Last updated: July 19, 2022

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Syncope is a sudden, transient loss of consciousness, which is thought to be secondary to cerebral hypoperfusion. It can be divided into cardiac syncope, e.g., due to arrhythmias or structural heart disease (potentially life-threatening), and noncardiac syncope, which includes frequently benign causes such as reflex syncope (due to vasovagal responses or carotid sinus syndrome) and orthostatic syncope. The diagnostic approach is focused on determining if loss of consciousness was due to syncope (ruling out differential diagnoses), ruling out immediately life-threatening causes of syncope, and determining the risk of serious adverse events from syncope, which further guide management and disposition. This involves obtaining a detailed history and performing a physical examination, including orthostatic vital sign measurements and an initial ECG. Further diagnostics should be guided by clinical suspicion of the underlying disease. In many cases, syncope is multifactorial and it is not possible to determine a specific etiology. The treatment strategy depends on the cause.

  • Loss of consciousness: a state characterized by the loss of awareness of self and the surroundings and an inability to respond to stimuli [1]
  • Transient loss of consciousness: a temporary; (short duration) and self-limited form of loss of consciousness; A term used predominantly during clinical evaluation while the pathogenesis is still unclear. [1][2]
  • Syncope: an abrupt transient loss of consciousness with rapid and spontaneous recovery, which is thought to be caused by cerebral hypoperfusion [1]
  • Presyncope: symptoms that usually precede syncope (e.g., lightheadedness, visual symptoms, possibly altered consciousness without loss of consciousness); may or may not progress to syncope. [1]

The following categories are consistent with nomenclature and classification used in the 2017 American Heart Association (AHA) syncope guidelines. [1]

Cardiac syncope

Includes arrhythmogenic, myocardial, and other vascular etiologies of syncope

Noncardiac syncope

Includes reflex syncope (most common type of syncope) and orthostatic syncope

Type of noncardiac syncope
Underlying mechanism(s) Examples of triggers and/or underlying causes
Reflex syncopes Vasovagal syncope (Neurocardiogenic syncope)
  • Prolonged standing
  • Emotional stress, e.g., fear, sight of blood, medical procedures
  • Pain or injury
  • Heat exposure
  • Can be idiopathic
Situational syncope
Carotid sinus syndrome
  • Pressure on the carotid sinuses (e.g., during a massage, when shaving, tightening a necktie)
Orthostatic syncopes


The following are lists of underlying causes of syncope. For a list of syncope mimics, i.e., other causes of transient loss of consciousness, see “Differential diagnosis of syncope.”

Cardiac and vascular causes [11]

This category includes life-threatening causes of syncope that require specialized management. See “Cardiac syncope” for further details.

Cardiac and vascular causes of syncope have a higher chance of being life-threatening and should be ruled out first!

Noncardiac causes

These typically benign etiologies can coexist in the same patient, i.e., they are not mutually exclusive. See “Noncardiac syncope” for further details.

Reflex-mediated and orthostatic causes of syncope occur more frequently and tend to be more benign than cardiac and vascular causes.

Vasovagal syncope and situational syncope can occur more easily in patients with preexisting orthostatic hypotension.

Patients with cardiac syncope often present without any prodrome, i.e., a sudden fall, which may be accompanied by injuries resulting from a lack of protective reflexes.

Thorough neurological and cardiopulmonary assessments, including pulse and blood pressure measurement in the supine, standing, and sitting positions, are crucial for identifying the underlying etiology!

The following recommendations are consistent with the 2017 American Heart Association (AHA) syncope guidelines. [1]

Initial management [1][2][11][12][13][14]

Syncope and presyncope can be multifactorial, with widely varying etiologies and diagnostic approaches. Focus on identifying the possible etiology of syncope while excluding differential diagnoses of syncope. [12]

Evaluate patients with presyncope similarly to those with syncope.

All forms of syncope are more likely to occur when multiple precipitating factors are present.

Rule out life-threatening causes of syncope such as pulmonary embolism, hemorrhage, and serious cardiac conditions!

Routine investigations [1][2][12][13]

Adding an ECG and orthostatic vital signs to a thorough clinical evaluation can help identify the etiology of syncope in up to 50% of patients. [12]


Orthostatic vital signs [15]

  • Method
    • Measure blood pressure and heart rate after the patient has been in a supine position for 5 minutes.
    • Ask the patient to stand up and retake vital signs after 1 minute and 3 minutes (a third measurement after 10 minutes is optional).
    • Document any symptoms that the patient experiences.
  • Findings

Laboratory studies

These are commonly requested as part of the initial workup. See “Further investigations” for more detailed diagnostics. [12]

Disposition [1][2][11][12][13][14]

Disposition decisions should take into account individual patient factors and follow local hospital policy (see also “Risk stratification”).

