Diagnostic Approach to Syncope

Classification and Diagnosis

The European Society of Cardiology recommends classifying syncope into three main categories: reflex (neuromediated), orthostatic hypotension, and cardiac, while excluding non-syncopal conditions that mimic loss of consciousness 1.
The American Heart Association suggests that epilepsy should be considered in the differential diagnosis of syncope, characterized by prolonged tonic-clonic movements, prolonged post-ictal confusion, and lateral tongue biting 2, 1.
The European Heart Journal notes that metabolic disorders, such as hypoglycemia, hypoxia, and hyperventilation with hypocapnia, can cause loss of consciousness and should be excluded in the diagnostic workup of syncope 2, 1.

The European Heart Journal states that vasovagal syncope is the most common form of reflex syncope, often triggered by emotional stress, medical instrumentation, or prolonged orthostatic stress 2, 1.
Typical prodromes of vasovagal syncope include nausea, sweating, pallor, blurred vision, and a sensation of heat 1, 4.

The European Heart Journal defines orthostatic hypotension as a decrease in systolic blood pressure of ≥20 mmHg or a decrease to <90 mmHg within 3 minutes of standing 3, 6.
The American Autonomic Society notes that primary autonomic failure, including pure autonomic failure and multiple system atrophy, can cause orthostatic hypotension 2, 1.

The European Heart Journal states that cardiac syncope can be caused by arrhythmias, including bradyarrhythmias and tachyarrhythmias 2, 1.
The American College of Cardiology recommends considering structural heart disease or cardiopulmonary disease as a cause of syncope, including obstructive valvular disease, acute myocardial infarction, and cardiomyopathy 2, 1, 4.

The European Heart Journal warns that syncope during exercise should always raise suspicion of a cardiac cause, even if a reflex vasodilation is possible 7.
The American Heart Association notes that post-exercise syncope is almost always due to autonomic failure or a neuromediated mechanism, typically in subjects without heart disease 7.