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.
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.
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.
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.
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.
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).
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.
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.
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.
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]
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]
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.
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.
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.
History and physical examination are the most specific and sensitive ways to evaluate syncope.[1] The diagnosis is achieved with a thorough history and physical examination in 50-85% of patients. No single laboratory test has greater diagnostic efficacy.
In older adults, syncope frequently manifests as falls owing to amnesia or loss of consciousness, or presyncope that results in a fall—particularly when they're prone to falls and have several other fall risk factors.[32] In this population, it is important to focus on syncope and presyncope when there's a history of unexplained falls or there are red flags for potential syncope.
The 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope listed history, physical examination, and 12-lead electrocardiography (ECG) as their only current level A recommendations.[2]
The 2017 American College of Cardiology (ACC), American Heart Association (AHA), and the Heart Rhythm Society (HRS) class I recommendations similarly indicate performing a detailed history and physical examination in individuals with syncope, with a resting 12-lead ECG helpful in the initial evaluation.[6] The ACC/AHA/HRS also recommend evaluating the cause and assessing the short- and long-term morbidity and mortality risk factors of syncope.
A detailed account of the event must be obtained from the patient. The account must include the circumstances surrounding the episode: the precipitant factors, the activity the patient was involved with prior to the event, and the patient's position when it occurred.
Precipitating factors can include fatigue, sleep or food deprivation, warm ambient environment, alcohol consumption, pain, and strong emotions such as fear or apprehension.
Activity prior to syncope may give a clue as to the etiology of symptoms. Syncope may occur at rest; with change of posture; on exertion; after exertion; or with specific situations such as shaving, coughing, voiding, or prolonged standing. Syncope occurring within 2 minutes of standing suggests orthostatic hypotension.[33]
Assess whether the patient was standing, sitting, or lying when the syncope occurred. Syncope while seated or lying is more likely to be cardiac.[34]
The following questions should be answered:
If the answers to these questions are positive, the episode has a high likelihood of being syncope. If one or more answers are negative, consider other forms of loss of consciousness prior to proceeding with syncope evaluation.[3] The clinician should attempt to gather all information with respect to symptoms preceding the syncope.
Prior faintness, dizziness, or light-headedness occurs in 70% of patients experiencing true syncope. Other symptoms, such as vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias, may also occur in the presyncopal period.
Symptoms of nausea or diaphoresis prior to the event may suggest syncope rather than seizure when the episode was not witnessed, whereas an aura may suggest seizure.
Patients with true syncope do not remember actually falling to the ground. Presyncope involves the same symptoms and pathophysiology but terminates prior to loss of consciousness and can occasionally include loss of postural tone.
The duration of symptoms preceding a syncopal episode has been reported to be an average of 2.5 minutes in vasovagal syncope and an average of only 3 seconds in arrhythmia-related cardiac syncope.
Clinicians should specifically inquire as to red-flag symptoms, such as exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event.
Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma, incontinence, or myalgias.
A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, and seizure.
Convulsive activity, automatisms, or attempts to elicit focality can indicate seizure. Witnesses may be able to estimate the duration of unconsciousness and to assist in ascertaining whether the patient experienced postevent confusion.
Postevent confusion is the most powerful tool for discriminating between syncope and seizure. A postictal phase suggests that a seizure has occurred. Postevent confusion has been described with syncope, but the confusion should not last more than 30 seconds. Seizurelike activity can occur with syncope if the patient is held in an upright posture.
A medication history must be obtained in all patients with syncope with special emphasis placed on cardiac and antihypertensive medications. Drugs commonly implicated in syncope include the following:
Inquiry must be made into any personal or familial past medical history of cardiac disease. Patients with a history of myocardial infarction (MI), arrhythmia, structural cardiac defects, cardiomyopathies, or congestive heart failure (CHF) have a uniformly worse prognosis than other patient groups.
Remember to consider the broad differential diagnosis of syncope. Assess whether the patient has a history of seizure disorder, diabetes, stroke (cerebrovascular accident [CVA]), deep vein thrombosis (DVT), or abdominal aortic aneurysm (AAA) or if pregnancy is a possibility.
A complete physical examination is requisite for all patients who present to the emergency department (ED). Special attention must be paid to certain aspects of the physical examination in patients who present with syncope.
Always analyze the vital signs. Fever may point to a precipitant of syncope, such as a urinary tract infection (UTI) or pneumonia. Postural changes in blood pressure (BP) and heart rate may point toward an orthostatic cause of syncope but are generally unreliable. Tachycardia may be an indicator of pulmonary embolism, hypovolemia, tachyarrhythmia, or acute coronary syndrome. Bradycardia may point toward a vasodepressor cause of syncope, a cardiac conduction defect, or acute coronary syndrome.
A glucose level, checked by rapid fingerstick (eg, Accu-Chek), should be evaluated in any patient with syncope. Hypoglycemia can produce a clinical picture identical to syncope, including the prodromal symptoms, absence of memory for the event, and spontaneous resolution.
