Syncope is a common clinical problem. Primary goal of evaluation is to determine whether the patient is at increased risk of SCD.
Sudden, self-limited loss of consciousness and postural tone caused by transient global cerebral hypoperfusion, followed by spontaneous, complete, and prompt recovery.
Four major categories based on etiology1
- Neurocardiogenic (most common): vasovagal, carotid sinus hypersensitivity, and situational.
- Orthostatic hypotension: hypovolemia, medication-induced (iatrogenic), and autonomic dysfunction.
- Arrhythmogenic: sinus node dysfunction, AV block, pacemaker malfunction, VT/VF, SVT (rare).
- Mechanical: HCM, valvular stenosis, aortic dissection, myxomas, pulmonary embolism, pulmonary HTN, acute MI, subclavian steal, etc.
- Miscellaneous (not true syncope): seizures, stroke/TIA, hypoglycemia, hypoxia, psychogenic, etc.
- Atherosclerotic cerebral artery disease is a rare cause of true syncope; the exception is severe obstructive four-vessel cerebrovascular disease (expect focal neurologic findings prior to syncope).
- Two components of neurocardiogenic syncope are described as cardioinhibitory, in which bradycardia or asystole results from increased vagal outflow to the heart, and vasodepression, where peripheral vasodilation results from sympathetic withdrawal to peripheral arteries. Most patients have a combination of both components as mechanism.
- Specific stimuli (e.g., micturition, defecation, coughing, swallowing) may evoke a neurocardiogenic mechanism, leading to situational syncope.
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