What causes fainting
Syncope is defined as transient loss of consciousness (TLOC) due to transient global cerebral hypoperfusion, with rapid onset, short duration and spontaneous complete recovery. It is distinct from other causes of TLOC including epileptic seizures and psychogenic pseudosyncope. Vasovagal syncope (neurally mediated syncope) is the most common cause, typically triggered by prolonged standing, emotion, pain or blood sampling, with prodromal symptoms (lightheadedness, nausea, sweating, visual dimming) followed by bradycardia and hypotension. Orthostatic syncope occurs on standing and is associated with dehydration, medication effects (antihypertensives, diuretics), autonomic failure or prolonged bed rest.
Cardiac syncope is the most dangerous cause and requires urgent evaluation. Mechanisms include cardiac arrhythmias (bradyarrhythmias, tachyarrhythmias), structural cardiac disease (aortic stenosis, hypertrophic cardiomyopathy, acute myocardial infarction) and pulmonary embolism. Cardiac syncope often occurs without warning or with minimal prodrome, during exertion or while supine, and may be associated with palpitations or chest pain. Neurological causes of syncope are less common than often assumed — most seizures with convulsive movements are mistaken for syncope and vice versa. True neurological syncope may result from subclavian steal, vertebrobasilar insufficiency or certain autonomic disorders. Accurate history from the patient and a witness is the single most important diagnostic tool.
- Vasovagal syncope — most common, triggered by standing, emotion, pain
- Orthostatic syncope — on standing, dehydration, medications, autonomic failure
- Cardiac syncope — arrhythmias, structural disease, most dangerous cause
- Neurological syncope — subclavian steal, vertebrobasilar insufficiency, autonomic disorders
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Evaluation approach (ECG, tilt table, neurological exam)
Evaluation of syncope follows a structured pathway beginning with clinical history (patient plus witness), physical examination including orthostatic blood pressure measurement, and a 12-lead electrocardiogram (ECG). The ECG screens for arrhythmias (bradycardia, heart block, ventricular tachycardia), conduction abnormalities (bundle branch block, prolonged QT) and structural markers (Q waves suggesting prior infarction). Blood tests may include full blood count (anaemia), glucose (hypoglycaemia) and renal function (electrolyte disturbance). Echocardiography is considered when structural cardiac disease is suspected.
Tilt-table testing is used when vasovagal or orthostatic syncope is suspected but the diagnosis is uncertain. The patient is tilted to 60–70 degrees while blood pressure and heart rate are monitored continuously; a positive test reproduces the syncope with documented hypotension and/or bradycardia. Carotid sinus massage (in patients over 40 in a monitored setting) assesses carotid sinus hypersensitivity. Electrophysiological studies (EPS) may be considered for patients with suspected cardiac arrhythmia when non-invasive evaluation is inconclusive. Neurological examination screens for focal deficits, signs of autonomic failure and carotid bruits. Electroencephalography (EEG) is not routine for syncope but is considered when seizure is suspected. The combined evaluation distinguishes cardiac, vasovagal, orthostatic and neurological causes, guiding appropriate treatment and risk stratification.
- 12-lead ECG — arrhythmias, conduction abnormalities, structural markers
- Orthostatic blood pressure — standing and lying measurements
- Tilt-table testing — vasovagal and orthostatic syncope confirmation
- Echocardiography — structural cardiac disease assessment
- Carotid sinus massage — carotid hypersensitivity in patients over 40
- EPS for suspected arrhythmia when non-invasive tests inconclusive