A detailed cardiopulmonary examination is essential. Irregular rhythms, ectopy, bradyarrhythmias, and tachyarrhythmias should be detected. Auscultation of heart sounds may reveal murmurs indicating high-grade valvular defects. Search for objective evidence of congestive heart failure, including jugular venous distension, lung rales, hepatomegaly, and pitting-dependent edema. Examine the abdomen for the presence of a pulsatile abdominal mass.
A detailed neurologic examination assists in establishing a baseline as well as defining new or worsening deficits. Patients with syncope should have a normal baseline mental status. Confusion, abnormal behavior, headache, fatigue, and somnolence must not be attributed to syncope; a toxic, metabolic, or central nervous system cause must be considered. The patient should have a detailed neurologic examination, including evaluation for carotid bruits, cranial nerve deficits, motor deficits, deep tendon reflex lateralization, and sensory deficits. Severe neuropathies may correlate with vasodepressor syncope.
The patient must be examined for signs of trauma. Trauma may be sustained secondary to syncope with resultant head injury, lacerations, and extremity fractures. Tongue trauma is thought to be more specific for seizures. Remember to consider antecedent head trauma resulting in loss of consciousness as opposed to syncope with resultant trauma if the history or findings are unclear.
Patients with syncope may require a stool guaiac examination, as appropriate based on their history. In one study, all patients with anemia contributing to syncope were guaiac-positive.
A few bedside examinations may help to elucidate the origin of a patient's syncope. The Hallpike maneuver may be performed in patients who describe short, intermittent prodromes with primarily vertiginous components to assess for benign paroxysmal positional vertigo.
Orthostatic changes marked by a decrease in systolic BP by 20 mm Hg, a decrease in diastolic BP by 10 mm Hg, or an increase in heart rate by 20 beats/min (bpm) with positional changes or systolic BP less than 90 mm Hg with the presence of symptoms may indicate postural hypotension. Bradycardia coinciding with the examination indicates vasodepressor syncope. Be aware that this examination is notoriously insensitive and has limited use.
Carotid sinus massage has been used with some success to diagnose carotid sinus syncope but can prompt prolonged sinus pauses and hypotension.
The American College of Cardiology (ACC), American Heart Association (AHA), and the Heart Rhythm Society (HRS) recommend investigation and management in a hospital in the presence of a serious medical condition identified during the initial assessment of individuals presenting with syncope that may be relevant to its cause.[6] They note that although targeted blood tests are reasonable for assessing selected patients with syncope identified from clinical evaluation, history and physical examination, and electrocardiographic (ECG) findings (class IIa), there's no clarity regarding the utility of brain natriuretic peptide and high-sensitivity troponin levels in patients suspected of having a cardiac etiology of syncope (class IIb). Furthermore, there is no benefit to obtaining routine and comprehensive laboratory tests for evaluating patients with syncope (class III).[6]
The frequency and nature of syncope events should determine the selection of specific cardiac monitoring (class I).[6] In the inpatient setting, telemetry is useful for individuals admitted for evaluation of suspected cardiac cause for syncope (class I).
In selected patients with syncope that has a suspected arrhythmic cause, electrophysiology studies (EPS) can be useful (class IIa).[6] However, EPS has no benefit and is not recommended in the evaluation of syncope in the setting of a normal ECG and normal cardiac structure and function—unless there is a suspected arrhythmic cause (class III).[6]
In selected patients with syncope who have known or suspected neurodegenerative disease, a referral for autonomic evaluation can help improve diagnostic and prognostic accuracy (class IIa).[6]
The American College of Radiology (ACR) considers no imaging studies as being appropriate in the setting of a low probability of cardiac or neurologic pathology, but chest radiography may be appropriate in select clinical scenarios.[9]
Suspected cardiovascular origin of syncope or presyncope
In the setting of a suspected cardiovascular origin of syncope or presyncope (on the basis of history, physical examination, and ECG findings), an appropriate initial imaging evaluation is resting transthoracic echocardiography (TTE).[9] Other initial imaging studies that may be appropriate in this clinical scenario are:
Initial imaging studies not usually appropriate in this clinical situation are[9] :
Low probability of cardiovascular origin of syncope or presyncope
Chest radiography may be appropriate initial imaging in the setting of syncope or presyncope that has a low probability of a cardiovascular origin on the basis of history, physical examination, and ECG results.[9]
Initial imaging studies not usually appropriate in this clinical situation are[9] :
Currently, no specific testing has sufficient power to be absolutely indicated for evaluation of syncope. Thus, tests may not be necessary and can be tailored to any signs or symptoms that raise concern for a specific underlying illness.[6, 35] Research-based and consensus guideline recommendations are listed below.