Most serious causes of syncope are identified within hours to days; however, it can take up to 2 weeks to identify arrhythmias, and syncope can be idiopathic up to 40% of cases. [1][11][12][13]


  • Consider individualized risk stratification in all patients with syncope.
  • Prioritize detailed risk stratification in patients with syncope of unclear etiology despite an initial diagnostic workup.
  • Consider using risk scores as an adjunct to clinical evaluation. [1]

Prognostic factors [1][2][12]

The following factors can affect the risk of death and serious underlying conditions, e.g., cardiac arrhythmias, MI, PE, and aortic dissection.

Risk of serious adverse events following a syncopal episode [1][2][12]
Features that lower risk Features that increase risk
Patient characteristics
Characteristics of the episode Triggers
  • Exercise
Additional features
  • Long history of recurrent syncope with similar characteristics
  • Occurs in the standing position
Physical examination
  • Normal
  • Normal
Laboratory studies
  • Normal

Risk scores

  • Clinical applications
    • Several scoring systems have been proposed but have limited utility.
    • Consider using risk scores to supplement but not replace clinical judgment. [1]
  • Examples
    • Canadian Syncope Risk Score [16][17][18][19][20]
    • San Francisco Syncope Rule [21][22]

Experts discourage using syncope risk scores in isolation. [1][23]

These recommendations are consistent with the 2017 AHA syncope guidelines, the 2018 European society of cardiology (ESC) syncope guidelines, the 2021 American College of Radiology (ACR) appropriateness criteria for syncope, and Choosing Wisely recommendations on patients with syncope from the American Academy of Neurology (AAN), American College of Physicians (ACP), American College of Emergency Physicians (ACEP), and American Epilepsy Society (AES). Further investigations are not routinely indicated and should be guided by clinical suspicion. [1][2][24][25][26][27][28][29]


  • Consider expanded investigations in patients with syncope of unclear etiology after an initial evaluation, especially if there is a high risk of serious adverse events from syncope.
  • Consider imaging studies based on the pretest probability (PTP) of cardiac syncope (see “Cardiovascular imaging”). [25]
    • Patients with a high PTP: A resting transthoracic echocardiogram is usually appropriate.
    • Patients with a low PTP: Consider CXR ; most other advanced imaging studies are usually inappropriate.
  • Consider syncope provocation studies in patients with a suspected but uncertain diagnosis of noncardiac syncope.
  • Avoid routine neurological investigations unless there is a strong clinical suspicion for an underlying neurological cause. [26][27][28][29]
  • Consider psychiatric evaluation for patients with suspected psychogenic pseudosyncope.

In many cases of syncope (30–40%), the underlying etiology remains unclear even after an exhaustive diagnostic workup has been completed. [1][12][13]

Cardiovascular studies [1][24]

Consider the following in consultation with a cardiologist in patients with high-risk features or suspected structural cardiac disease.

Syncope provocation studies [1][2][24]

Carotid sinus massage is contraindicated in patients with a history of TIA, stroke, or myocardial infarction in the past 3 months, patients with ventricular arrhythmias, and those with a history of complications from a previous massage. [31]

Neurological investigations [1][2][24]

These studies are not routinely recommended in patients with simple syncope without neurological features. [12][27][28]

Avoid routine neuroimaging, neurovascular studies, and EEG when evaluating patients with simple syncope without neurological symptoms or abnormal neurological findings. [12][26][27][28][33]

The term cardiac syncope is used in the 2017 AHA syncope guidelines to denote arrhythmogenic, myocardial, and vascular causes of syncope that are more often life-threatening. [1]

General principles

Syncope may be the first manifestation of a life-threatening cardiac condition.

Management [1][2][12][13]

Cardiac and vascular causes of syncope [1][12]
Conditions Characteristic features Diagnostic findings Management
Arrhythmogenic syncope
Cardiomyopathy [34][35]
Acute myocardial infarction
Valvular heart diseases [36]
  • Cardiac imaging: variable depending on the affected valve(s)
    • Chamber dilation or hypertrophy
    • Valve thickening
    • Calcifications
Cardiac tamponade [37]
Acute aortic dissection [38]
  • ECG: nonspecific changes
  • CTA chest or MRI chest: visualization of dissecting segment
Pulmonary hypertension [39][40]
Pulmonary embolism [41]

Recommendations in this article are consistent with the 2017 AHA syncope guidelines and the 2015 Heart Rhythm Society guidelines on vasovagal syncope and POTS. The term noncardiac syncope is used in the 2017 AHA syncope guidelines to denote typically benign causes of syncope that are not directly cardiogenic or vascular in origin but are mediated by neurological, hormonal, or metabolic effects on cardiovascular physiology. [1][2][42]

General principles

  • Noncardiac syncope is frequently associated with a prodrome and specific physiological or environmental triggers, which vary depending on the etiology.
  • When performed, syncope provocation studies (e.g., tilt table test) may aid the diagnosis.
  • Other studies (e.g., laboratory studies, ECG) usually do not show significant findings.

