Syncope: Practice Essentials, Background, Pathophysiology (original) (raw)

Practice Essentials

Syncope is defined as a transient, self-limited loss of consciousness [1] with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients.

Signs and symptoms

History and physical examination are the most specific and sensitive ways of evaluating syncope. These measures, along with 12-lead electrocardiography (ECG), were the only current level A recommendations listed in the 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope. [2]

A detailed account of the event must be obtained from the patient, including the following:

The following questions should be asked:

If the answers are positive, syncope is highly likely; if one or more are negative, other forms of loss of consciousness should be considered. [3]

Presyncopal symptoms reported may include the following:

Other information that should be obtained includes the following:

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

See Presentation for more detail.

Diagnosis

No specific laboratory testing has sufficient power to be absolutely indicated for evaluation of syncope. Tests may not be necessary and can be tailored to any signs or symptoms that raise concern for a specific underlying illness. Research-based and consensus guideline recommendations are as follows:

Imaging studies that may be helpful include the following:

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

Other diagnostic tests and procedures include the following:

See Workup for more detail.

Management

Prehospital management of syncope may require the following:

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

In patients brought to the emergency department with a presumptive diagnosis of syncope, appropriate initial interventions may include the following:

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

See Treatment and Medication for more detail.

eMedicine Logo

Background

Syncope is defined as a transient, self-limited loss of consciousness [1] with an inability to maintain postural tone that is followed by spontaneous recovery. [6] The term syncope excludes seizures, coma, shock, or other states of altered consciousness.

Syncope is a prevalent disorder, accounting for 1-3% of emergency department (ED) visits and as many as 6% of hospital admissions each year in the United States. As much as 50% of the population may experience a syncopal event during their lifetime.

Although many etiologies for syncope are recognized, categorization into reflex (neurally mediated), orthostatic, and cardiac (cardiovascular) may be helpful during the initial evaluation. Cardiac syncope is associated with increased mortality, whereas noncardiac syncope is not. Syncope may result in significant morbidity and disability due to falls or accidents that occur as a result. [7] In the United States alone, an estimated $2 billion annually is spent on patients hospitalized with syncope.

Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients. It is unclear whether hospital inpatient admission of asymptomatic patients after syncope affects outcomes. No current criterion standard exists for diagnosing undifferentiated syncope.

Many physicians have admitted patients because of perceived risk. Reviews of the 2001 American College of Emergency Physician (ACEP) clinical policy suggested that evidence-based criteria may decrease admission rates by nearly half by identifying cardiac causes of syncope. Inpatient admission should be reserved for patients in whom identification of specific immediate risk is needed (eg, those with structural heart disease or a history of ventricular arrhythmia). Outpatient management can be used for patients who are at low risk for a cardiac etiology to define a precise cause so that mechanism-specific treatment can be effected.

eMedicine Logo

Pathophysiology

Syncope occurs as a consequence of global cerebral hypoperfusion. [1] Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of the high-energy phosphates found elsewhere in the body; consequently, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope.

Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output (CO), systemic vascular resistance (SVR), mean arterial pressure (MAP), intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these systems or subclinical defects in several of them may cause syncope.

CO can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. SVR can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. MAP decreases with all causes of hypovolemia. Medications can affect CO, SVR, or MAP.

Other conditions can mimic syncope. A central nervous system (CNS) event, such as a hemorrhage or an unwitnessed seizure, can present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia, hypercarbia).

eMedicine Logo

Etiology

Cardiac (cardiopulmonary) syncope may be due to vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction and predicts a worse short-term and long-term prognosis. Obtaining an initial electrocardiogram (ECG) is mandatory if any of these causes are possible for the differential diagnosis.