In one study, two of 170 patients with syncope tested for serum glucose were found to be hypoglycemic.[36] Despite this low yield, rapid blood glucose assessment is easy, fast, and may be diagnostic, leading to efficient intervention.
If performed empirically, a CBC has an exceedingly low yield in syncope. Some risk stratification protocols use a low hematocrit level as a poor prognostic indicator.
A prospective evaluation of syncope found that four of 170 patients had signs and symptoms of gastrointestinal (GI) hemorrhage with a confirmatory CBC. No occult bleeding was diagnosed on the basis of an empiric CBC in this study.
Anemia has been shown in several studies to suggest poor short-term outcomes.
These tests have an exceedingly low yield in syncope if performed empirically. Some risk stratification protocols use electrolyte level abnormalities and renal insufficiency as poor prognostic indicators.
In a study by Martin et al, 134 patients with syncope had electrolytes drawn as part of the routine workup.[36] One patient was unexpectedly found to be hyponatremic secondary to diuretic use.
Serum electrolyte tests are indicated in patients with altered mental status or in patients in whom seizure is being considered. If arrhythmia is noted, evaluation of electrolytes may be useful.
These tests are indicated in patients who give a history of chest pain with syncope, dyspnea with syncope, or exertional syncope; those with multiple cardiac risk factors; and those in whom a cardiac origin is strongly suspected.
A rise in creatine kinase (CK) levels may be associated with prolonged seizure activity or muscle damage secondary to a prolonged period of loss of consciousness.
Levels of B-type natriuretic peptide (BNP) over 300 pg/mL are a predictor of serious outcomes at 30 days.[26]
In elderly and debilitated patients, urinary tract infection (UTI) is common, easily diagnosed and treated, and may precipitate syncope. UTIs may occur in the absence of fever, leukocytosis, and symptoms in this population.
The American College of Cardiology (ACC), American Heart Association (AHA), and the Heart Rhythm Society (HRS) indicate no benefit to obtaining routine cardiac imaging in evaluating patients with syncope unless there is suspicion of a cardiac origin from findings on an initial assessment, including the patient's history, physical examination, or electrocardiogram (class III).[6] Furthermore, in the absence of focal neurologic findings that support further investigation in patients with syncope (class III)[6] :
In elderly patients and in patients who are debilitated, pneumonia is common, easily diagnosed, and treatable and may precipitate syncope. Pneumonia may occur in the absence of fever, leukocytosis, and symptoms in this population.
Evaluation of a select number of etiologies of syncope may be aided by chest radiography. Pneumonia, congestive heart failure (CHF), lung mass, effusion, and widened mediastinum can all be seen if present and may guide therapy.
Head (noncontrast)
Noncontrast CT scanning of the head is not indicated in a nonfocal patient after a syncopal event. This test has a low diagnostic yield in syncope.
Of 134 patients prospectively evaluated for syncope using CT scanning, 39 patients had abnormal findings on scans.[36] Only one head CT scan was diagnostic in a patient not expected to have intracranial pathology. Of the remaining scans, five showed subdural hematomas thought to be secondary to syncope.
Head CT may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope.
Chest and abdomen
CT scanning of these areas may be useful in selected patients with syncope of suspected cardiac cause(s).[6] CT of the chest and abdomen is indicated only in select cases, such as cases in which aortic dissection, ruptured abdominal aortic aneurysm (AAA), or pulmonary embolism (PE) is suspected.
MRI of the brain and magnetic resonance arteriography (MRA) may be required in select cases to evaluate the vertebrobasilar vasculature and are more appropriately performed on an inpatient basis in consultation with a neurologist or a neurosurgeon. MRI may be useful in selected patients with syncope of suspected cardiac origin.[6]
Ventilation-perfusion (V/Q) scanning is appropriate for patients in whom PE is suspected.
In patients with known heart disease, left ventricular function and ejection fraction have been shown to have an accurate predictive correlation with death. Echocardiography is the test of choice for evaluating suspected mechanical cardiac causes of syncope.
If a clinical suspicion of structural heart disease exists, transthoracic echocardiography can be useful in selected patients with syncope.[6]
Obtain a standard 12-lead electrocardiogram (ECG) in patients with syncope. This is a level A recommendation in the 2007 American College of Emergency Physicians (ACEP) consensus guidelines for syncope[2] and a class I recommendation in the 2017 American College of Cardiology (ACC), American Heart Association (AHA), and Heart Rhythm Society (HRS) syncope guidelines.[6] ECG is used in virtually every clinical decision rule for risk stratification.
Normal ECG findings are a good prognostic sign. ECG can be diagnostic for acute myocardial infarction (MI) or myocardial ischemia and can provide objective evidence of preexisting cardiac disease or dysrhythmia, such as Wolff-Parkinson-White syndrome, Brugada syndrome, atrial flutter, or atrioventricular (AV) blocks.[37]
Bradycardia, sinus pauses, nonsustained ventricular tachycardia and sustained ventricular tachycardia, and atrioventricular conduction defects occur with increasing frequency with age and are truly diagnostic only when they coincide with symptoms.
