Last updated: September 15, 2023

Summarytoggle arrow icon

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.

Definitionstoggle arrow icon

  • 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]

Overviewtoggle arrow icon

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

Types 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., due to 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


Etiologytoggle arrow icon

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.

Clinical featurestoggle arrow icon

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.


Managementtoggle arrow icon

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]

Risk stratificationtoggle arrow icon


  • 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]

Further investigationstoggle arrow icon

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]

Cardiac syncopetoggle arrow icon

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]

Noncardiac syncopetoggle arrow icon

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]

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

Vasovagal syncope (VVS; neurocardiogenic syncope)

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 [1][2][12]

Postprandial orthostatic hypotension [46][47]

Postural tachycardia syndrome (POTS) [42][51]

Postural tachycardia syndrome typically causes presyncope with significant orthostatic tachycardia. Orthostatic hypotension is minimal and a complete loss of consciousness is rare. [51]

Exercise-associated postural hypotension (EAPH) [52]

  • Definition: inability to stand or walk without assistance (i.e., collapse) after vigorous exertion
  • Epidemiology: : occurs most commonly in athletes (especially upon completion of endurance running)
  • Risk factors: mild dehydration, excessive exercise (overexertion), and reduced baroreflex response to hypotension due to long-term endurance training [53]
  • Pathophysiology
    • During exercise, ↑ blood flow to muscles of the lower extremities; ↑ skeletal muscle pump activity → ↑ venous return to the heart
    • Sudden cessation of exercise → loss of skeletal muscle pump activity → venous return → large volumes of blood pool in the lower extremities → postural hypotension → collapse
  • Clinical features
  • Diagnostics: diagnosis of exclusion
  • Management
  • Prevention
    • Adequate hydration before and during exercise
    • Continued walking upon completion of vigorous exercise to prevent venous pooling in the lower extremities

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

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.

Nonpharmacological management of noncardiac syncope [1][2][42]

  • 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
    • If possible, instruct patients to avoid or anticipate triggers.
    • Advise patients with a short prodrome to lie down when prodrome is detected (to avoid injuries from falls).
    • Patients with long prodromes may benefit from acute water ingestion and physical counterpressure measures, e.g.: [1][54]
      • Squatting
      • Leg crossing
      • Muscle tensing (e.g., abdominal contraction)
      • Muscle pumping (e.g., marching in place)
      • Bending over
    • Advise the patient to educate friends and family on basic first aid for syncope. [55]
  • Compression stockings (at least thigh high) : Consider for patients with orthostatic syncope.

Overview of pharmacological therapy

If symptoms persist despite nonpharmacological management, consider trialing medication.

Medications for noncardiac syncope [1][12][42]
Medication Indications Cautions
Beta blockers, e.g., propranolol [51]
Octreotide [56][57][58]
Acarbose [48]
Pyridostigmine [60]

Most drugs used in the management of noncardiac syncope are not licensed for this use; usage is off-label and local protocols should be followed where available.

Acute management checklisttoggle arrow icon

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

Differential diagnosestoggle arrow icon

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 [61]
  • 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 [62]
  • 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.