The American College of Cardiology (ACC), American Heart Association (AHA), and Heart Rhythm Society (HRS) guidelines indicate short-term risk factors (≤30 days) include male sex, age older than 60 years, palpitations occuring before loss of consciousness, exertional syncope, heart failure, structural heart disease, cerebrovascular disease, family history of sudden cardiac death, and trauma, as well as some physical evaluation or laboratory anomalies (evidence of bleeding, persistent abnormal vital signs, abnormal electrocardiogram [ECG], positive troponin level). [6] Long-term risk factors (>30 days) also include male sex, age older than 60 years, structural heart disease, heart failure, cerebrovascular disease, in addition to the presence of ventricular arrhythmias, cancer, diabetes, a high CHADS-2 score (congestive heart heart failure, hypertension, age ≥75 years, diabetes, stroke/transient ischemic attack), an abnormal ECG, and lower glomerular filtration rate. [6]

Low flow states, such as those associated with advanced cardiomyopathy, congestive heart failure, and valvular insufficiency, may result in hypotension and cause transient global cerebral hypoperfusion. Often, these patients are on medications that reduce afterload, which may contribute to the cause of syncope.

Ventricular arrhythmias, such as ventricular tachycardia and torsade de pointes, tend to occur in older patients with known cardiac disease. These patients tend to have fewer recurrences and have a more sudden onset with few, if any, presyncopal symptoms. Associated chest pain or dyspnea may be present. This type of syncope is generally unrelated to posture and can occur during lying, sitting, or standing. Often, these arrhythmias are not revealed on the initial ECG but may be captured with prolonged monitoring.

Supraventricular tachyarrhythmias include supraventricular tachycardia and atrial fibrillation with rapid response. These may be associated with palpitations, chest pain, or dyspnea. Patients typically have prodromal symptoms and may have syncope while attempting to stand or walk because of resultant hypotension. These symptoms may spontaneously resolve prior to evaluation but are often noted during initial triage and assessment. Be sure to scrutinize ECG findings for evidence of Wolff-Parkinson-White syndrome, Brugada syndrome, and long QT syndrome.

Bradyarrhythmias include sick sinus syndrome, sinus bradycardia, high-grade atrioventricular blocks, pacemaker malfunction, and adverse medication reactions. Generally, these patients have a history of cardiac problems and are symptomatic. Chest pain, dyspnea, decreased exercise tolerance, and fatigue may all be present. Consider cardiac ischemia and medication side effects as additional causes.

Cardiac outflow obstruction may also result in sudden-onset syncope with little or no prodrome. One critical clue is the exertional nature, and the other is the presence of a cardiac murmur. Young athletes may present with this etiology for syncope. Specific pathology includes aortic stenosis, hypertrophic obstructive cardiomyopathy, mitral stenosis, pulmonary stenosis, pulmonary embolus, left atrial myxoma, and pericardial tamponade.

Syncope can also result from an acute myocardial infarction (MI), acute aortic dissection, and pulmonary embolus. These conditions can have associated chest pain, neck pain, shoulder pain, dyspnea, epigastric pain, hypotension, alteration of mental status and can result in sudden death.

Reflex (neurally mediated) syncope may be due to vasovagal syncope, which is mediated by emotional distress such as fear or physical pain. Situational syncope describes syncope that occurs with a fixed event such as micturition, deglutition, exercise induced, and carotid sinus syncope. These causes tend to be more benign and do not predict poor outcomes.

Vasovagal syncope is the most common type in young adults [8] but can occur at any age. It usually occurs in a standing position and is precipitated by fear, emotional stress, or pain (eg, after a needlestick). Autonomic symptoms are predominant. Classically, nausea, diaphoresis, fading or "graying out" of vision, epigastric discomfort, and light-headedness precede syncope by a few minutes. The syncope is thought to occur secondary to efferent vasodepressor reflexes by a number of mechanisms, resulting in decreased peripheral vascular resistance. It is not life-threatening and occurs sporadically.

Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defecation, deglutition, tussive, and carotid sinus syncope are types of situational syncope. These stimuli result in autonomic reflexes with a vasodepressor response, ultimately leading to transient cerebral hypotension. These are not life-threatening but can cause morbidity. The treatment involves avoidance of the precipitant when possible and the initiation of counter maneuvers when anticipated.