This is an outpatient test. In the past, all patients with syncope were monitored for 24 hours in a hospital. Later, loop recorders and signal-averaged event recorders allowed for monitoring over longer time periods, which increased the yield of detecting an arrhythmia.
Studies showed that age-matched asymptomatic populations have an equivalent number of arrhythmic events recorded by ambulatory monitoring. Loop recorders have a higher diagnostic yield than Holter monitor evaluation with a marginal cost savings.[4]
In a prospective, randomized, controlled study, Sulke et al evaluated the first-line use of a remotely monitored implantable loop recorder (ILR) in the initial investigation of unexplained syncope, in comparison with conventional therapy and a dedicated Syncope Clinic (SC).[38] A total of 246 patients were randomly allocated to conventional management, SC alone, ILR alone, or SC + ILR, with a median follow-up of 20 months. ILRs offered rapid diagnosis, increased the likelihood of syncope being reported, showed a high rate of intermittent bradycardia that required pacing, and reduced recurrent syncope.
A study completed through an ECG outpatient registry in Vermont by Gibson and Heitzman, involving 1512 patients referred for syncope, showed that symptomatic arrhythmias were found in just 0.5% of patients.[5] In fact, patients had symptoms without arrhythmias more often than symptoms with arrhythmias, advancing the notion that the negative diagnostic yield of ambulatory monitoring is a higher than its positive yield.
This test is useful for confirming autonomic dysfunction and can generally be safely arranged on an outpatient basis.[1, 39] The tilt-table test may be indicated when the initial evaluation doesn't provide a clear, highly likely, or potential diagnosis, but does raise the suspicion of reflex syncope, orthostatic hypotension, postural orthostatic tachycardia syndrome, or psychogenic pseudosyncope.[40]
It involves using a tilt table to stand a patient at 70º for 45 minutes. Various modified protocols with concomitant medications, fasting, and maneuvers exist. Normally, norepinephrine (NE) levels initially rise, and they are maintained to hold blood pressure (BP) constant. A positive result occurs when NE levels fatigue with time and a falling BP and pulse rate produce symptoms.
In the pediatric population, in conjunction with a detailed history and physical evaluation, the head-up tilt-table test may differentiate between presyncopal and syncopal episodes in children who present with seizurelike events.[41]
The head-up tilt-table test is less sensitive than electrophysiologic stress testing, and a negative result does not exclude the diagnosis of neurogenic syncope. In a study aimed at determining whether a statistical model could be used for an early prediction of head-up tilt-table test outcome from heart rate variability and baroreflex sensitivity parameters in 105 Italian patients with a previous history of vasovagal syncope, investigators found no syncopal predictions that were of practical value.[42]
Class IIa recommendations for tilt-table testing from the ACC/AHA/HRS guidelines include the following[6] :
However, the ACC/AHA/HRS does not recommend tilt-table testing for prediction of a response to medical therapy for VVS (class III).[6]
EEG can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis.
Stress testing/electrophysiologic studies (EPS) have a higher diagnostic yield than the Holter monitor and should be obtained for any patient with a suspected arrhythmia as a cause of syncope.
A cardiac stress test is appropriate for patients in whom cardiac syncope is suspected and who have risk factors for coronary atherosclerosis. Exercise stress testing may be beneficial in determining syncope origin in selected patients with syncope or presyncope that occurs during exertion.[6] This test can assist with cardiac risk stratification and can guide future therapy.
Carotid sinus massage has been used with some success to diagnose carotid sinus syncope. Patients are placed on a cardiac monitor and beat-to-beat BP-monitoring device. Atropine is kept at the bedside.
Longitudinal massage lasting 5 seconds is initiated at the point of greatest carotid pulse intensity at the level of the thyroid cartilage on one side at a time.
The maximal response occurs after approximately 18 seconds, and a positive result is one that produces 3 seconds of asystole or syncope. If the result is negative, the process is repeated on the other carotid sinus.
Carotid sinus massage may theoretically precipitate an embolic stroke in persons with preexisting carotid artery disease.
The American College of Cardiology (ACC), American Heart Association (AHA), and the Heart Rhythm Society (HRS) recommend guideline-directed medical therapy (all class I) for patients with[6] :
In individuals with arrhythmogenic right ventricular cardiomyopathy with syncope and[6] :
In patients with cardiac sarcoidosis[6] :
In patients with long QT syndrome and syncope of suspected arrhythmic origin who have no contraindications, beta-blocker therapy is a first-line treatment (class I).[6] Furthermore, in those with long QT syndrome and:
The ACC/AHA/HRS recommend exercise restriction in individuals with catecholaminergic polymorphic ventricular tachycardia (CPVT) and syncope of suspected arrhythmic origin (class I).[6] In those with CPVT and stress-induced syncope, beta blockers without intrinsic sympathomimetic activity are recommended (class I). In patients with CPVT with persistent syncope of suspected VA despite beta-blocker therapy, flecainide is reasonable (class IIa). Placement of and ICD is reasonable in those with CPVT and previous exercise- or stress-induced syncope despite the use of optimal medical therapy or LCSD (class IIa).[6]
In patients with vasovagal syncope (VVS), physical counterpressure maneuvers can be beneficial to those who have a sufficiently long prodromal period (class IIa).[6] In those with recurrent VVS without a history of hypertension, heart failure, or urinary retention, use of midodrine is reasonable (class IIa).
