Syncope

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

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

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

Cardiac syncope

Includes arrhythmogenic, myocardial, and other vascular etiologies of syncope

Noncardiac syncope

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

References:^{[3][4][5][6][7][8][9][10]}

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

Cardiac and vascular causes ^[11]

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

• Cardiac dysrhythmias
  • Bradyarrhythmias, e.g., Mobitz II or 3^rd-degree AV block
  • Ventricular tachyarrhythmias, e.g., sustained VT, ARVC-associated VT
  • SVT: e.g., AVNRT
  • Arrhythmias associated with sudden cardiac arrest: e.g., LQTS, Brugada syndrome
  • Malfunction or failure of pacemaker/AICD
• Myocardial dysfunction
  • Myocardial infarction or acute coronary syndrome
  • Acute heart failure
  • Myocarditis
  • Cardiomyopathies
  • Ventricular outflow tract obstruction: e.g., hypertrophic obstructive cardiomyopathy
• Valvular heart disease: e.g., severe aortic stenosis
• Extracardiac vascular disorders
  • Circulatory shock: e.g., cardiogenic shock, hemorrhagic shock, other types of hypovolemic shock, septic shock
  • Acute aortic syndromes
  • Pericardial tamponade
  • Pulmonary: e.g, pulmonary embolism, pulmonary hypertension, tension pneumothorax
  • Intracranial: e.g., subarachnoid hemorrhage, pontine stroke

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

Noncardiac causes

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

• Reflex-mediated
  • Vasovagal syncope (neurocardiogenic syncope)
  • Carotid sinus hypersensitivity
  • Situational syncope: e.g., micturitional syncope
• Orthostasis-related
  • Orthostatic hypotension
    • Hypovolemia: e.g., GI fluid loss, diuretic use, adrenal insufficiency
    • Medication-induced: e.g., beta blockers, calcium channel blockers, alpha blockers
    • Neurogenic (a type of dysautonomia): e.g., diabetic neuropathy, Parkinson disease
  • Postural (orthostatic) tachycardia syndrome (POTS)

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

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

• Prodrome
  • Vasovagal: impairment of senses; , nausea, pallor, warmth, diaphoresis, lightheadedness, and hyperventilation
  • Orthostatic: lightheadedness, nausea, and dizziness
• Rapid onset loss of consciousness
  • Accompanied by complete loss of muscle tone
  • Last seconds to minutes followed by spontaneous recovery
  • Convulsive syncope: common form in which loss of consciousness is accompanied by myoclonic movements

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

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

References:^[5][7]

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

Initial management ^{[1][2][11][12][13][14]}

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

• Stabilization (as needed)
  • Consider stabilizing measures for acutely syncopal patients, e.g., ABCDE survey, POC glucose, supine positioning, IV access, cardiac monitoring, fluid resuscitation.
  • Identify and treat life-threatening causes of syncope concurrently.
• Initial evaluation: Perform a detailed clinical assessment with select routine investigations.
  • Obtain medication, medical, and family history ^[12]
  • Determine triggers and ask witnesses (if available) for details about the event.
  • Conduct a thorough physical examination.
  • Obtain ECG and orthostatic vital signs
  • Consider basic laboratory studies
• Risk stratification: Consider performing on all patients based on clinical features, historical factors, and results of the initial evaluation to help guide disposition and need for further investigations.
• Next steps
  • Detailed diagnostics: Consider as guided by clinical suspicion, especially in patients without a clear cause of syncope identified on initial evaluation (see “Further investigations”).
  • Definitive management: Depends on underlying etiology, risk stratification, and disease severity (see “Cardiac syncope” and “Noncardiac syncope”).
  • Manage complications: e.g., fall injuries

Evaluate patients with presyncope similarly to those with syncope.

