Syncope is a short-term loss of consciousness and loss of postural stability followed by spontaneous return of consciousness to the previous neurologic baseline without the need for resuscitation. The condition is caused by transient interruption of cerebral blood flow that may be benign or related to a underlying life-threatening condition. Syncope is not a distinct disease entity; rather, it is a symptom of another pathologic process, whether it be transient or a more established disease process. Syncope may be accompanied by other symptoms, such as light-headedness, sweating, palpitations, nausea, feeling warm or cold, and visual blurring. Workup includes a detailed history and physical examination, electrocardiography, echocardiography, provocative testing (tilt-table test), or imaging of the suspected culprit vasculature. In many cases, a definite etiology is not found. Management is based on the underlying cause and can include physical countermaneuvers, stopping offending drugs, volume resuscitation, blood transfusion, and/or cardiac or vascular interventions.

Last update:

Table of Contents

Share this concept:

Share on facebook
Share on twitter
Share on linkedin
Share on reddit
Share on email
Share on whatsapp

Definition and Epidemiology


Syncope is a self-limiting, transient loss of consciousness caused by inadequate cerebral blood flow that results in inadequate cerebral perfusion. 

  • There is associated loss of postural integrity. 
  • A spontaneous return to baseline levels of neurologic function without the need for resuscitation or intervention is typical.

Presyncope (also known as near-syncope) is part of the syncope spectrum.

  • Like syncope, it may present with prodromal symptoms. 
  • However, there is no loss of consciousness.


  • Accounts for: 
    • > 2% of all ED encounters
    • > 5% of all hospital admissions
  • Lifetime prevalence in general population: approximately 10%–20%
  • Occurrence has a bimodal age distribution:
    • A peak in late adolescence to early adulthood (mostly vasovagal origin)
    • Second peak in older age, with a sharp rise thereafter


Regardless of the underlying cause, syncope is a manifestation of hypoperfusion to either the cerebral cortex (bilateral) or the reticular activating system (RAS).

Neurocardiogenic syncope

  • Also known as vasovagal syncope
  • Neurocardiogenic symptoms most common cause of syncope
  • Usually a benign, self-limited episode of systemic hypotension caused by a reflex that increases vagal tone and/or decreases sympathetic tone (i.e., excessive autonomic reflex activity)
  • Manifestations affecting perfusion include:
    • Vasodilation
    • Reduced cardiac filling 
    • Bradycardia
  • These dynamics result in: 
    • Cerebral hypoperfusion 
    • Loss of consciousness
    • Loss of cortical stimulation of postural tone
  • Situational causes (as a group, referred to as “situational syncope”) include:
    • Emotional stress:
      • Witnessing trauma
      • Sight of needles or blood
      • Extreme anxiety or panic attack
      • Extreme pain 
    • Prolonged standing
    • Micturition
    • Defecation
    • Swallowing
    • Coughing/sneezing
    • Carotid hypersensitivity:
      • Syncope (or presyncope) resulting from excessive reflex response to carotid sinus stimulation
      • Stimuli include head turning, tight neckwear, shaving.

Orthostatic hypotension

Orthostatic hypotension is defined by a drop in systolic blood pressure ≥ 20 mm Hg  or reflex tachycardia > 20 beats per minute with positional change (i.e., failure or inadequacy of the autonomic reflex response).

Volume depletion:

  • Hemorrhage:
    • Traumatic hemorrhage
    • Retroperitoneal hemorrhage
    • GI blood loss
    • Splenic rupture
    • Obstetric/gynecologic blood loss
  • GI losses:
    • Vomiting
    • Diarrhea
  • Diminished thirst drive (primarily in older individuals)
  • Water deprivation
  • Diuretic use
  • Immobility/deconditioning

Autonomic dysfunction:

  • Primary: 
    • Pure autonomic failure
    • Parkinson disease
    • Multiple system atrophy
    • Lewy body dementia
  • Secondary: 
    • Diabetes mellitus
    • Amyloidosis
    • Spinal cord injury 
    • Autoimmune neuropathy
    • Paraneoplastic neuropathy

Cardiac syncope

  • Heart rhythm disturbances:
    • Tachyarrhythmias:
      • Supraventricular tachycardias
      • Ventricular tachycardias
    • Bradyarrhythmias (with inadequate ventricular compensation): 
      • Sinus node dysfunction
      • Atrioventricular block
    • Other:
      • Long QT syndrome
      • Brugada syndrome
      • Pacemaker failure
  • Myocardial ischemia:
    • MI
    • Ischemic cardiomyopathy
    • Left ventricular free wall rupture
  • Structural heart disease:
    • Hypertrophic cardiomyopathy
    • Cardiac tamponade
    • Severe native valve disease:
      • Mitral valve stenosis
      • Aortic valve stenosis
      • Aortic insufficiency
    • Prosthetic valve dysfunction
    • Congenital coronary anomalies
    • Cardiac masses and tumors (e.g., atrial myxoma)

Syncope related to pathology of the great vessels

  • Pulmonary embolism (PE; saddle embolus)
  • Severe pulmonary hypertension
  • Aortic dissection

Cerebrovascular causes of syncope

  • Bilateral carotid artery disease
  • Subclavian steal syndrome
  • Global cerebral hypoperfusion
  • Epidural hematoma (“lucid interval”)
  • Subarachnoid hemorrhage
  • Transient ischemic attack

Medication-related syncope

Medication-related syncope is generally related to orthostasis or an effect on cardiovascular function.  

  • Diuretics (e.g., thiazides or loop diuretics):
    • May induce volume depletion
    • May induce electrolyte disturbances
  • Vasoactive medications (e.g., calcium channel blockers, beta blockers, alpha blockers, nitrates, etc.):
    • May induce vasodilation
    • May induce bradycardia or suppress vascular autoregulation
  • Antiarrhythmics:
    • May predispose to development of prolonged QT interval
    • Prolonged QT interval predisposes to torsade de pointes
  • Antidepressants (e.g., tricyclic drugs, selective serotonin reuptake inhibitors (SSRIs), etc.):
    • Indirect mechanism related to suppression of sympathetic neurotransmitters
    • May suppress vascular autoregulation

Toxic metabolic causes of syncope

  • Electrolyte disturbance
  • Hypoxia
  • Hypoglycemia
  • Intoxication:
    • Alcohol
    • Illicit drugs
    • Prescription medication abuse
Dynamics of neurocardiogenic syncope

Dynamics of neurocardiogenic (also known as vasovagal, reflex, or neurally mediated) syncope:
Normally, the heart and the CNS provide hemodynamic inputs to the brain stem, which then balances sympathetic and parasympathetic tone to maintain perfusion.
A failure of this mechanism, in the face of physiologic stress, results in a paradoxical withdrawal of sympathetic tone simultaneous to increased parasympathetic discharge.
Vasodilation and relative hypotension combined with bradycardia lead to poor cerebral perfusion and syncope.

Image by Lecturio.


Causes of syncope “SVNCOPE”

  • Situational
  • Vasovagal
  • Neurogenic
  • Cardiac
  • Orthostatic hypotension
  • Psychiatric
  • Everything else

Clinical Presentation

Presenting symptoms

  • Witnessed or unwitnessed loss of consciousness
    • May or may not be preceded by prodromal symptoms
    • May or may not be associated with an identifiable trigger associated with situational syncope
    • May or may not be attributed to an underlying pathologic disturbance
  • Loss of postural tone (e.g., a fall if standing, a slump if seated)
    • May or may not be accompanied by brief convulsive activity
      • May be mistaken for seizure
      • Distinguished from seizure by brevity of convulsions and absence of postictal state
    • Postural tone returns to normal after individual regains consciousness
  • Major or minor trauma associated with loss of postural tone
  • Spontaneous return of consciousness:
    • Individual may report fatigue or tiredness.
    • Generally, return to neurologic baseline level of function, unless:
      • Cause of syncope is cerebrovascular in nature.
      • Neurologic trauma is sustained during postural loss.

Prodromal symptoms

The following symptoms are associated with imminent syncope or presyncope:

  • Light-headedness
  • A feeling of being warm or cold
  • Sweating
  • Palpitations
  • Nausea or nonspecific abdominal discomfort
  • Visual blurring; can proceed to temporary darkening
  • Diminution of hearing and occurrence of unusual sounds
  • Pallor reported by onlookers

Red flags

Certain presentations suggest more serious causes of syncope:

  • Syncope during exertion
  • Syncope while supine
  • Multiple recurrences within a short period of time
  • Heart murmur or other findings suggesting structural abnormalities
  • Older age
  • Significant injury during syncope
  • Family history of: 
    • Sudden unexplained death
    • Exertional syncope
    • Unexplained recurrent syncope
    • Seizures


The etiology of approximately ½ of syncope cases remains undetermined despite an exhaustive workup. It is imperative to rule out life-threatening etiologies, such as cardiac syncope, PE, subarachnoid hemorrhage, and blood loss.


  • Number, frequency, and duration of episodes
  • Onset
  • Position
  • Trauma sustained during loss of postural tone
  • Provocative factors:
    • During or immediately after exertion/exercise (red flag)
    • During or immediately after:
      • Micturition
      • Defecation
      • Coughing
      • Swallowing
    • While in a warm and/or crowded place
    • During prolonged standing
    • During the postprandial period
    • In association with:
      • Emotional stress
      • Fear
      • Intense pain
    • Immediately following carotid sinus stimulation
    • While supine (suggestive of a serious problem)
  • Associated symptoms preceding and/or following the event:
    • Nausea
    • Vomiting
    • Feeling cold or clammy
    • Visual auras or blurry vision
    • Palpitations
    • Shortness of breath
    • Chest pain
  • Additional symptoms following the syncopal event:
    • Confusion
    • Fatigue
    • Injury
    • Bladder or bowel incontinence
    • Recurrent syncope 
  • Witnessed signs:
    • Manner in which collapse happened
    • External appearance of individual
    • Estimated duration of loss of consciousness
    • Physical movements noted
    • Any breathing changes seen
    • Associated trauma
  • Preexisting medical conditions:
    • Structural heart disease:
      • Ischemic heart disease
      • Valvular heart disease
      • Congenital heart disease
      • Cardiomyopathies
      • Prior cardiac surgery
    • Neurologic conditions:
      • Seizure disorders
      • Migraine headaches
      • Parkinson disease
      • Stroke
    • Diabetes mellitus:
      • Predisposition to cardiovascular/cerebrovascular disease
      • Prone to development of autonomic neuropathy
    • Intoxication:
      • Alcohol
      • Illicit drugs
      • Prescription narcotics (e.g., opioids, benzodiazepines, amphetamines)
  • Medications:
    • Diuretics
    • Antihypertensive agents 
    • Antiarrhythmic agents 
  • Family history:
    • Sudden death (< 40 years of age)
    • Familial cardiomyopathy
    • Seizure disorders or migraine headaches
    • Familial predisposition to syncope

Physical examination

  • Vital signs:
    • Pulse and blood pressure taken with individual supine, seated, and standing (orthostatic vital signs)
      • Drop of systolic BP > 20 mm Hg diagnostic of orthostatic hypotension
      • Drop of systolic BP > 30 mm Hg in hypertensive individuals
    • Note speed and regularity of pulse.
    • Note rate, regularity, and intensity of breathing effort.
  • Cardiac examination:
    • Note presence of heart murmur, especially if new or worsened.
    • Comparative pulse timing and blood pressure: 
      • Incongruence between upper limbs indicative of proximal aortic dissection
      • Incongruence between upper and lower limbs indicative of distal aortic dissection
    • Note presence of jugular venous distention (JVD), pulmonary rales, peripheral edema.
    • Note presence of bruits, especially if new or worsened.
  • Neurologic examination:
    • Note cognitive status, presence of disorientation, or confusion.
    • Note level of consciousness, especially if deteriorating.
    • Note presence of focal neurologic deficit(s).


ECG is indicated for all individuals presenting with syncope, regardless of suspected etiology. ECG monitoring should be continued throughout the ED or hospital stay. Notable findings may include:

  • Arrhythmias
  • ECG changes suggestive of cardiac ischemia
  • PR segment, QRS duration, QT interval prolongation (especially if new or worsened)
  • Right heart strain pattern (S1, Q3, T3) suggestive of PE
  • Conduction blocks
  • Specific signs of congenital or acquired structural heart disease


  • Used to screen for structural heart disease in known or suspected cases
  • May detect:
    • Valvular abnormalities
    • Wall-motion abnormalities
    • Left ventricular dysfunction
    • Elevated pulmonary pressures (suggestive of PE)
    • Pericardial effusion
    • Masses
    • Vegetations

Laboratory evaluation

  • CBC:
    • RBC indices for: 
      • Anemia
      • Blood loss
      • Erythrocytosis
    • WBC indices for: 
      • Evidence of infection
      • Lymphoproliferation
    • Platelet count for: 
      • Bleeding
      • Thrombotic tendencies
  • CMP to evaluate for:
    • Renal or hepatic dysfunction
    • Electrolyte disturbance
    • Acid–base imbalance
    • Hypoglycemia
  • Coagulation studies:
    • PT/PTT to evaluate for coagulopathy
    • Especially in suspected intracerebral/cerebrovascular or GI hemorrhage
  • Cardiac biomarkers:
    • Includes:
      • MB isoenzyme of creatine kinase (CKMB)
      • Cardiac troponins
      • Beta-natriuretic peptide
    • Evaluate for the presence of ischemic heart disease and/or heart failure
  • Urine toxicology screen
  • Urine hCG for women of childbearing age


  • Neuroimaging (CT, MRI of head/brain) for: 
    • Suspected intracranial mass
    • Intracranial hemorrhage
    • Cerebrovascular accident
    • Traumatic brain injury
  • CTA of the chest or ventilation/perfusion (VQ) scan for suspected PE
  • Carotid Doppler scan for suspected carotid vascular disease
  • Abdominal CT or ultrasonography to evaluate for: 
    • Splenic rupture
    • Aortic aneurysm
    • Intraabdominal and retroperitoneal bleeding
  • Abdominoplevic ultrasonography to evaluate for ectopic pregnancy or gynecologic sources of hemorrhage 
  • Lower-extremity ultrasonography to evaluate for deep vein thrombosis (DVT)
  • Specific imaging indicated for evaluation of other suspected etiologies

Other tests

  • Tilt-table test: changes in posture from lying to standing to evaluate cause of syncope
  • Electroencephalography to evaluate for possible seizure
  • Holter monitoring or loop recording for cardiac rhythm disturbances that manifest during the initial ED visit or hospital stay
  • Other specific testing indicated for evaluation of other suspected etiologies


Much of the management of syncope will be specific to the confirmed or suspected etiology. Because the specific etiology of syncope often goes undiagnosed, general measures are discussed here.

Treatment of prodromal symptoms

This includes physical countermaneuvers, such as: 

  • Leg crossing: simultaneous tensing of leg, abdominal, and buttock muscles
  • Handgrip: consists of maximum grip on a rubber ball or similar object
  • Arm tensing: involves gripping one hand with the other while simultaneously abducting both hands

Immediate treatment

  • Assist the individual to the ground, chair, or stretcher to avoid traumatic injury.
  • Lay individual supine with legs elevated to help with venous return to the heart and to eventually restore cerebral perfusion.
  • Assess vital signs (blood pressure, pulse, respiratory rate).
  • Observe other signs (pallor, diaphoresis, seizure activity).
  • Get additional assistance:
    • Call 911.
    • “Is there a doctor in the house?”
  • Attempt to arouse the individual.
  • If high-risk factors are present, admit to the most appropriate unit in the hospital (e.g., telemetry, ICU).

Risk assessment

  • Low risk for poor outcomes if no evidence of heart disease is identified
  • High-risk features associated with poor outcomes:
    • Evidence of structural or ischemic heart disease
    • History of structural or ischemic heart disease
    • Older age
    • Syncope while supine
    • Syncope during exertion
    • Palpitations at time of syncope
    • Chest pain at time of syncope
    • Dyspnea at time of syncope
    • Syncope without prodrome
    • Family history of sudden cardiac death
    • Association with thunderclap headache
    • High-risk physical examination findings:
      • Abnormal vital signs
      • Abnormal cardiac exam
      • Abnormal pulmonary exam
      • Abnormal neurologic exam
    • Abnormal ECG
    • Persistently low blood pressure
    • Low hematocrit
  • Promptly rule out life-threatening causes of syncope or syncope mimics (seizure and cerebrovascular accident are not true causes of syncope):
    • MI
    • Nonperfusing cardiac arrhythmia
    • PE
    • Cerebrovascular accident
    • Intracranial hemorrhage
    • Aortic rupture
    • Massive hemorrhage
    • Seizure

Therapies to prevent syncope recurrence

Reflex syncope: carotid sinus syncope:

  • Reassurance and education about nature, risks, and prognosis
  • Avoid mechanical manipulation of the carotid sinuses (e.g., abrupt turning of the neck, wearing tight collars).
  • Vasodilators should be avoided or reduced where possible.
  • Medication:
    • Midodrine
    • Beta blockers
    • Paroxetine
    • Disopyramide 
  • Pacemakers (those with cardioinhibitory responses)

Orthostatic hypotension: 

  • Medication-induced:
    • Discontinue offending medication.
    • Substitute with an alternative agent.
    • Adjust dose.
    • Change timing of drug administration.
  • Volume depletion: 
    • Volume resuscitation
    • Discontinue/adjust dose of diuretics.
    • Counsel about hydration and salt intake.
    • Treat underlying cause (e.g., gastroenteritis, hemorrhage).

Causes of syncope that warrant immediate admission/intervention

Cardiac emergencies:

  • Arrhythmias:
    • Documented, suspected, or induced ventricular tachycardia:
      • Advanced cardiac life support (ACLS) protocol if indicated
      • Antiarrhythmics
      • Catheter ablation
      • Implantable cardioverter–defibrillator
    • Supraventricular arrhythmias: 
      • ACLS protocol if indicated
      • Antiarrhythmics
      • Catheter ablation
    • Bradyarrhythmias: permanent pacemakers
  • Ischemic heart disease (IHD) or acute coronary syndrome (ACS):
    • Activate ACS protocol if indicated.
    • Coronary intervention or cardiac surgery if indicated 
  • Obstruction to left ventricular outflow caused by aortic stenosis: 
    • Balloon valvuloplasty
    • Aortic valve replacement

Cerebrovascular emergencies:

  • Immediate noncontrast CT of head if cerebrovascular accident (hemorrhagic or ischemic) or intracranial hemorrhage is suspected
  • Appropriate admission/transfer/consultation depending on findings:
    • Neurology
    • Neurosurgery
    • Interventional vascular team:
      • Interventional radiology
      • Interventional vascular surgery/neurosurgery
    • Neurologic ICU monitoring

Hemorrhagic emergencies:

  • Hemodynamic stabilization:
    • Volume resuscitation
    • Administration of appropriate blood products
  • Stop/reverse anticoagulation
  • Appropriate surgical consultation if indicated:
    • Gastroenterology
    • Interventional vascular team
    • Obstetrics/gynecology

Differential Diagnosis

  • Seizure: abnormal electrical activity of the neurons in the cerebral cortex that can manifest in numerous ways depending on the region of the brain affected. There are numerous etiologies, and investigation of the root cause should be part of the initial evaluation. Diagnosis is made by a clinical evaluation, lab testing, neuroimaging, electroencephalography, and antiseizure drug levels. Treatment is by elimination of the cause, if possible, antiseizure drugs, and surgery when drugs are ineffective. 
  • Traumatic brain injury: physical injury to brain tissue that temporarily or permanently impairs brain function. Traumatic brain injury can be caused by falls, motor vehicle accidents, assaults, and sports activities. Individuals may present with loss of consciousness, confusion, amnesia, seizures, and focal neurologic deficits. Diagnosis is by initial rapid trauma assessment, neurologic examination, and CT scan. Initial treatment is optimizing brain perfusion and supportive care. Severe injuries may require timely surgical intervention.  
  • Intoxication: reversible syndrome associated with substance use, which may cause physical and mental changes (varies depending on the substance that was ingested). Intoxication may lead to accidental death via overdose, and various substances may carry significant complications that increase morbidity and mortality. Management is usually supportive, although some substances have reversible pharmacologic agents. 
  • Conversion disorders: also called functional neurologic symptom disorder. Conversion disorders are psychiatric disorders with prominent motor or sensory impairment that is not compatible with any known neurologic medical condition. The deficits are not consciously produced. Individuals are typically impaired in their social and professional life, but can also be inappropriately unconcerned with their symptoms. Treatment centers around education and psychotherapy.


  1. McDermott, D. (2020). Approach to the adult patient with syncope in the emergency department. Retrieved September 25, 2021, from
  2. Chen-Scarabelli, C., Scarabelli, T. M. (2004). Neurocardiogenic syncope. BMJ 329:336–341.
  3. Kharsa A, Wadhwa R. Carotid sinus hypersensitivity. StatPearls. Retrieved September 25, 2021, from
  4. Benditt D. (2021). Syncope in adults: epidemiology, pathogenesis, and etiologies. UpToDate. Retrieved September 1, 2021, from
  5. Benditt D. (2021). Syncope in adults: clinical manifestations and initial diagnostic evaluation. UpToDate. Retrieved September 1, 2021, from
  6. Benditt D. (2019). Syncope in adults: management. UpToDate. Retrieved September 2, 2021, from
  7. Thompson A.D., Shea M.J. (2020). Syncope.  MSD Manual Professional Version. Retrieved September 2, 2021, from
  8. Kenaan M., Eagle K. (2018). Syncope. Oxford Medicine Online. Retrieved September 2, 2021, from
  9. Morag R. (2017). Syncope. Medscape. Retrieved September 2, 2021, from

Study on the Go

Lecturio Medical complements your studies with evidence-based learning strategies, video lectures, quiz questions, and more – all combined in one easy-to-use resource.

Learn even more with Lecturio:

Complement your med school studies with Lecturio’s all-in-one study companion, delivered with evidence-based learning strategies.

🍪 Lecturio is using cookies to improve your user experience. By continuing use of our service you agree upon our Data Privacy Statement.