In patients with carotid sinus syndrome that is cardioinhibitory or mixed, permanent cardiac pacing is reasonable (class IIa).[6]
VVS
In a 2023 systematic review and meta-analysis of 18 studies comprising data from 1130 participants to evaluate the utility of nonpharmacologic and nonpacing therapies to prevent VVS, Alharbi et al reported yoga (largest effect size), physical counterpressure maneuvers, and yoga (lowest effect size) show potential in preventing recurrent VVS and can be considered as viable treatment options.[43] More investigation is needed.
Serotonin-specific reuptake inhibitors appear to show potential in preventing vasovagal syncope. In a 2024 systematic review and meta-analysis of 3 studies comprising data from 204 patients, Raj et al found these agents substantially lowered the likelihood of a patient having at least one recurrence of vasovagal syncome as well as provided significant protection against clinical presyncope.[44]
Prehospital management of syncope covers a wide spectrum of acute care and includes rapid assessment of airway, breathing, circulation, and neurologic status.
Treatment may require the following:
Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.
See also a 2024 consensus statement of the European Society for Emergency Medicine (EUSEM) Syncope Group regarding syncope core management process in the emergency department (ED) under Guidelines.[45]
In patients brought to the ED with a presumptive diagnosis of syncope, appropriate initial interventions include the following:
Electrocardiography (ECG) and rapid blood glucose evaluation should be promptly performed. A study to determine the sensitivity and specificity of the San Francisco Syncope Rule (SFSR) ECG criteria for determining cardiac outcomes found that when used correctly, the criteria can help predict which syncope patients are at risk of cardiac outcomes.[46] The SFSR ECG criteria predicted 36 of 42 patients with cardiac outcomes, with a sensitivity of 86%, a specificity of 70%, and a negative predictive value of 99%.
Syncope may be the manifestation of an acute life-threatening process but is generally not an emergency. Clinically ruling out certain processes is important. The treatment choice for syncope depends on the cause or precipitant of the syncope. Patients in whom a cause cannot be ascertained in the ED, especially if they have experienced significant trauma, should receive supportive care and monitoring.
Situational syncope treatment focuses on educating patients about the condition. For example, in carotid sinus syncope, patients should be instructed to avoid wearing tight collars, to use a razor rather than electric shaver, and to maintain good hydration status; they should also be informed of the possibility of pacemaker placement in the future.
Orthostatic syncope treatment also focuses on educating the patient. Inform patients about avoiding postprandial dips in blood pressure (BP), teach them to elevate the head of their bed to prevent rapid BP fluctuations on arising from bed, and emphasize the importance of assuming an upright posture slowly.
Additional therapy may include thromboembolic disease (TED) stockings, mineralocorticoids (eg, fludrocortisone for volume expansion), and other drugs such as midodrine (an alpha1-agonist with vasopressor activity). Patients' medications must be reviewed carefully to eliminate drugs associated with hypotension. Intentional oral fluid consumption is useful in decreasing frequency and severity of symptoms in these patients.[47]
The Syncope Evaluation in the Emergency Department Study (SEEDS) data suggested that specialized syncope units with protocoled approaches to ruling out cardiac causes of syncope reduce hospital costs and length of stay without compromising quality of care.[48] Data from subsequent studies confirmed these findings.[1]
Cardiac arrhythmic syncope is treated with antiarrhythmic drugs or pacemaker placement. Consider cardiologist evaluation or inpatient management, in that this is more commonly associated with poor outcomes.[2] Trials assessing beta-blockade to prevent syncope have conflicting results,[49] but no clear effect has been demonstrated.
In the prospective, multicenter Syncope Unit Project 2 (SUP 2) study, Brignole et al investigated the long-term effects and determinants of success of cardiac pacing in patients with severe unpredictable recurrent reflex syncope. Patients underwent carotid sinus massage (CSM), followed by tilt testing (TT) if CSM was negative, followed by implantation of an implantable loop recorder (ILR) if TT was negative; patients with an asystolic response to one of these tests received a dual-chamber pacemaker. The benefit of cardiac pacing was maintained at 3 years and was greatest in patients with negative TT.[50]
In a single-center observational study (2014-2020) that compared the clinical utility of ILR in 43 patients with heart disease and a history of symptomatic syncope versus 77 patients with heart disease without syncopal symptoms over a 3-year cumulative event rate, Assaf et al found no difference between the groups regarding the primary endpoint of an actionable event (arrhythmic event resulting in a change in clinical management) and that of the secondary endpoint of an event leading to device implantation.[51]
Cardiac mechanical syncope may be treated with beta-blockade to decrease outflow obstruction and myocardial workload. Valvular disease may require surgical correction. This, too, is associated with increased future morbidity and mortality.