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

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

Routine investigations ^{[1][2][12][13]}

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

ECG

• Indicated in all patients
• Potential findings ^[13]
  • Arrhythmias and conduction abnormalities
  • Brugada syndrome
  • Ischemic changes
  • Ventricular hypertrophy

Orthostatic vital signs ^[15]

• Method
  • Measure blood pressure and heart rate after the patient has been in a supine position for 5 minutes.
  • Ask the patient to stand up and retake vital signs after 1 minute and 3 minutes (a third measurement after 10 minutes is optional).
  • Document any symptoms that the patient experiences.
• Findings
  • Normal: Minimal or no variation in blood pressure or heart rate
  • Abnormal
    • Significant drop in systolic and/or diastolic BP (See “Orthostatic hypotension.”)
    • Significant increase in heart rate (See “POTS.”)

Laboratory studies

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

• Glucose (may detect hypoglycemia)
• CBC (may show ↓ serum hemoglobin)
• BMP (e.g., ↑ BUN/creatinine ratio may suggest dehydration)
• Pregnancy test

Disposition ^{[1][2][11][12][13][14]}

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

• Admission: e.g., for further investigations (e.g., provocation studies, cardiovascular imaging), continuous cardiac monitoring, and targeted management
  • Typically indicated for patients with cardiac syncope: e.g., structural heart disease, pulmonary embolism, shock, SAH
  • In patients with noncardiac syncope (i.e., reflex syncope or orthostatic syncope) OR syncope of unclear origin after initial evaluation, consider admission if there is a high risk of serious adverse events following syncope.
  • Consider critical care unit admission for patients with immediately life-threatening causes of syncope.
• Discharge ^[1][12][13]
  • In patients with noncardiac syncope OR syncope of unclear origin, consider discharge with reassurance and instructions if there is a low risk of serious adverse events following syncope.
  • Consider outpatient cardiac monitoring (e.g., loop recorder, Holter monitoring) for recurrent or frequent syncopal episodes of unclear origin.
• Consultations: as guided by suspected underlying cause and severity (e.g., cardiology, ICU).

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

Approach

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

Prognostic factors ^[1][2][12]

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

Risk scores

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

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

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

Approach

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

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

Cardiovascular studies ^[1][24]

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

• Rhythm monitoring
  • Consider if there is clinical suspicion of arrhythmia.
  • Choose the monitoring device based on the frequency of events (to increase the diagnostic yield), e.g.: ^[1]
    • ECG Holter monitor: symptoms likely to recur within 24–72 hours
    • External loop recorders: symptoms likely to recur within 2–6 weeks
    • Implantable loop recorders: for recurrent but infrequent symptoms ^[2]
  • Findings include:
    • Sinus bradycardia < 40 bpm
    • Sinus pauses > 3 seconds
    • AV blocks
    • Bundle branch blocks
• Cardiothoracic imaging: Consider for patients with high-risk features or if there is clinical suspicion of structural disease.
  • Echocardiogram: common initial imaging modality to exclude or confirm structural disease ^[25]
  • CTA chest: Consider if pulmonary artery disease (e.g., PAH, PE) or acute aortic syndromes are suspected.
  • Coronary CTA: Can help identify coronary artery disease or anomalous coronary anatomy (e.g., in young patients with exertional syncope).
  • Cardiac MRI: Can help identify infiltrative cardiomyopathies or areas of scarring that could represent arrhythmogenic foci (e.g., in ARVC).
• Cardiac stress testing: Consider to detect ischemic heart disease in patients who experience syncope during exertion.
• Cardiac enzymes: Consider troponin only if acute coronary syndrome is suspected (may be elevated). ^[1]
• Electrophysiological studies
  • Consider in select patients with suspected arrhythmia despite a normal initial evaluation. ^[1][2]
  • Avoid if cardiac imaging and an ECG are both normal.