Syncope due to orthostatic hypotension can occur through several mechanisms. Pure autonomic failure can be associated with Parkinson disease or dementia. Secondary autonomic insufficiency can be due to diabetes, uremia, or spinal injury. Drugs such as alcohol cause orthostatic intolerance, and medications such as vasodilators and antidepressants block orthostatic reflexes. Volume depletion due to blood loss, vomiting, diarrhea, poor oral intake, and diuretics also causes orthostatic syncope.

Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relation between orthostatic hypotension and syncope. Orthostatic hypotension increases in prevalence with age as a blunted baroreceptor response results in failure of compensatory cardioacceleration. In elderly patients, 45% of these cases are related to medications. Limited evidence suggests that polydipsia may reduce recurrences. Orthostasis is a common cause of syncope and tends to be recurrent. Bedside orthostatics cannot exclude this as an etiology; if it is suspected, patients should be referred to a primary care provider for outpatient tilt-table testing.

eMedicine Logo

Epidemiology

Data regarding epidemiology and demographics of syncope vary with the populations under investigation as well as with how syncope is defined and/or characterized. [6] Estimated prevalence has been reported to be as high at 41%, with a 13.5% prevalence of recurrent syncope. [6] In adults, vasovagal syncope is the most common form of syncope.

United States statistics

An estimated 1 million plus US emergency department visits are from syncope or presyncope. [9]

Framingham data demonstrated a first occurrence rate of 6.2 cases per 1000 patient-years. [10, 11] Syncope reoccurs in 3% of affected individuals, and approximately 10% of affected individuals have a cardiac etiology.

International statistics

Data from Europe and Japan suggest an occurrence rates similar to that in the United States, accounting for 1-3.5% of ED visits. In a 2024 report of findings from a multicenter European prospective study of 952 adults aged at least 18 years who presented to EDs with undifferentiated or suspected syncopal-related transient loss of consciousness (TLOC), Reed et al found a 1% prevalence of syncope in the ED, with about 4 in 10 patients admitted. [12] This Syncope Evaluation in the Emergency Department (SEED) study noted admission rates rose with the presence of increasing high-risk factors (on the basis of the European Society of Cardiology criteria. See the Guidelines section.), which 75% of patients exhibited. [12]

Race-, sex-, and age-related demographics

No significant differences regarding race are observed with respect to syncope risk. Although large prospective studies fail to show clinically significant differences between men and women, data from Olmsted County, Minnesota, found a higher prevalence reported among females. [6]

National Hospital Ambulatory Medical Care Survey (NHAMCS) data show that syncope occurs in all age groups but is most common in older adult populations. Noncardiac causes tend to be more common in young adults, whereas cardiac syncope is more common with male sex and becomes increasingly more frequent with advancing age. [6]

Syncope is relatively uncommon in pediatric populations. A retrospective study by Pratt and Fleisher reported a prevalence of less than 0.1% in children. [13] Pediatric syncope warrants prompt detailed evaluation.

Advancing age is an independent risk factor for both syncope and death. [6] Various studies suggest categorizing patients older than 45 years, 65 years, and 80 years as being at higher risk. Advancing age correlates with increasing frequency of coronary artery and myocardial disease, arrhythmia, vasomotor instability, autonomic failure, polyneuropathy, and use of polypharmacy. Predictors of recurrent syncope in this population include aortic stenosis, atrioventricular or left bundle branch block, atrial fibrillation, heart failure, impaired kidney function, and chronic obstructive pulmonary disorder. [6]

eMedicine Logo

Prognosis

Cardiac syncope has a poorer prognosis than other forms of syncope; the 1-year endpoint mortality has been shown to be as high as 45%. [14] Studies evaluating mortality within 4 weeks of presentation and 1 year after presentation both report statistically significant increases in this patient group. Patients with cardiac syncope may be significantly restricted in their daily activities, and the occurrence of syncope may be a symptom of their underlying disease progression.