Patients with select etiologies of syncope may require transfer for specialty evaluation or procedures.
The etiology of syncope dictates the need, if any, for specialty consultation. Select cases may require consultation with a neurosurgeon, a neurologist, a cardiologist, a vascular surgeon, a cardiothoracic surgeon, an endocrinologist, or a toxicologist.
In August 2017, the American College of Cardiology (ACC), American Heart Association (AHA), and the Heart Rhythm Society (HRS) released their recommendations for evaluating and managing patients with syncope.[6] Select definitions and class I (strong) recommendations are summarized below.
Syncope is defined as a symptom that presents suddenly, transiently, and with total loss of consciousness (LOC); is associated with an inability to maintain postural tone; and has quick and spontaneous recovery. No clinical features of other nonsyncope LOC causes should be present (eg, seizure, previous head trauma, or apparent LOC [ie, pseudosyncope]).
LOC is a state of cognition wherein an individual lacks awareness of themself and their situation, and is not able to respond to stimuli.
Transient LOC is a self-limited LOC that is classified as syncope or nonsyncope conditions (eg, seizures, hypoglycemia, metabolic conditions, drug/alcohol intoxication, head trauma-related concussion).
Presyncope or near-syncope relates to symptoms that occur before syncope (eg, extreme lightheadness, visual sensations, different degrees of altered consciousness without total LOC). There may be progression to syncope, or it may abort without syncope.
Orthostatic hypotension occurs when there is a drop in systolic blood pressure (SBP) of at least 20 mm Hg or diastolic BP (DBP) of at least 10 mm Hg when assuming an upright posture.
Cardiac/cardiovascular syncope results from bradycardia, tachycardia, or hypotension as a result of low cardiac index, obstructed blood flow, vasodilatation, or acute vascular dissection.
Noncardiac syncope results from causes other than those related to the heart or its vascular system (eg, reflex syncope, orthostatic hypotension, volume depletion, dehydration, blood loss).
Reflex or neurally mediated syncope occurs from a reflex that leads to vasodilation, bradycardia, or both.
Vasovagal syncope (VVS) is the predominant form of reflex syncope mediated by the vasovagal reflex, frequently preceded by identifiable triggers and/or by a characteristic prodrome. It may occur with upright posture or with exposure to emotional stress, pain, or clinical settings; often features diaphoresis, warmth, nausea, and pallor; has associated vasodepressor hypotension and/or inappropriate bradycardia; and has fatigue as its usual aftermath.
Carotid sinus syndrome is reflex syncope that occurs in the setting of carotid sinus hypersensitivity (ie, a pause ≥3 seconds and/or a fall in SBP ≥50 mm Hg when the carotid sinus is stimulated).
Psychogenic pseudosyncope is a syndrome that seems to be but is not true LOC and lacks an identifiable cardiac, reflex, neurologic, or metabolic etiology.
Perform a detailed history and physical examination in individuals with syncope. In the initial evaluation, a resting 12-lead electrocardiogram (ECG) is helpful.
Evaluate the cause and assess the short- and long-term morbidity and mortality risk factors of syncope.
In the presence of a serious medical condition identified during the initial assessment of individuals presenting with syncope that may be relevant to its cause, the ACC/AHA/HRS recommend investigation and management in a hospital.
The frequency and nature of syncope events should determine the selection of specific cardiac monitoring. In the inpatient setting, telemetry is useful for individuals admitted for evaluation of suspected cardiac syncope.
Guideline-directed medical therapy is recommended for patients with:
Placement of an implantable cardioverter-defibrillator is recommended in patients with syncope, documented ventricular arrhythmia (VA), and:
In patients with long QT syndrome and syncope of suspected arrhythmic origin who have no contraindications, beta-blocker therapy is a first-line treatment.
Restricting exercise in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) who present syncope of suspected arrhythmia origin is recommended. Use of beta-blocking agents that lack intrinsic sympathomimetic activity is recommended for those with CPVT and stress-induced syncope.
Recommendations on the diagnosis and management of syncope were released in June 2018 by the European Society of Cardiology (ESC).[52]
Transient loss of consciousness (TLOC) has four specific characteristics: short duration, abnormal motor control, loss of responsiveness, and amnesia for the period of LOC.
TLOC is probably syncope when: (1) there are signs and symptoms specific for reflex syncope, syncope due to orthostatic hypertension (OH), or cardiac syncope, and (2) signs and symptoms specific for other forms of TLOC (head trauma, epileptic seizures, psychogenic TLOC, and/or rare causes) are absent.
