Table 1.3-2. Syncope: causes and management suggestions

Etiology

Causes

Triggers

Diagnosis

Management

VVS

– Inappropriate reflex response leading to vasodilation or bradycardia

– Most common type of syncope in all ages (46% of all events)

– Usually benign and not requiring specific treatment; ensure adequate salt intake and hydration

– Sudden, unexpected, or unpleasant stimulus (sight, sound, smell, pain)

– Following long periods of standing in crowded hot places

– After meals; concomitant nausea or vomiting

– Typical history

– Calgary Syncope Symptom Score (see table 1.3-4)

– Tilt table testing can be considered in case of diagnostic uncertainty

– Trigger avoidance

– Advice on episodic management (sitting down, isometric exercises)

– Orthostatic training (unproven benefit)

– Dual-chamber pacemaker indicated in selected patients with episodes of prolonged asystole

Carotid sinus syndrome

– Hypersensitivity of afferent or efferent limbs of carotid sinus leading to bradycardia and/or vasodilation

– Rarely in adults aged <50 years

Syncope after head turning (eg, changing traffic lanes)

– Carotid sinus massage

– Asystole >3 s or fall in SBP >50 mm Hg

– Dual-chamber pacemaker

– Pharmacotherapy only in exceptional cases with specialist consultation (unproven benefit)

Orthostatic hypotension

Occurs when autonomic sympathetic vasomotor system fails to respond to challenges imposed by upright position, causing hypotension

– Primary causes: Parkinson disease, MSA, pure autonomic failure

– Secondary causes (more common): volume depletion due to alcohol or drugs (diuretics, beta and alpha blockade, vasodilators)

– Sustained drop in BP (≥20 mm Hg drop in SBP, or SBP <90 mm Hg) within 3 min of standing

– Consistent medical history

– Discontinue offending drugs

– Avoid circumstances that may trigger syncope

– Increase intravascular volume with fluids or drugs: fludrocortisone 0.1-0.4 mg/d PO or midodrine 5-40 mg/d PO

Cardiac syncope

Can be structural or arrhythmogenic, leading to decreased cardiac output and drop in cerebral perfusion

– Significant organic heart disease; syncope during physical exercise or in supine position, syncope preceded by palpitations, family history of SCD

– Patients at high risk for VTE

– ECG or telemetry changes of conduction delay, QT prolongation, IHD, hypertrophy

– Echocardiography

– Referral to cardiologist for management of underlying cardiac disease

– Interrogate pacemaker if in situ

Cerebrovascular syncope

Decreased cerebrovascular blood flow, can occur with:

– Subclavian steal syndrome

– TIA affecting vertebral and posterior arteries

– Migraine variant

– Subclavian steal syndrome: stenosis of subclavian artery proximal to vertebral artery causing reversal of flow during strenuous upper limb exercise

– Ischemic risk factors (hypertension, dyslipidemia, prior CVA, smoker, DM)

– Migraine triggers

– Subclavian and/or carotid artery bruit, BP differential

– Carotid US

– Vertebral and subclavian angiography

– MRA/MRI

Referral to specialists for management of underlying disease depending on etiology (eg, neurologist for migraines, TIA; vascular surgeon for subclavian steal)

BP, blood pressure; CVA, cerebrovascular accident; DM, diabetes mellitus; ECG, electrocardiography; IHD, ischemic heart disease; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; MSA, multiple system atrophy; PO, oral; SBP, systolic blood pressure; SCD, sudden cardiac death; TIA, transient ischemic attack; US, ultrasonography; VTE, venous thromboembolism; VVS, vasovagal syncope.