Coll Cardiol. 2006;47(2):473–484.

30. Benditt DG, Adkisson WO. Approach to the patient with syncope: venues, presentations, diagnoses. Cardiol Clin. 2013;31(1):9–25.

31. Parry SW, Tan MP. An approach to the evaluation and management of syncope in adults. BMJ. 2010;340:c880.

32. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40(1):142–148.

33. Moya A, Sutton R, Ammirati F, et al.; Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631–2671.

34. Lemonick DM. Evaluation of syncope in the emergency department. Am J Clin Med. 2010;7(1):11–19.

35. Ooi WL, Hossain M, Lipsitz LA. The association between orthostatic hypotension and recurrent falls in nursing home residents. Am J Med. 2000;108(2):106–111.

36. Krediet CT, Parry SW, Jardine DL, Benditt DG, Brignole M, Wieling W. The history of diagnosing carotid sinus hypersensitivity: why are the current criteria too sensitive? Europace. 2011;13(1):14–22.

37. Costantino G, Furlan R. Syncope risk stratification in the emergency department. Cardiol Clin. 2013;31(1):27–38.

38. Reed MJ, Mills NL, Weir CJ. Sensitive troponin assay predicts outcome in syncope. Emerg Med J. 2012;29(12):1001–1003.

39. Krahn AD, Andrade JG, Deyell MW. Selecting appropriate diagnostic tools for evaluating the patient with syncope/collapse. Prog Cardiovasc Dis. 2013;55(4):402–409.

40. Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med. 2009;169(14):1299–1305.

41. Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Ann Emerg Med. 2004;43(2):224–232.

42. Anderson KL, Limkakeng A, Damuth E, Chandra A. Cardiac evaluation for structural abnormalities may not be required in patients presenting with syncope and a normal ECG result in an observation unit setting. Ann Emerg Med. 2012;60(4):478–484.e1

43. Sarasin FP, Junod AF, Carballo D, Slama S, Unger PF, Louis-Simonet M. Role of echocardiography in the evaluation of syncope: a prospective study. Heart. 2002;88(4):363–367.

44. Ruwald MH, Zareba W. ECG monitoring in syncope. Prog Cardiovasc Dis. 2013;56(2):203–210.

45. Davis S, Westby M, Pitcher D, Petkar S. Implantable loop recorders are cost-effective when used to investigate transient loss of consciousness which is either suspected to be arrhythmic or remains unexplained. Europace. 2012;14(3):402–409.

46. Edvardsson N, Frykman V, van Mechelen R, et al.; PICTURE Study Investigators. Use of an implantable loop recorder to increase the diagnostic yield in unexplained syncope: results from the PICTURE registry. Europace. 2011;13(2):262–269.

47. Edvardsson N, Wolff C, Tsintzos S, Rieger G, Linker NJ. Costs of unstructured investigation of unexplained syncope: insights from a micro-costing analysis of the observational PICTURE registry. Europace. 2015;17(7):1141–1148.

48. Krahn AD, Klein GJ, Yee R, Hoch JS, Skanes AC. Cost implications of testing strategy in patients with syncope: randomized assessment of syncope trial. J Am Coll Cardiol. 2003;42(3):495–501.

49. Forleo C, Guida P, Iacoviello M, et al. Head-up tilt testing for diagnosing vasovagal syncope: a meta-analysis. Int J Cardiol. 2013;168(1):27–35.

50. Chiu DT, Shapiro NI, Sun BC, Mottley JL, Grossman SA. Are echocardiography, telemetry, ambulatory electrocardiography monitoring, and cardiac enzymes in emergency department patients presenting with syncope useful tests? A preliminary investigation. J Emerg Med. 2014;47(1):113–118.

51. Johnson PC, Ammar H, Zohdy W, Fouda R, Govindu R. Yield of diagnostic tests and its impact on cost in adult patients with syncope presenting to a community hospital. South Med J. 2014;107(11):707–714.

52. van Dijk N, Quartieri F, Blanc JJ, et al.; PC-Trial Investigators. Effectiveness of physical counterpressure maneuvers in preventing vasovagal syncope: the Physical Counterpressure Manoeuvres Trial (PC-Trial). J Am Coll Cardiol. 2006;48(8):1652–1657.

53. Di Girolamo E, Di Iorio C, Sabatini P, Leonzio L, Barbone C, Barsotti A. Effects of paroxetine hydrochloride, a selective serotonin reuptake inhibitor, on refractory vasovagal syncope: a randomized, double-blind, placebo-controlled study. J Am Coll Cardiol. 1999;33(5):1227–1230.

54. Brignole M, Menozzi C, Moya A, et al. Pacemaker therapy in patients with neurally mediated syncope and documented asystole: Third International Study on Syncope of Uncertain Etiology (ISSUE-3): a randomized trial. Circulation. 2012;125(21):2566–2571.

55. Benditt DG, Nguyen JT. Syncope: therapeutic approaches. J Am Coll Cardiol. 2009;53(19):1741–1751.

56. Gauer RL. Evaluation of syncope. Am Fam Physician. 2011;84(6):640–650.

57. Miller TH, Kruse JE. Evaluation of syncope. Am Fam Physician. 2005;72(8):1492–1500.

 

 

Copyright © 2017 by the American Academy of Family Physicians.
This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact afpserv@aafp.org for copyright questions and/or permission requests.

Want to use this article elsewhere? Get Permissions


More in AFP


Editor's Collections


Related Content


More in Pubmed

MOST RECENT ISSUE


Aug 15, 2018

Access the latest issue of American Family Physician

Read the Issue


Email Alerts

Don't miss a single issue. Sign up for the free AFP email table of contents.

Sign Up Now

Navigate this Article