A prodrome characterized by diaphoresis and pallor is commonly reported in patients with all types of noncardiac syncope.

Reflex syncope [1][2][12][42]

  • Includes all types of neurally mediated syncope
  • Common mechanism: parasympathetic hyperactivity (cardioinhibitory response), sympathetic hypoactivity (vasodepressor response), or a combination of both vasodilatation (vasodepressor response) and/or bradycardia (cardioinhibitory response) → reduced BP → reduced cerebral perfusion

Reflex syncope is the most common cause of syncope. It is benign and usually self-limiting.

Vasovagal syncope (VVS; neurocardiogenic syncope)

  • Epidemiology
    • Common in younger patients (the first episode is rare after 40 years of age)
    • Can be recurrent
  • Mechanism (vasovagal response): Trigger activates vagus nerve → ↑ parasympathetic nervous tone → ↓ heart rate, ↓ blood pressure, ↓ cardiac contractility, ↑ peripheral vasodilation
  • Clinical features
  • Possible triggers
    • Prolonged standing
    • Emotional stress, e.g., fear, the sight of blood, medical procedures
    • Pain or injury
    • Heat exposure
    • Can be idiopathic
  • Diagnosis is clinical and requires presyncope or syncope associated with the following:

Situational syncope

Carotid sinus syndrome

Orthostatic syncope [1][2][12]

Although orthostasis is most often benign in origin, there may be more serious underlying etiologies and it can increase the risk of other types of syncope.

If there is evidence of underlying hypovolemia, determine its severity and rule out serious cardiac and vascular causes (see “Cardiac syncope”).

Neurogenic orthostatic hypotension

Postural tachycardia syndrome (POTS) [42][44]

Postural tachycardia syndrome typically causes presyncope with significant orthostatic tachycardia. Orthostatic hypotension is minimal and a complete loss of consciousness is rare. [44]

Management of noncardiac syncope [1][2][12][42][44]

Once life-threatening causes have been excluded, the remaining possible noncardiac causes for syncope are often benign and usually self-limiting or can be successfully managed with nonpharmacological treatment to prevent future episodes. Rarely, medication or pacemakers may be necessary.

Nonpharmacological treatment

  • Fluid management: Increase fluid (2–3 liters/day) and sodium intake (6–9 g of salt/day) unless contraindicated. [1]
  • Medication adjustment: Consider discontinuing or decreasing the dosage of offending or contributing drugs (e.g., diuretics, antihypertensives).
  • Patient education
  • Compression stockings (at least thigh high): Consider for patients with orthostatic syncope (including neurogenic orthostatic hypotension and POTS).
  • Other specific measures [1]
    • Counterpressure maneuvers
      • Physical maneuvers (e.g., squatting, leg crossing, tensing, abdominal contraction, and acute water ingestion) to increase blood pressure in patients with a syncopal prodrome
      • Recommended in all patients with VVS or orthostatic hypotension who have a significantly long prodrome.
    • Orthostatic training
      • For example, patients are instructed to stand against a wall daily for 30 minutes to 1 hour.
      • Consider for patients with VVS if syncope recurs despite counterpressure maneuvers and increased salt and fluid intake.
    • Aerobic exercise programs: may improve symptoms in patients with POTS [44]

Pharmacological therapy

Cardiac pacemakers

The following is suggested for patients with an acute syncopal episode or transient loss of consciousness of unclear origin.

The following is a list of syncope mimics, i.e., other causes of transient loss of consciousness. For a list of underlying causes of syncope, see “Etiology of syncope.”

Differential diagnoses for syncope [2]
Common clinical features and patient history Characteristic diagnostic findings
Psychogenic pseudosyncope [45]
  • Prolonged duration of the event
  • Eyes closed
  • Frequent episodes
  • Unusual triggers and/or prodromes
Subclavian steal syndrome
  • Patients with diabetes: glucose < 70 mg/dL
  • Patients without diabetes: glucose < 50 mg/dL
Traumatic brain injury
  • History of trauma
Heatstroke [46]
  • Induced by significant heat, exertion
  • High body temperature
Acute hyperventilation syndrome
Drop attacks
  • Diagnostic studies are indicated based on clinical evaluation: e.g., CT or MRI head , audiometry and ENT evaluation


The differential diagnoses listed here are not exhaustive.

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