Most episodes result from brief global cerebral hypoperfusion. Syncope is commonly categorized as vasovagal (neurocardiogenic), orthostatic, cardiac arrhythmia or structural heart disease–related, and, less commonly, neurologic or other causes. Distinguishing syncope from seizures, intoxication, or metabolic disturbances is essential.
Clinical features include a prodrome of lightheadedness, nausea, diaphoresis, and pallor, often followed by loss of consciousness and rapid recovery. Exertional syncope or syncope with palpitations or chest pain is more suggestive of a cardiac cause. Post-event confusion is not typical; seizures may have prolonged postictal states and tongue biting.
Evaluation begins with history and targeted examination. Red flags include exertional syncope, syncope with chest pain or dyspnea, trauma, family history of sudden death, known heart disease, or abnormal ECG. Essential tests are resting ECG, orthostatic blood pressure measurements, and basic labs. Further assessment may include echocardiography if a heart condition is suspected, ambulatory rhythm monitoring, event recording or tilt-table testing for suspected vasovagal syncope. Neuroimaging is reserved for focal neurological signs.
Management focuses on preventing injury and treating underlying causes. Immediate measures during a syncopal episode include lying flat and elevating the legs; avoid standing quickly. For vasovagal or orthostatic syncope, counseling on hydration, salt intake (if appropriate), physical counterpressure maneuvers, and, in select cases, compression stockings are used. Medications are rarely first-line; options such as fludrocortisone or midodrine may be considered for orthostatic intolerance. Cardiac syncope requires rapid cardiology assessment; treatment may involve pharmacologic therapy, pacemaker or implantable cardioverter-defibrillator, or catheter ablation.