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

• Carotid sinus massage: Perform in patients > 40 years of age to determine if reflex syncope is due to carotid sinus syndrome.
• Tilt table test: Consider only for patients with recurrent syncopal episodes and if the diagnosis remains unclear following an initial evaluation.
  • Clinical applications ^[30]
    • Distinguish between different types of reflex syncope (i.e., vasovagal and orthostatic hypotension)
    • Investigate differential diagnoses of syncope
      • To distinguish syncope from psychogenic pseudosyncope
      • To distinguish convulsive syncope from epilepsy
  • Method
    • The patient is strapped onto a table and positioned at predetermined inclinations (possibly with an additional pharmacological provocation agent ).
    • Variation in blood pressure and heart rate are registered and compared to the expected variations in healthy individuals.
  • Contraindications include ischemic heart disease, uncontrolled hypertension, left ventricular outflow tract obstruction, and aortic stenosis

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

Neurological investigations ^[1][2][24]

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

• CT or MRI head: Only consider if there is suspicion of a cerebrovascular event, intracranial hypertension, or a head injury from a fall. ^[27][28]
• Carotid ultrasound with Doppler: Only consider if there are accompanying neurological features that suggest TIA or stroke. ^[26]
• Autonomic evaluation (specialized studies): Consider in patients with suspected autonomic dysfunction to provoke and assess autonomic reflexes. ^[32]
• EEG: Only consider for patients with a high pretest probability of seizures. ^[29]

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

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

General principles

• In cardiac syncope, reduced cerebral perfusion results from insufficient cardiac output due to acute cardiac and/or circulatory failure.
• This can manifest as transient loss of consciousness for different reasons, for example:
  • The underlying cause is paroxysmal and self-limiting, e.g., PSVT.
  • The underlying cause is dynamic and is triggered by specific physiological circumstances, e.g., dynamic LVOT obstruction, such as in HOCM, causes syncope if oxygen demand is increased.
  • Cerebral perfusion is reduced during the delay between the onset of an inciting event (MI, PE, hemorrhage) and the effect of compensatory physiological responses (e.g., sympathetic activation).
• Cardiac syncope is associated with one-year mortality rates of up to 33%.

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

Management ^{[1][2][12][13]}

• Consider cardiac causes in patients who present with:
  • A sudden fall without any prodrome
  • A brief prodrome characterized by specific cardiovascular symptoms, e.g., palpitations, chest pain
• Place patients under continuous cardiac monitoring.
• Imaging (e.g., TTE, CTA), laboratory studies (e.g., cardiac enzymes), and cardiac rhythm monitoring may confirm the diagnosis.
• Common therapeutic measures include:
  • Cardiac pacing
  • Antiarrhythmic drugs
  • AICD placement
  • Catheter ablation
  • Fluid resuscitation
• Definitive management depends on the specific underlying condition.
• Consult cardiology for prompt treatment of cardiac conditions.

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

General principles

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

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

Reflex syncope ^{[1][2][12][42]}

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

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

Vasovagal syncope (VVS; neurocardiogenic syncope)

• Epidemiology
  • Common in younger patients (the first episode is rare after 40 years of age)
  • Can be recurrent
• Mechanism (vasovagal response): trigger activates vagus nerve → ↑ parasympathetic nervous tone → ↓ heart rate, blood pressure, and cardiac contractility, ↑ peripheral vasodilation
• Clinical features
  • Prodrome: includes nausea, diaphoresis, pallor, and flushing
  • Commonly followed by fatigue
• Possible triggers
  • Prolonged standing
  • Emotional stress, e.g., fear, the sight of blood, medical procedures
  • Pain or injury
  • Heat exposure
  • Can be idiopathic
• Diagnosis is clinical and requires presyncope or syncope associated with the following:
  • Typical trigger and prodrome
  • Hypotension with or without any of the following cardioinhibitory responses during the episode: ^[43]
    • Documented bradycardia
    • Asystole ≥ 3 seconds
• Treatment ^[1]
  • Initiate nonpharmacological management of noncardiac syncope.
  • If symptoms persist, consider: ^[1]
    • Midodrine or fludrocortisone (for dosages see “Medications for noncardiac syncope”)
    • Orthostatic training ^[44][45]
    • If > 40 years of age with prolonged spontaneous pauses: dual chamber pacemaker