Special patient groupstoggle arrow icon

Syncope in children

Referencestoggle arrow icon

  1. Shen W-K, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope. J Am Coll Cardiol. 2017; 70 (5): p.e39-e110.doi: 10.1016/j.jacc.2017.03.003 . | Open in Read by QxMD
  2. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis.. Am Fam Physician. 2017; 95 (5): p.303-312.
  3. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018; 39 (21): p.1883-1948.doi: 10.1093/eurheartj/ehy037 . | Open in Read by QxMD
  4. Sabatine M. Pocket Medicine. Lippincott Williams & Wilkins ; 2019
  5. Thiruganasambandamoorthy V, Sivilotti MLA. Annals for Hospitalists Inpatient Notes - Identifying High-Risk Patients With Syncope—What Hospitalists Need to Know. Ann Intern Med. 2021; 174 (2): p.HO2-HO3.doi: 10.7326/m20-8081 . | Open in Read by QxMD
  6. Michele Brignole. ‘Ten Commandments’ of ESC Syncope Guidelines 2018. Eur Heart J. 2018; 39 (21): p.1870-1871.doi: 10.1093/eurheartj/ehy210 . | Open in Read by QxMD
  7. Juraschek SP, Daya N, Rawlings AM, et al. Association of History of Dizziness and Long-term Adverse Outcomes With Early vs Later Orthostatic Hypotension Assessment Times in Middle-aged Adults. JAMA Internal Medicine. 2017; 177 (9): p.1316.doi: 10.1001/jamainternmed.2017.2937 . | Open in Read by QxMD
  8. Bejar D, Colombo PC, Latif F, Yuzefpolskaya M. Infiltrative Cardiomyopathies. Clinical Medicine Insights: Cardiology. 2015; 9s2: p.CMC.S19706.doi: 10.4137/cmc.s19706 . | Open in Read by QxMD
  9. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Circulation. 2010; 121 (13): p.1533-1541.doi: 10.1161/circulationaha.108.840827 . | Open in Read by QxMD
  10. Maganti K, Rigolin VH, Sarano ME, Bonow RO. Valvular Heart Disease: Diagnosis and Management. Mayo Clin Proc. 2010; 85 (5): p.483-500.doi: 10.4065/mcp.2009.0706 . | Open in Read by QxMD
  11. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015; 36 (42): p.2921-2964.doi: 10.1093/eurheartj/ehv318 . | Open in Read by QxMD
  12. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. Circulation. 2010; 121 (13): p.e266-369.doi: 10.1161/CIR.0b013e3181d4739e . | Open in Read by QxMD
  13. Galiè N, McLaughlin VV, Rubin LJ, Simonneau G. An overview of the 6th World Symposium on Pulmonary Hypertension. Eur Respir J. 2019; 53 (1): p.1802148.doi: 10.1183/13993003.02148-2018 . | Open in Read by QxMD
  14. Fares W, Bazan I. Pulmonary hypertension: diagnostic and therapeutic challenges. Therapeutics and Clinical Risk Management. 2015: p.1221.doi: 10.2147/tcrm.s74881 . | Open in Read by QxMD
  15. Agnelli G, Becattini C. Acute Pulmonary Embolism. N Engl J Med. 2010; 363 (3): p.266-274.doi: 10.1056/nejmra0907731 . | Open in Read by QxMD
  16. Sheldon RS, Grubb BP, Olshansky B, et al. 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope. Heart Rhythm. 2015; 12 (6): p.e41-e63.doi: 10.1016/j.hrthm.2015.03.029 . | Open in Read by QxMD
  17. Barón-Esquivias G, Barón-Solís C, Ordóñez A. Pacing for Patients Suffering From Cardioinhibitory Vasovagal Syncope Using the Closed-Loop System. Frontiers in Cardiovascular Medicine. 2020; 6.doi: 10.3389/fcvm.2019.00192 . | Open in Read by QxMD
  18. Podd S, Hunt J, Sulke N. Home Orthostatic Training In Elderly Patients With Vasovagal Syncope — A Prospective Randomised Controlled Trial. Eur Cardiol. 2015; 10 (2): p.1.doi: 10.15420/ecr.2015.10.2.1 . | Open in Read by QxMD
  19. Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A. Usefulness of a Tilt Training Program for the Prevention of Refractory Neurocardiogenic Syncope in Adolescents. Circulation. 1999; 100 (17): p.1798-1801.doi: 10.1161/01.cir.100.17.1798 . | Open in Read by QxMD
  20. Fedorowski A, Ricci F, Hamrefors V, et al. Orthostatic Hypotension: Management of a Complex, But Common, Medical Problem. Circ Arrhythm Electrophysiol. 2022; 15 (3).doi: 10.1161/circep.121.010573 . | Open in Read by QxMD
  21. Freeman R, Abuzinadah AR, Gibbons C, Jones P, Miglis MG, Sinn DI. Orthostatic Hypotension. J Am Coll Cardiol. 2018; 72 (11): p.1294-1309.doi: 10.1016/j.jacc.2018.05.079 . | Open in Read by QxMD
  22. Park JW, Okamoto LE, Shibao CA, Biaggioni I. Pharmacologic treatment of orthostatic hypotension. Autono Neurosci. 2020; 229: p.102721.doi: 10.1016/j.autneu.2020.102721 . | Open in Read by QxMD