When epileptic seizures or psychogenic attacks are likely, appropriate steps should be taken. By using a detailed clinical history, physicians can differentiate syncope from other forms of TLOC in approximately 60% of cases.
The starting point of the diagnostic evaluation of TLOC of suspected syncopal nature is the initial syncope evaluation, which consists of careful history taking concerning present and previous attacks, as well as eyewitness accounts, in person or through a telephone interview; physical examination, including supine and standing blood pressure (BP) measurements; and an electrocardiogram (ECG).
Additional examinations may be performed when needed: immediate ECG monitoring when there is a suspicion of arrhythmic syncope; echocardiogram when there is previous known heart disease, data suggestive of structural heart disease, or syncope secondary to cardiovascular cause; carotid sinus massage (CSM) in patients aged >40 years; head-up tilt testing when there is suspicion of syncope due to OH or reflex syncope; blood tests when clinically indicated (eg, hematocrit or hemoglobin when hemorrhage is suspected, oxygen saturation and blood gas analysis when hypoxia is suspected, troponin when cardiac ischemia-related syncope is suspected, or D-dimer when pulmonary embolism is suspected).
Clinical features that can suggest a diagnosis on initial evaluation:
Long history of recurrent syncope, in particular occurring before the age of 40 years
After unpleasant sight, sound, smell, or pain
Prolonged standing
During a meal
Being in crowded and/or hot places
Autonomic activation before syncope: pallor, sweating, and/or nausea/vomiting
With head rotation or pressure on the carotid sinus (as in tumors, shaving, tight collars)
Absence of heart disease
Clinical features that can suggest a diagnosis on initial evaluation:
While or after standing
Prolonged standing
Standing after exertion
Post-prandial hypotension
Temporal relationship with start or changes of dosage of vasodepressive drugs or diuretics leading to hypotension
Presence of autonomic neuropathy or parkinsonism
Clinical features that can suggest a diagnosis on initial evaluation:
During exertion or when supine
Sudden onset palpitation immediately followed by syncope
Family history of unexplained sudden death at young age
Presence of structural heart disease or coronary artery disease
ECG findings suggesting arrhythmic syncope
These patients do not need further diagnostic tests in the emergency department (ED) as they are likely to have reflex, situational, or orthostatic syncope. They may benefit from reassurance, or counseling.
These patients should be classified as HIGH RISK; they require an intensive diagnostic approach and may need urgent treatment and admission. These patients should be monitored (although it is unclear for how long this should be, most studies suggesting up to 6 hours in the ED and up to 24 hours in hospital) in a setting where resuscitation can be performed in case of deterioration.
These patients will require expert syncope opinion, which can probably be safely managed in an outpatient setting. There is no direct evidence that admitting patients to hospital changes their outcome, while there is evidence that management in an ED observation unit and/or fast-track to a syncope outpatient unit is beneficial.
There is strong consensus that the diagnosis of carotid sinus syndrome (CSS) requires both the reproduction of spontaneous symptoms during carotid sinus massage (CSM) and clinical features of spontaneous syncope compatible with a reflex mechanism.
Tilt testing is widely accepted as a useful tool to demonstrate susceptibility of the patient to reflex syncope, especially a hypotensive (vasodepressive) tendency, and thereby to initiate treatment. The endpoint of tilt testing is the reproduction of symptoms along with the induction of reflex hypotension/bradycardia, OH, postural orthostatic tachycardia syndrome (POTS), or psychogenic pseudosyncope (PPS).
There is strong evidence that the absence of a BP overshoot and an absence of a heart rate (HR) increase during the Valsalva is pathognomonic for neurogenic OH.
Deep breathing test: There is strong consensus that blunted or abolished variation is suggestive of parasympathetic dysfunction.
The gold standard for the diagnosis of arrhythmic syncope is when there is a correlation between the symptoms and an ECG recording. The presence of asymptomatic significant arrhythmias—defined as prolonged asystole (≥3 s), rapid supraventricular tachycardias (SVTs) (ie, >160 bpm for >32 beats), or ventricular tachycardias (VTs)—has been considered by several authors to be a diagnostic finding.
Even if the quality of evidence is moderate, there is strong consensus that a positive electrophysiologic study (EPS) indicates that the likely mechanism of syncope is paroxysmal atrioventricular (AV) block.
Angiography alone is not diagnostic of the cause of syncope. Therefore, cardiac catheterization techniques should be carried out in suspected myocardial ischemia or infarction with the same indications as for patients without syncope.
The efficacy of therapy aimed at preventing syncope recurrence is largely determined by the mechanism of syncope rather than its etiology. Bradycardia is a frequent mechanism of syncope. Cardiac pacing is the most powerful therapy for bradycardia, but its efficacy is less if hypotension coexists.