Syncope of any etiology in a patient with cardiac conditions (to be differentiated from cardiac syncope) has also been shown to imply a poor prognosis. Patients with New York Heart Association (NYHA) functional class III or IV who have any type of syncope have a mortality as high as 25% within 1 year.

However, some patients do well after definitive surgical treatment or pacemaker placement. Evaluation by a cardiologist for pacemaker placement should be considered in select patients older than 40 years who have recurrent syncope that is confirmed to be neurally mediated syncope (NMS) with a documented period of asystole. Preliminary data suggests that although syncope may recur in this subset of patients, the frequency is reduced by more than 50%. [15]

Noncardiac syncope seems to have no effect on overall mortality and includes syncope due to vasovagal response, autonomic insufficiency, situations, and orthostatic positions.

Vasovagal syncope has a uniformly excellent prognosis. This condition does not increase the mortality, and recurrences are infrequent.

Situational syncope and orthostatic syncope also have an excellent prognosis. They do not increase the risk of death; however, recurrences do occur and are sometimes a source of significant morbidity in terms of quality of life and secondary injury.

Syncope of unknown etiology generally has a favorable prognosis, with 1-year follow-up data showing a low incidence of sudden death (2%), a 20% chance of recurrent syncope, and a 78% remission rate.

Recurrent falls due to syncope can result in lacerations, orthopedic injuries, and intracranial trauma.

Morbidity/mortality

Data suggest that patients with cardiac syncope are more likely to experience a poor outcome. Patients who have a significant cardiac history and those who seem to have a cardiac syncope (because of associated chest pain, dyspnea, cardiac murmur, signs of congestive heart failure (CHF), or ECG abnormalities) should be considered to be at increased risk. Most published methods of risk stratification take into account cardiac symptoms and risk factors. [16]

Morbidity from syncope includes recurrent syncope, which occurs in 20% of patients within 1 year of the initial episode. Lacerations, extremity fractures, head injuries, and motor vehicle accidents can occur secondary to syncope.

Syncope in a patient with poor baseline cardiac function portends a poor prognosis, irrespective of etiology. Middlekauff et al studied 491 patients with NYHA functional class III or IV disease and noted that, regardless of the cause, 45% of those with syncope died within 1 year, whereas 12% of those without syncope died during the same interval. [17]

Patients with cardiac syncope appear to do worse than patients with noncardiac syncope. Soteriades et al followed 7814 patients with syncope for 17 years and found a higher mortality for patients with cardiac syncope than for those with noncardiac syncope. [18] Suzuki et al studied 912 patients with syncope for an average of 3 years and found the same result. [19]

Risk of serious outcome and death in patients with syncope increases with higher peak troponin concentrations, according to a prospective cohort study of 338 patients who had plasma troponin I levels measured with a sensitive assay 12 hours after syncope. [20] The percentage of patients with a serious outcome increased across patients divided into quintiles on the basis of peak troponin concentration at 1 month (0%, 9%, 13%, 26%, 70%) and at 1 year (10%, 22%, 26%, 52%, 85%). [20]

Decision rules may assist in identifying patients who are at risk. Martin et al described a risk stratification system that predicted an increased incidence of death at 1 year on the basis of abnormal ECG findings, a history of ventricular arrhythmia, a history of CHF, and age older than 45 years. [21]

Sarasin et al demonstrated a risk of arrhythmia that is proportional to the number of cardiac risk factors, including abnormal ECG findings, history of CHF, and age older than 65 years. [22]

The San Francisco Syncope Rule (SFSR) was determined to have a 96% sensitivity for identifying patients at immediate risk for serious outcomes within 7 days, on the basis of the presence of abnormal ECG findings, a history of CHF, dyspnea, a hematocrit level lower than 0.30, and hypotension. [23] The presence of these findings should prompt serious consideration for hospital admission.