Situational syncope

• Description: : Mechanism, clinical features, and diagnosis are identical to vasovagal syncope, except the trigger of the vasovagal response is a specific voluntary or involuntary action or physiological function, e.g., micturition syncope
• Possible triggers
  • Coughing
  • Swallowing
  • Laughing
  • Defecation (bowel movements)
  • Micturition (commonly seen in individuals with prostatic hyperplasia)
• Treatment ^[1]
  • Initiate nonpharmacological management of noncardiac syncope.
  • For controllable triggers (e.g., laughing, coughing): avoidance when possible

Carotid sinus syndrome

• Description: a type of recurrent reflex syncope that primarily occurs in individuals with carotid sinus hypersensitivity when pressure is applied to the carotid sinus
• Mechanism: increased carotid sinus sensitivity (due to, e.g., increased baroreceptor or peripheral receptor response)
• Risk factors: coronary atherosclerosis, previous history of neck surgery or irradiation, age (> 50 years)
• Trigger: pressure on the carotid sinuses (e.g., during a massage, when shaving, tightening a necktie)
• Diagnosis: carotid sinus hypersensitivity confirmed, e.g., pause in heart rate ≥ 3 seconds AND/OR fall in systolic blood pressure ≥ 50 mm Hg when pressure is applied by carotid sinus massage
• Treatment ^[1]
  • Educate patients to avoid triggers, e.g., tight-collared clothing.
  • Consider a pacemaker for patients with carotid sinus syndrome with a cardioinhibitory response.
  • See also “Nonpharmacological management of noncardiac syncope.”

Orthostatic syncope ^[1][2][12]

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

• Common mechanism
  • Orthostatic hypotension: standing up/postural change PLUS insufficient counterregulation, i.e., reflex tachycardia and vasoconstriction are impaired (due to autonomic dysfunction) or overwhelmed → dependent pooling of blood → hypotension (can be symptomatic or asymptomatic)
  • Symptomatic orthostasis: Decreased cerebral perfusion leads to a decrease in both muscle tone and level of consciousness.
• Common underlying causes
  • Hypovolemia (e.g., dehydration, hemorrhage, use of diuretics such as thiazides)
  • Medications that cause vasodilation or limit tachycardia (e.g., beta blockers, alpha blockers, calcium channel blockers)
  • Prolonged bed rest
  • Age-related loss of baroreceptor sensitivity
  • Anemia
  • Pregnancy
• Diagnosis: Determine the likelihood of orthostasis based on its pretest probability (PTP) PLUS evidence on physical examination (i.e., orthostatic vital signs) or tilt table test.
  • Features associated with high PTP for orthostasis include:
    • History of syncope while standing
    • Absence of syncope while laying down
    • Symptoms worsen in high temperatures
    • Evidence of a typical underlying cause: e.g., clinical or laboratory findings of hypovolemia, responsible medications, anemia
  • Orthostasis on examination
    • Orthostatic hypotension: change from supine or seated position to a standing position → systolic BP decreases by ≥ 20 mm Hg AND/OR diastolic BP decreases by ≥ 10 mm Hg ^[2]
    • Orthostatic tachycardia: See “POTS.”
  • Combined results ^[2]
    • Low PTP: Orthostatic syncope is unlikely; further testing is needed independent of BP changes.
    • High PTP and documented symptomatic orthostatic hypotension: Orthostatic syncope is highly likely.
    • High PTP and documented asymptomatic orthostatic hypotension: Orthostatic syncope is possible.
• Treatment
  • Initiate nonpharmacological management of noncardiac syncope.
  • If symptoms persist, consider midodrine (see “Medications for noncardiac syncope”).