  23. Palma JA, Kaufmann H. Management of Orthostatic Hypotension. Continuum (Minneap Minn). 2020; 26 (1): p.154-177.doi: 10.1212/con.0000000000000816 . | Open in Read by QxMD
  24. Jenkins DJA, Sahye-Pudaruth S, Khodabandehlou K, et al. Systematic review and meta-analysis examining the relationship between postprandial hypotension, cardiovascular events, and all-cause mortality. Am J Clin Nutr. 2022; 116 (3): p.663-671.doi: 10.1093/ajcn/nqac158 . | Open in Read by QxMD
  25. Raj SR. Postural Tachycardia Syndrome (POTS). Circulation. 2013; 127 (23): p.2336-2342.doi: 10.1161/circulationaha.112.144501 . | Open in Read by QxMD
  26. Asplund CA, O'Connor FG, Noakes TD. Exercise-associated collapse: an evidence-based review and primer for clinicians.. Br J Sports Med. 2011; 45 (14): p.1157-62.doi: 10.1136/bjsports-2011-090378 . | Open in Read by QxMD
  27. Holtzhausen LM, Noakes TD. The prevalence and significance of post-exercise (postural) hypotension in ultramarathon runners.. Med Sci Sports Exerc. 1995; 27 (12): p.1595-601.
  28. Wieling W, van Dijk N, Thijs RD, de Lange FJ, Krediet CTP, Halliwill JR. Physical countermeasures to increase orthostatic tolerance. J Intern Med. 2014; 277 (1): p.69-82.doi: 10.1111/joim.12249 . | Open in Read by QxMD
  29. Benditt DG, Goldstein M. Fainting. Circulation. 2002; 106 (9): p.1048-1050.doi: 10.1161/01.cir.0000028398.85327.b4 . | Open in Read by QxMD
  30. Hauser SL, Josephson SA. Harrison's Neurology in Clinical Medicine, 4th Edition. McGraw Hill Professional ; 2016
  31. Shibao CA, Kaufmann H. Pharmacotherapy of Cardiovascular Autonomic Dysfunction in Parkinson Disease. CNS Drugs. 2017; 31 (11): p.975-989.doi: 10.1007/s40263-017-0473-5 . | Open in Read by QxMD
  32. Alagiakrishnan K, Banach M. Hypotensive Syndromes in Geriatric Patients. Springer Nature ; 2019
  33. Eschlböck S, Wenning G, Fanciulli A. Evidence-based treatment of neurogenic orthostatic hypotension and related symptoms. J Neural Transm. 2017; 124 (12): p.1567-1605.doi: 10.1007/s00702-017-1791-y . | Open in Read by QxMD
  34. Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008; 7 (5): p.451-458.doi: 10.1016/s1474-4422(08)70088-7 . | Open in Read by QxMD
  35. McLeod KA. Syncope in childhood. Arch Dis Child. 2003; 88 (4): p.350-353.doi: 10.1136/adc.88.4.350 . | Open in Read by QxMD
  36. Massin MM, Bourguignont A, Coremans C, Comté L, Lepage P, Gérard P. Syncope in pediatric patients presenting to an emergency department. J Pediatr. 2004; 145 (2): p.223-228.doi: 10.1016/j.jpeds.2004.01.048 . | Open in Read by QxMD
  37. Benditt D. Syncope in adults: Clinical manifestations and diagnostic evaluation. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: October 12, 2016. Accessed: February 17, 2017.
  38. Morag R. Syncope. Syncope. New York, NY: WebMD. Updated: January 13, 2017. Accessed: March 15, 2017.
  39. Lakkireddy D. Psychogenic Pseudosyncope: Clinical Features, Diagnosis and Management. Journal of Atrial Fibrillation. 2020; 13 (1).doi: 10.4022/jafib.2399 . | Open in Read by QxMD
  40. Hifumi T, Kondo Y, Shimizu K, Miyake Y. Heat stroke. Journal of Intensive Care. 2018; 6 (1).doi: 10.1186/s40560-018-0298-4 . | Open in Read by QxMD
  41. Lima Neto A, Bittar R, Gattas G, et al. Pathophysiology and diagnosis of vertebrobasilar insufficiency: A review of the literature. Int Arch Otorhinolaryngol. 2016; 21 (3): p.302-307.doi: 10.1055/s-0036-1593448 . | Open in Read by QxMD
  42. Thiruganasambandamoorthy V, Sivilotti MLA, Le Sage N, et al. Multicenter Emergency Department Validation of the Canadian Syncope Risk Score. JAMA Internal Medicine. 2020; 180 (5): p.737.doi: 10.1001/jamainternmed.2020.0288 . | Open in Read by QxMD
  43. Chan J, Ballard E, Brain D, et al. External validation of the Canadian Syncope Risk Score for patients presenting with undifferentiated syncope to the emergency department. Emergency Medicine Australasia. 2020.doi: 10.1111/1742-6723.13641 . | Open in Read by QxMD
  44. Meisenheimer ES, Rogers TS, Saguil A. Canadian Syncope Risk Score: A Validated Risk Stratification Tool.. Am Fam Physician. 2021; 103 (6): p.375-376.
  45. Safari S, Khasraghi ZS, Chegeni MA, Ghabousian A, Amini A. The ability of Canadian Syncope risk score in differentiating cardiogenic and non-cardiogenic syncope; a cross-sectional study. Am J Emerg Med. 2021; 50: p.675-678.doi: 10.1016/j.ajem.2021.07.034 . | Open in Read by QxMD