In an external retrospective review, validation of the SFSR in a Canadian ED was undertaken. The rule performed with a sensitivity of 90% (44/49 outcomes; 95% confidence interval [CI] 79-96%) and a specificity of 33%, which was much lower than previously reported. The results of this study suggested that implementation of the rule would have significantly increased admission rates. The authors concluded that further study was needed. [24] & Another study was also unable to validate the rule, with a sensitivity of 74% and a specificity of 57% reported. [25]

The ROSE (Risk stratification Of Syncope in the Emergency department) criteria suggested that an elevated B-type natriuretic peptide (BNP), Hemoccult-positive stool, anemia, low oxygen saturation, and presence of Q waves on ECG predict serious outcomes at 30 days. [26] These rules had a 87% sensitivity and a 98.5% negative predictive value to help risk-stratify patients. In this study, the isolated finding of BNP greater than 300 pg/mL was a major predictor of serious outcomes and was present in 89% of patients who died within 30 days.

Constantino et al discovered that 6.1% of patients had severe outcomes within 10 days of syncope evaluation. [27] The mortality was 0.7%, and 5.4% of patients were readmitted or experienced major therapeutic intervention. Risk factors associated with severe short-term outcomes included abnormal ECG, history of CHF, age older than 65 years, male gender, history of chronic obstructive pulmonary disease (COPD), structural heart disease, presence of trauma, and lack of prodromal symptoms.

The Evaluation of Guidelines in SYncope Study 2 (EGSYS 2) prospectively followed nearly 400 patients at 1 month and 2 years. The death rate was 2% at 1 month and 9% at 2 years. Patients with advancing age, presence of structural heart disease, and/or abnormal ECG had higher risk. [28]

Clinical judgment, Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score, [29] and SFSR criteria all have relatively low sensitivities individually for predicting severe short-term outcomes. Some evidence suggests that combining various risk stratification tools may increase sensitivity and reduce unnecessary admissions. [30] A review and meta-analysis by Serrano et al assessed the methodologic quality and prognostic accuracy of the SFSR and the OESIL risk score. [31] The analysis of 18 eligible studies determined that the quality and accuracy of both sets of clinical decision rules are limited.

eMedicine Logo

Patient Education

Patients who present to the ED with syncope should be cautioned to avoid tall ledges and instructed not to drive. Syncope-related injury during driving is rare, but it has been documented.

Education may have a substantial impact on the prevention of recurrence, especially in situational and orthostatic syncope.

Patients may be trained to avoid situations that prompt syncope in situational cases.

In orthostatic syncope, patients should drink 500 mL of fluid each morning in addition to their usual routine and should avoid standing up too quickly.