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

Neurogenic orthostatic hypotension ^[1][2][12]

• Description: A subtype of orthostatic hypotension where the autonomic dysfunction that impairs or blunts the reflex tachycardia and/or vasoconstriction is caused by a neurological disorder.
• Possible underlying conditions include dysfunction of the:
  • Central autonomic system: e.g., due to Parkinson disease, Lewy body dementia
  • Peripheral autonomic system: e.g., due to pure autonomic failure, diabetic neuropathy, vitamin B12 deficiency
• Diagnosis: similar to orthostatic syncope; other evidence of dysautonomia or signs of an underlying neurological disorder may also be present.
• Treatment ^[1]
  • Initiate nonpharmacological management of noncardiac syncope.
  • Optimize treatment of underlying causes, e.g., management of diabetes.
  • If symptoms persist, consider pharmacological therapy.
    • First line: fludrocortisone, droxidopa, midodrine
    • Refractory symptoms: pyridostigmine or octreotide
    • For further information including dosages, see “Medications for noncardiac syncope.”

Postprandial orthostatic hypotension ^[46][47]

• Description: a subtype of orthostatic hypotension that occurs after eating ^[46]
• Mechanism: not fully known; involves splanchnic venous pooling and is exacerbated by autonomic dysfunction ^[47][48]
• Risk factors
  • Adults ≥ 65 years old
  • Autonomic dysfunction
• Clinical features
  • Decrease in blood pressure after meals, especially ones that are large, high-carbohydrate, or include alcohol
  • Can be asymptomatic or associated with presyncope and/or syncope
• Diagnosis
  • Diagnosis is confirmed if, within 2 hours of a meal, either: ^[47]
    • SBP decreases by ≥ 20 mm Hg ^[49]
    • OR postprandial SBP is ≤ 90 mm Hg following a preprandial SBP ≥ 100 mm Hg
  • Consider:
    • ABPM ^[2][46]
    • Referral for autonomic evaluation ^[1]
• Treatment
  • Initiate nonpharmacological management of noncardiac syncope.
  • Additionally advise patients to: ^[47]
    • Avoid large, high-carbohydrate meals.
    • Allow foods to cool to room temperature before eating.
    • Decrease alcohol intake.
    • Avoid physical activity or quickly standing after meals.
  • If symptoms persist, consider octreotide or acarbose (see “Medications for noncardiac syncope”). ^[1][50]

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

• Description: A poorly understood subtype of orthostatic syncope; Often occurs following other medical conditions (e.g., pregnancy, trauma, surgery, viral illness)
• Clinical features
  • Cardiac symptoms: e.g., lightheadedness, presyncope, palpitations, chest discomfort
  • Noncardiac symptoms: e.g., tremors, nausea, fatigue, brain fog, blurred vision, sleep disturbance, exercise intolerance
  • Symptoms are aggravated in the upright position and alleviated in the recumbent position.
• Diagnosis
  • Requires the presence of characteristic clinical features for > 6 months with no alternate explanation PLUS the following during physical examination or tilt table testing:
    • Orthostatic heart rate increase by ≥ 30 beats/minutes within 10 minutes of standing ^[42]
    • Absence of significant orthostatic hypotension
  • CBC and thyroid function studies can be helpful to exclude anemia and thyrotoxicosis.
  • Consider extended testing (e.g., TTE, exercise stress test) on a case-by-case basis.
• Treatment
  • Initiate nonpharmacological management of noncardiac syncope.
  • Aerobic exercise programs may improve symptoms. ^[42][51]
  • If symptoms persist, consider midodrine, fludrocortisone, or propranolol (see “Medications for noncardiac syncope”). ^[42][51]

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

Exercise-associated postural hypotension (EAPH) ^[52]