Syncopal recurrences often decrease spontaneously after medical assessment, even in the absence of a specific therapy; in general, syncope recurs in < 50% of patients within 1–2 years.
Despite its benign course, recurrent and unpredictable reflex syncope may be disabling. The cornerstone of management of these patients is non-pharmacological treatment, including education, lifestyle modification, and reassurance regarding the benign nature of the condition.
Careful avoidance of agents that lower BP (ie, any antihypertensive agents, nitrates, diuretics, neuroleptic antidepressants, or dopaminergic drugs) is key in the prevention of recurrence of syncope.
There is moderate evidence that discontinuation/reduction of hypotensive therapy targeting an SBP of 140 mmHg should be effective in reducing syncopal recurrences in patients with hypotensive susceptibility.
There is moderate evidence that fludrocortisone may be effective in reducing syncopal recurrences in young patients with low–normal values of arterial BP and without comorbidities.
There is sufficient evidence from multiple trials that beta-blockers are not appropriate in reducing syncopal recurrences. Desirable and undesirable effects are closely balanced.
There is sufficient evidence that dual-chamber cardiac pacing should be considered to reduce recurrence of syncope when the correlation between symptoms and ECG is established in patients ≥40 years of age with the clinical features of those in the ISSUE studies.
Despite the lack of large randomised controlled trials (RCTs), there is sufficient evidence that dual-chamber cardiac pacing should be considered to reduce syncopal recurrences in patients affected by dominant cardioinhibitory carotid sinus syndrome (CSS).
There is strong consensus that reduction or discontinuation of hypotensive drugs and psychotropic drugs clearly outweighs the undesirable effects (eg, complications) of high BP.
Syncope in childhood is common, the majority being of reflex origin, with only a minority having a potentially life-threatening cause.
Discriminating benign from serious causes is made primarily by history, physical examination, and ECG results.
Children with a history suggesting vasovagal syncope (VVS), a normal ECG, and no family history of arrhythmia should not undergo further cardiac investigations.
The cornerstone of therapy for young patients with reflex syncope includes education and reassurance.
In August 2024, the European Society for Emergency Medicine (EUSEM) Syncope Group released a consensus statement that provided information on the general process to work up and care for patients with suspected syncope as well as rules for sufficient and systematic management of syncope in the emergency department (ED) that initially presents as transient loss of consciousness (TLOC).[45] Essential components of the risk-based approach comprise processes such as excluding life-threatening causes, differentiating syncope from nonsyncopal TLOCs, and using syncope risk stratification to make informed decisions on whether to admit or discharge patients.[45] Summaries of selected standard operating procedures are outlined below.
Assess the available triage vital signs; evaluate blood pressure (BP), heart rate (HR), peripheral oxygen saturation, respiratory rate, and body temperature. Document in detail.
If recommended in specific clinical scenarios, the recommended minimal laboratory studies to obtain are levels of blood glucose and hemoglobin.
Additional tests that may be obtained include a complete blood cell (CBC) count; levels of electrolytes, creatine kinase (CK), lipase, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), lactate, and C-reactive protein (CRP), as well as a coagulation profile for patients on anticoagulant treatment.
On the basis of suspected diagnoses, other tests may include levels of serial cardiac troponin and/or copeptin as a quick method of excluding myocardial infarction, and/or level of D-dimer to exclude a diagnosis of pulmonary embolism or aortic dissection.
Obtain and evaluate electrocardiography (ECG). Only a normal ECG is considered low risk. An expert ECG interpretation should occur within 10 minutes of a patient's registration, with documentation of the results according to the institutional and local standards.
The presence of major high-risk features should prompt obtaining an ECG. Such features include:
Characteristics considered minor high risk (only if the patient's history is consistent with arrhythmogenic syncope) include:
The goals of pharmacotherapy are to prevent complications and to reduce morbidity.
Clinical Context: Anticholinergic (or parasympatholytic) drug that exerts its action by competitively inhibiting acetylcholine at muscarinic receptors on postganglionic smooth muscle. Can counteract rapidly heightened vagal tone in response to pathologic carotid sinus syndrome. Additionally, can reverse bradycardia and lessen degree of heart block when vagal activity is etiologic factor. Usual doses are used to reduce severe bradycardia and syncope associated with hyperactive carotid sinus reflex.
These agents improve conduction through the atrioventricular node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective.
Clinical Context: Nutrient replenisher, serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose, whereas each 100 mL of 10% dextrose contains 10 g of dextrose.
Should be given only after demonstrated hypoglycemia.
Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations.
Clinical Context: Indicated for treatment of anxiety and management of panic attacks. Following PO administration, absorbed readily. Peak concentrations in plasma occur 1-2 h following administration.
CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis.
Clinical Context: Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect persisting for 2-3 h. Has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.
Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist that acts on receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of BP. This drug has minimal beta effects and diffuses poorly across the blood-brain barrier.