eMedicine Logo

  1. Walsh K, Hoffmayer K, Hamdan MH. Syncope: diagnosis and management. Curr Probl Cardiol. 2015 Feb. 40(2):51-86. [QxMD MEDLINE Link].
  2. [Guideline] Huff JS, Decker WW, Quinn JV, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007 Apr. 49(4):431-44. [QxMD MEDLINE Link]. [Full Text].
  3. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009): the Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Eur Heart J. 2009 Nov. 30(21):2631-71. [QxMD MEDLINE Link].
  4. Rockx MA, Hoch JS, Klein GJ, et al. Is ambulatory monitoring for "community-acquired" syncope economically attractive? A cost-effectiveness analysis of a randomized trial of external loop recorders versus Holter monitoring. Am Heart J. 2005 Nov. 150(5):1065. [QxMD MEDLINE Link].
  5. Gibson TC, Heitzman MR. Diagnostic efficacy of 24-hour electrocardiographic monitoring for syncope. Am J Cardiol. 1984 Apr 1. 53(8):1013-7. [QxMD MEDLINE Link].
  6. [Guideline] Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS Guideline for the evaluation and management of patients with syncope: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2017 Aug 1. 136 (5):e60-e122. [QxMD MEDLINE Link]. [Full Text].
  7. Ungar A, Mussi C, Nicosia F, et al. The "syncope and dementia" study: a prospective, observational, multicenter study of elderly patients with dementia and episodes of "suspected" transient loss of consciousness. Aging Clin Exp Res. 2015 Dec. 27(6):877-82. [QxMD MEDLINE Link].
  8. Tretter JT, Kavey RE. Distinguishing cardiac syncope from vasovagal syncope in a referral population. J Pediatr. 2013 Dec. 163(6):1618-1623.e1. [QxMD MEDLINE Link].
  9. Kligerman SJ, Bykowski J, Hurwitz Koweek LM, et al, for the Expert Panels on Cardiac Imaging and Neurological Imaging. ACR Appropriateness Criteria syncope. J Am Coll Radiol. 2021 May. 18 (5S):S229-38. [QxMD MEDLINE Link]. [Full Text].
  10. Chen L, Chen MH, Larson MG, Evans J, Benjamin EJ, Levy D. Risk factors for syncope in a community-based sample (the Framingham Heart Study). Am J Cardiol. 2000 May 15. 85(10):1189-93. [QxMD MEDLINE Link].
  11. Savage DD, Corwin L, McGee DL, Kannel WB, Wolf PA. Epidemiologic features of isolated syncope: the Framingham Study. Stroke. 1985 Jul-Aug. 16(4):626-9. [QxMD MEDLINE Link].
  12. Reed MJ, Karuranga S, Kearns D, et al, for the SEED investigators. Management of syncope in the emergency department: a European prospective cohort study (SEED). Eur J Emerg Med. 2024 Apr 1. 31 (2):136-46. [QxMD MEDLINE Link].
  13. Pratt JL, Fleisher GR. Syncope in children and adolescents. Pediatr Emerg Care. 1989 Jun. 5(2):80-2. [QxMD MEDLINE Link].
  14. Mizrachi EM, Sitammagari KK. Cardiac Syncope. StatPearls [Internet]. 2023 Jan. [QxMD MEDLINE Link]. [Full Text].
  15. 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 May 29. 125(21):2566-71. [QxMD MEDLINE Link].
  16. Benditt DG, Can I. Initial evaluation of "syncope and collapse" the need for a risk stratification consensus. J Am Coll Cardiol. 2010 Feb 23. 55(8):722-4. [QxMD MEDLINE Link].
  17. Middlekauff HR, Stevenson WG, Stevenson LW, Saxon LA. Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope. J Am Coll Cardiol. 1993 Jan. 21(1):110-6. [QxMD MEDLINE Link].
  18. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002 Sep 19. 347(12):878-85. [QxMD MEDLINE Link].
  19. Suzuki M, Hori S, Nakamura I, Soejima K, Aikawa N. Long-term survival of Japanese patients transported to an emergency department because of syncope. Ann Emerg Med. 2004 Sep. 44(3):215-21. [QxMD MEDLINE Link].
  20. Reed MJ, Mills NL, Weir CJ. Sensitive troponin assay predicts outcome in syncope. Emerg Med J. 2012 Dec. 29(12):1001-3. [QxMD MEDLINE Link].