  46. Sweanor RAL, Redelmeier RJ, Simel DL, Albassam OT, Shadowitz S, Etchells EE. Multivariable risk scores for predicting short‐term outcomes for emergency department patients with unexplained syncope: A systematic review. Academic Emergency Medicine. 2021; 28 (5): p.502-510.doi: 10.1111/acem.14203 . | Open in Read by QxMD
  47. Serrano LA, Hess EP, Bellolio MF, et al. Accuracy and Quality of Clinical Decision Rules for Syncope in the Emergency Department: A Systematic Review and Meta-analysis. Ann Emerg Med. 2010; 56 (4): p.362-373.e1.doi: 10.1016/j.annemergmed.2010.05.013 . | Open in Read by QxMD
  48. Saccilotto RT, Nickel CH, Bucher HC, Steyerberg EW, Bingisser R, Koller MT. San Francisco Syncope Rule to predict short-term serious outcomes: a systematic review. Can Med Assoc J. 2011; 183 (15): p.E1116-E1126.doi: 10.1503/cmaj.101326 . | Open in Read by QxMD
  49. Costantino G, Sun BC, Barbic F, et al. Syncope clinical management in the emergency department: a consensus from the first international workshop on syncope risk stratification in the emergency department. Eur Heart J. 2015; 37 (19): p.1493-1498.doi: 10.1093/eurheartj/ehv378 . | Open in Read by QxMD
  50. Herold G. Internal Medicine. Herold G ; 2014
  51. Agabegi SS, Agabegi ED. Step-Up To Medicine. Wolters Kluwer Health ; 2015
  52. Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. N Engl J Med. 2016; 375: p.1524-1531.doi: 10.1056/NEJMoa1602172 . | Open in Read by QxMD
  53. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. 2004; 329 (7461): p.336-341.doi: 10.1136/bmj.329.7461.336 . | Open in Read by QxMD
  54. O’Mahony D. Pathophysiology of carotid sinus hypersensitivity in elderly patients. Lancet. 1995; 346 (8980): p.950-952.doi: 10.1016/s0140-6736(95)91563-x . | Open in Read by QxMD
  55. Kaufmann H, Freeman R. Postural Tachycardia Syndrome. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: March 3, 2015. Accessed: March 2, 2018.
  56. Goldberger ZD, Petek BJ, Brignole M, et al. ACC/AHA/HRS Versus ESC Guidelines for the Diagnosis and Management of Syncope. J Am Coll Cardiol. 2019; 74 (19): p.2410-2423.doi: 10.1016/j.jacc.2019.09.012 . | Open in Read by QxMD
  57. Kligerman SJ, Bykowski J, Hurwitz Koweek LM, et al. ACR Appropriateness Criteria® Syncope. Journal of the American College of Radiology. 2021; 18 (5): p.S229-S238.doi: 10.1016/j.jacr.2021.02.021 . | Open in Read by QxMD
  58. Five Things Physicians and Patients Should Question. Updated: February 21, 2013. Accessed: November 29, 2021.
  59. Five Things Physicians and Patients Should Question. Updated: April 4, 2012. Accessed: November 29, 2021.
  60. Ten Things Physicians and Patients Should Question. Updated: June 18, 2018. Accessed: November 29, 2021.
  61. Five Things Physicians and Patients Should Question. Updated: August 15, 2018. Accessed: November 29, 2021.
  62. Sandhu KS, Khan P, Panting J, Nadar S. Tilt-table test: its role in modern practice. Clin Med (Northfield Il). 2013; 13 (3): p.227-232.doi: 10.7861/clinmedicine.13-3-227 . | Open in Read by QxMD
  63. Pasquier M, Clair M, Pruvot E, Hugli O, Carron P-N. Carotid Sinus Massage. N Engl J Med. 2017; 377 (15): p.e21.doi: 10.1056/nejmvcm1313338 . | Open in Read by QxMD
  64. Zygmunt A, Stanczyk J. Methods of evaluation of autonomic nervous system function. Archives of Medical Science. 2010; 1: p.11-18.doi: 10.5114/aoms.2010.13500 . | Open in Read by QxMD
  65. Udoetuk S, Dongarwar D, Salihu HM. Racial and Gender Disparities in Diagnosis of Malingering in Clinical Settings. J Racial Ethn Health Disparities. 2020; 7 (6): p.1117-1123.doi: 10.1007/s40615-020-00734-6 . | Open in Read by QxMD
  66. Olshansky B. Reflex syncope. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: August 14, 2014. Accessed: February 17, 2017.
  67. Mellusi J. Differential diagnosis of syncope.. Anesth Prog. 1967; 14 (1): p.4-11.
  68. Stern SDC, Cifu AS, Altkorn D. Symptom to Diagnosis An Evidence Based Guide, Fourth Edition. McGraw-Hill Education / Medical ; 2019

Icon of a lock3 free articles remaining

You have 3 free member-only articles left this month. Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer