• Clinical science



Syncope is a sudden, completely reversible loss of consciousness secondary to an acute reduction of cerebral perfusion, which may last from several seconds up to minutes. The most frequent form is vasovagal syncope, which is triggered by emotional stress or prolonged standing, and may be diagnosed with the tilt table test. Orthostatic syncope may occur upon suddenly standing up after prolonged sitting or lying down. It is caused by a drop in blood pressure. This relatively benign cause may, however, lead to life-threatening injuries as a result of falls. A thorough medical investigation is necessary as syncopes may also be the result of a serious cardiovascular disorder (e.g., cardiac arrhythmia or valvular stenosis). The treatment strategy is dependent on the cause of the syncopes.


  • TLOC (transient loss of consciousness): temporary syncope of unknown origin
Overview of possible causes of syncopes
Pathophysiology Subtype Etiology Examples
Cardiac syncope
  • Heart's inability to meet an increased oxygen demand (e.g., during exertion)
  • reduced cerebral perfusion
Arrhythmogenic syncope Bradycardia/tachycardiaejection fraction
Cardiovascular syncope Structural outflow obstruction

Reflex syncope (Most common cause)

  • Neurally mediated syncope that can be due to 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
Neurocardiogenic syncope (subtype of vasovagal syncope) Prolonged standing (and no compensatory heart rate acceleration)
  • Common in younger patients (unusual to have first episode after age 40)
  • Can be recurrent
Emotional syncope (subtype of vasovagal syncope) Pain or emotional stress
  • Pain
  • Fear
  • Sight of blood
  • Injury
Carotid sinus syndrome Increased carotid sinus sensitivity (frequently associated with arteriosclerotic changes in the carotid sinus) → systolic blood pressure when pressure is applied to the carotid sinus
Other situational syncopes Vagotonic, peripheral vascular dilation
  • Cough
  • Swallow
  • Micturition syncopes (commonly seen in males with prostatic hyperplasia)
Orthostatic syncope (postural hypotension)
  • Standing up/postural change
  • insufficient counterregulation due to autonomic dysfunction (e.g. decreased baroreceptor sensitivity in the elderly)
  • reduced cerebral perfusion
Sympathotonic orthostatic hypotension When standing up: systolic blood pressure despite excessive sympathotonic counter regulation (significant heart rate increase) → reduced cerebral perfusion
Asympathotonic orthostatic hypotension When standing up: systolic blood pressure without sympathotonic counterregulation (steady or even reduced heart rate) → reduced cerebral perfusion
Postural tachycardia syndrome (PoTS, orthostatic intolerance) When standing up: no significant drop in blood pressure, but massive heart rate increase within 10 minutes of standing up


Clinical features

  • Prodrome: presyncope
    • Vasovagal: impairment of senses; , nausea, pallor, warmth, diaphoresis, lightheadedness, and hyperventilation
    • Orthostatic: lightheadedness, nausea, and dizziness
    • Cardiac: no prodrome; often sudden fall
  • 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

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!


  • Patient history: Determine triggers; , ask witnesses how patient behaved during event, and medication/medical/family history.
  • Routine investigations
    • ECG (for all patients!)
    • CBC (↓ serum Hb)
  • Additional tests
    • Cardiac origin suspected (see also cardiac arrhythmia)
      • Cardiac monitoring (If ECG is not diagnostic and a cardiac cause is strongly suspected): sinus bradycardia < 40/min, sinus pauses > 3 seconds, atrioventricular (AV) or bundle branch blocks
      • Stress ECG (ischemia)
      • Echocardiography: if structural heart disease is suspected or ECG is abnormal
      • Cardiac enzymes
      • Carotid ultrasound with doppler
    • Pulmonary origin suspected : chest x-ray (suspected pneumonia, lung mass) and ventilation/perfusion scanning (suspected pulmonary embolus)
    • Neurological origin suspected : head imaging (CT, MRI, or MRA showing ischemia or hemorrhage) and EEG (seizure)
    • Other laboratory tests: : abnormal electrolytes, abnormal urinalysis BUN/creatinine ratio (assess for signs of hypovolemia in orthostatic hypotension), stool occult blood test
    • Maneuvers
      • Testing for orthostatic hypotension or vasodepressor syncope
        • Patient is asked to stand after being in supine position for at least 5 minutes → Blood pressure is measured each minute for at least 3 minutes.
        • If systolic BP decreases by ≥ 20 mm Hg and the diastolic BP decreases by ≥ 10 mm Hg, or the heart rate increases by 20 bpm, or BP < 90 mm Hgorthostatic hypotension
        • Coinciding bradycardiavasodepressor syncope
      • Tilt table test
        • Determines if vasovagal or orthostatic syncope is present
        • Procedure
          • The patient is strapped onto a tilt table in a supine position for 15 minutes, and then is raised passively to an angle of around 70°.
          • Positive: reflex hypotension (systolic blood pressure < 90 mm Hg) and bradycardia (vasovagal) or slow progressive hypotension (orthostatic) with presyncope or syncope
          • Negative (normal): increased heart rate along with barely changed blood pressure and no clinical signs of syncope or presyncope

It is important to rule out life-threatening causes of syncope such as pulmonary embolism, hemorrhage, or serious cardiac conditions!

Differential diagnoses

Non-syncopal events Medical history and clinical features Diagnosis
  • Epileptic symptoms (e.g., aura, postictal state, lateral tongue biting, bladder/bowel incontinence)
  • Abnormal EEG
  • Brain lesions visible in imaging (CT, MRI)
Subclavian steal syndrome
  • Occurs when straining the ipsilateral arm
  • Rare: complete loss of consciousness
  • Focal-neurological signs during an attack (e.g., double images, dysarthria)
Vertebrobasilar insufficiency
  • Drop attacks can be seen with a TIA in the vertebrobasilar circulation.
  • Other neurologic deficits will be seen as well.
  • CT/MRI
  • Diabetes
  • Clinical symptoms: symptoms of autonomic counterregulation (e.g., restlessness, sweating, pale skin)
  • ↓ Blood glucose
Craniocerebral injury
  • Pathology on imaging (CT, MRI)
  • The body is unable to regulate the core body after it becomes elevated.
  • Syncope can precede exertional heatstroke.
  • Can occur when stressed
  • Often occurs in patients with panic disorders
Cryptogenic drop attacks
  • The cause of many falls, especially in older patients, remains elusive despite extensive diagnostic testing. These falls/attacks are called cryptogenic drop attacks.


The differential diagnoses listed here are not exhaustive.


  • Treat underlying condition
  • Vasovagal syncopes
    • Physiological counterstrategies: Crossing the legs, tensing muscles, lying down, and elevating the legs can reverse the syncope.
    • Avoid triggers
  • Orthostatic syncopes
    • Sufficient intake of sodium and fluids
    • Compression stockings
    • Adjust medications (e.g., diuretics)
    • Fludrocortisone if unable to manage episodes with nonpharmacological interventions




We list the most important complications. The selection is not exhaustive.