  21. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with syncope. Ann Emerg Med. 1997 Apr. 29(4):459-66. [QxMD MEDLINE Link].
  22. Sarasin FP, Hanusa BH, Perneger T, Louis-Simonet M, Rajeswaran A, Kapoor WN. A risk score to predict arrhythmias in patients with unexplained syncope. Acad Emerg Med. 2003 Dec. 10(12):1312-7. [QxMD MEDLINE Link].
  23. 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 Feb. 43(2):224-32. [QxMD MEDLINE Link].
  24. Thiruganasambandamoorthy V, Hess EP, Alreesi A, Perry JJ, Wells GA, Stiell IG. External validation of the San Francisco Syncope Rule in the Canadian setting. Ann Emerg Med. 2010 May. 55(5):464-72. [QxMD MEDLINE Link].
  25. Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ. Failure to validate the San Francisco Syncope Rule in an independent emergency department population. Ann Emerg Med. 2008 Aug. 52(2):151-9. [QxMD MEDLINE Link].
  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 Feb 23. 55(8):713-21. [QxMD MEDLINE Link].
  27. Costantino G, Perego F, Dipaola F, et al. Short- and long-term prognosis of syncope, risk factors, and role of hospital admission: results from the STePS (Short-Term Prognosis of Syncope) study. J Am Coll Cardiol. 2008 Jan 22. 51(3):276-83. [QxMD MEDLINE Link].
  28. Ungar A, Del Rosso A, Giada F, et al, for the Evaluation of Guidelines in Syncope Study 2 Group. Early and late outcome of treated patients referred for syncope to emergency department: the EGSYS 2 follow-up study. Eur Heart J. 2010 Aug. 31(16):2021-6. [QxMD MEDLINE Link].
  29. Colivicchi F, Ammirati F, Melina D, et al, for the 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 May. 24(9):811-9. [QxMD MEDLINE Link].
  30. Dipaola F, Costantino G, Perego F, et al, for the STePS investigators. San Francisco Syncope Rule, Osservatorio Epidemiologico sulla Sincope nel Lazio risk score, and clinical judgment in the assessment of short-term outcome of syncope. Am J Emerg Med. 2010 May. 28(4):432-9. [QxMD MEDLINE Link].
  31. 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 Oct. 56(4):362-373.e1. [QxMD MEDLINE Link].
  32. Jansen S, van der Velde N. Syncope in older adults: challenges, approach and treatment. Age Ageing. 2024 Feb 1. 53 (2):[QxMD MEDLINE Link]. [Full Text].
  33. Atkins D, Hanusa B, Sefcik T, Kapoor W. Syncope and orthostatic hypotension. Am J Med. 1991 Aug. 91(2):179-85. [QxMD MEDLINE Link].
  34. Calkins H, Shyr Y, Frumin H, Schork A, Morady F. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med. 1995 Apr. 98(4):365-73. [QxMD MEDLINE Link].
  35. Guse SE, Neuman MI, O'Brien M, et al. Implementing a guideline to improve management of syncope in the emergency department. Pediatrics. 2014 Nov. 134(5):e1413-21. [QxMD MEDLINE Link].
  36. Martin GJ, Adams SL, Martin HG, Mathews J, Zull D, Scanlon PJ. Prospective evaluation of syncope. Ann Emerg Med. 1984 Jul. 13(7):499-504. [QxMD MEDLINE Link].
  37. Dovgalyuk J, Holstege C, Mattu A, Brady WJ. The electrocardiogram in the patient with syncope. Am J Emerg Med. 2007 Jul. 25(6):688-701. [QxMD MEDLINE Link].
  38. Sulke N, Sugihara C, Hong P, Patel N, Freemantle N. The benefit of a remotely monitored implantable loop recorder as a first line investigation in unexplained syncope: the EaSyAS II trial. Europace. 2016 Jun. 18(6):912-8. [QxMD MEDLINE Link].
  39. Rangel I, Freitas J, Correia AS, et al. The usefulness of the head-up tilt test in patients with suspected epilepsy. Seizure. 2014 May. 23(5):367-70. [QxMD MEDLINE Link].