• Definition: inability to stand or walk without assistance (i.e., collapse) after vigorous exertion
• Epidemiology: : occurs most commonly in athletes (especially upon completion of endurance running)
• Risk factors: mild dehydration, excessive exercise (overexertion), and reduced baroreflex response to hypotension due to long-term endurance training ^[53]
• Pathophysiology
  • During exercise, ↑ blood flow to muscles of the lower extremities; → ↑ skeletal muscle pump activity → ↑ venous return to the heart
  • Sudden cessation of exercise → loss of skeletal muscle pump activity → ↓ venous return → large volumes of blood pool in the lower extremities → postural hypotension → collapse
• Clinical features
  • Dizziness, weakness; (usually, no loss of consciousness)
  • Body temperature is normal or mildly elevated.
• Diagnostics: diagnosis of exclusion
• Management
  • Oral hydration and Trendelenburg position
  • Rule out life-threatening causes of collapse (e.g., cardiac arrest, exertional heatstroke, exercise-associated hyponatremia.
• Prevention
  • Adequate hydration before and during exercise
  • Continued walking upon completion of vigorous exercise to prevent venous pooling in the lower extremities

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

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

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

• Fluid management: : Increase fluid (2–3 liters/day) and sodium intake (6–9 g of salt/day) unless contraindicated. ^[1]
• Medication adjustment: Consider discontinuing or decreasing the dosage of offending or contributing drugs (e.g., diuretics, antihypertensives).
• Patient education
  • If possible, instruct patients to avoid or anticipate triggers.
  • Advise patients with a short prodrome to lie down when prodrome is detected (to avoid injuries from falls).
  • Patients with long prodromes may benefit from acute water ingestion and physical counterpressure measures, e.g.: ^[1][54]
    • Squatting
    • Leg crossing
    • Muscle tensing (e.g., abdominal contraction)
    • Muscle pumping (e.g., marching in place)
    • Bending over
  • Advise the patient to educate friends and family on basic first aid for syncope. ^[55]
• Compression stockings (at least thigh high) : Consider for patients with orthostatic syncope.

Overview of pharmacological therapy

If symptoms persist despite nonpharmacological management, consider trialing medication.

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

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

• Perform rapid ABCDE survey.
• Place the patient supine and consider leg elevation.
• Obtain a full set of vitals.
• Begin cardiac monitoring.
• Obtain IV access.
• Check POC glucose.
• Perform thorough clinical evaluation.
• Ask about medication use and triggers on history.
• Examine for neurological abnormalities and injuries.
• Obtain an ECG.
• Measure orthostatic vital signs
• Consider basic laboratory studies (e.g., CBC, BMP).
• Identify and treat life-threatening causes of syncope.
• Rule out serious differential diagnoses of syncope.
• Perform risk stratification to determine the risk of serious adverse events from syncope.
• Consider using risk scores to supplement clinical judgment.
• Consult a specialist (e.g., cardiology) and begin targeted therapy if cardiac syncope is highly suspected or identified.
• Consider nonpharmacological therapy for noncardiac syncope, e.g., fluids, adjust or discontinue the offending medication.
• Determine disposition based on etiology and risk stratification.

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

References:^[7][63]

The differential diagnoses listed here are not exhaustive.

Syncope in children

• Epidemiology: Approx. 20% of children have experienced at least one episode of syncope before the age of 15. ^[64]
• Etiology
  • Benign causes (common)
    • Vasovagal syncope (most common) ^[65]
    • Breath-holding spells
    • Orthostatic hypotension
    • Non-life-threatening arrhythmias (e.g., bradycardia, supraventricular tachycardia)
  • Life-threatening causes (rare)
    • Cardiac: e.g., long QT syndrome, congenital heart defects
    • Metabolic: e.g., hypoglycemia, electrolyte disturbances (e.g., hyperkalemia)
    • Infectious: e.g., sepsis
    • Other: e.g., heat stroke, poisoning (e.g., sedatives, alcohol, and/or recreational drugs), anaphylaxis
  • Syncope-mimicking conditions (e.g., seizures, hyperventilation, narcolepsy)
• Clinical features: same as clinical features in adults
• Management
  • Rule out life-threatening causes of syncope.
  • See “Management” section above.