  40. van Zanten S, Sutton R, Hamrefors V, Fedorowski A, de Lange FJ. Tilt table testing, methodology and practical insights for the clinic. Clin Physiol Funct Imaging. 2024 Mar. 44 (2):119-30. [QxMD MEDLINE Link]. [Full Text].
  41. Azizi Malamiri R, Momen AA, Nikkhah A, et al. Usability of the head upright tilt test for differentiating between syncopal and seizure-like events in children. Acta Neurol Belg. 2015 Dec. 115(4):575-9. [QxMD MEDLINE Link].
  42. Klemenc M, Strumbelj E. Predicting the outcome of head-up tilt test using heart rate variability and baroreflex sensitivity parameters in patients with vasovagal syncope. Clin Auton Res. 2015 Dec. 25(6):391-8. [QxMD MEDLINE Link].
  43. Alharbi A, Shah M, Gupta M, et al. The efficacy of non-pharmacological and non-pacing therapies in preventing vasovagal syncope: Tilt training, physical counter pressure maneuvers, and yoga - A systematic review and meta-analysis. Auton Neurosci. 2024 Feb. 251:103144. [QxMD MEDLINE Link]. [Full Text].
  44. Raj P, Lei L, Flevaris P, Raj S, Sheldon R. Serotonin reuptake inhibition for the prevention of vasovagal syncope: a systematic review and meta-analysis. Clin Auton Res. 2023 Dec. 33 (6):811-9. [QxMD MEDLINE Link].
  45. [Guideline] Möckel M, Catherine Janssens KA, et al, for the EUSEM Syncope Group. The syncope core management process in the emergency department: a consensus statement of the EUSEM syncope group. Eur J Emerg Med. 2024 Aug 1. 31 (4):250-9. [QxMD MEDLINE Link]. [Full Text].
  46. Quinn J, McDermott D. Electrocardiogram findings in emergency department patients with syncope. Acad Emerg Med. 2011 Jul. 18(7):714-8. [QxMD MEDLINE Link].
  47. Claydon VE, Schroeder C, Norcliffe LJ, Jordan J, Hainsworth R. Water drinking improves orthostatic tolerance in patients with posturally related syncope. Clin Sci (Lond). 2006 Mar. 110(3):343-52. [QxMD MEDLINE Link].
  48. Shen WK, Decker WW, Smars PA, et al. Syncope Evaluation in the Emergency Department Study (SEEDS): a multidisciplinary approach to syncope management. Circulation. 2004 Dec 14. 110(24):3636-45. [QxMD MEDLINE Link].
  49. Sheldon R, Connolly S, Rose S, et al. Prevention of Syncope Trial (POST): a randomized, placebo-controlled study of metoprolol in the prevention of vasovagal syncope. Circulation. 2006 Mar 7. 113(9):1164-70. [QxMD MEDLINE Link].
  50. Brignole M, Arabia F, Ammirati F, et al., for the Syncope Unit Project 2 (SUP 2) investigators. Standardized algorithm for cardiac pacing in older patients affected by severe unpredictable reflex syncope: 3-year insights from the Syncope Unit Project 2 (SUP 2) study. Europace. 2016 Sep. 18(9):1427-33. [QxMD MEDLINE Link].
  51. Assaf A, Sakhi R, Michels M, et al. Implantable loop recorders in patients with heart disease: comparison between patients with and without syncope. Open Heart. 2021 Aug. 8 (2):e001748. [QxMD MEDLINE Link]. [Full Text].
  52. [Guideline] Brignole M, Moya A, de Lange FJ, et al, for the ESC Scientific Document Group . 2018 ESC guidelines for the diagnosis and management of syncope. Eur Heart J. 2018 Jun 1. 39(21):1883-948. [QxMD MEDLINE Link]. [Full Text].
  53. [Guideline] Brignole M. 'Ten Commandments' of ESC syncope guidelines 2018: The new European Society of Cardiology (ESC) Clinical Practice Guidelines for the diagnosis and management of syncope were launched 19 March 2018 at EHRA 2018 in Barcelona. Eur Heart J. 2018 Jun 1. 39(21):1870-1. [QxMD MEDLINE Link].
  54. Goldberger ZD, Petek BJ, Brignole M, et al. ACC/AHA/HRS Versus ESC guidelines for the diagnosis and management of syncope: JACC guideline comparison. J Am Coll Cardiol. 2019 Nov 12. 74 (19):2410-23. [QxMD MEDLINE Link]. [Full Text].