Syncope – ECG-Based Causes (Cardiogenic Focus)

Syncope – ECG-Based Causes (Cardiogenic Focus)

General Principles

• Most syncopal patients do not need extensive labs or imaging unless history/PE suggests (e.g., GI bleed → CBC, vomiting/diarrhea → electrolytes, trauma → head CT).

• The one test everyone should get: 12-lead ECG.

• What to look for:

  • Ischemia/MI

  • Arrhythmias/AV block

  • “Killers” that are often missed on ECG

1. Hypertrophic Cardiomyopathy (HCM)

ECG Clues

• High QRS voltage

• Deep, narrow (“dagger-like”) Q waves

  • Most common in lateral leads (I, aVL, V5–V6)

  • Sometimes inferior leads

• Q waves are narrow (≠ infarction Q waves which are wide and ≥⅓ QRS amplitude).

• T wave abnormalities possible due to repolarization changes.

Next Steps

• Order Doppler echocardiogram to confirm.

• While awaiting cardio consult: no exertion, consider beta-blockers.

• Urgent referral to cardiology.

2. Brugada Syndrome

ECG Clues (usually V1–V2)

• Incomplete RBBB pattern + ST elevation

• Morphologies:

  • Coved (convex or straight ST ↑ with inverted T) → most specific, highest risk

  • Saddleback → less specific, but still concerning in syncope context

• Normal RBBB usually shows ST depression in V1–V2, not elevation.

Clinical Features

• Sodium channelopathy → polymorphic VT/VF → sudden death.

• Often occurs at rest, during sleep, or post-prandial (↑ vagal tone).

• Can mimic ST-elevation MI → history matters (syncope vs chest pain).

Next Steps

• Consult electrophysiology (EP), not general cardiology.

• Confirm with sodium-channel blocker challenge (e.g., ajmaline).

• Treatment: AICD placement.

• Echo, stress test, MRI usually normal (structural disease absent).

3. Wolff–Parkinson–White (WPW) Syndrome

Classic Triad

• Short PR interval (<120 ms)

• Delta wave (slurred QRS upstroke)

• Wide QRS (slightly widened due to pre-excitation)

Tips

• Delta waves may appear in only a few leads. Always check intervals.

• Clue: if PR short, scan all 12 leads for delta.

Risk

• Accessory pathway allows rapid conduction of atrial fibrillation → very high ventricular rates (250–300+ bpm).

• ECG:

  • Irregularly irregular

  • Some narrow, some wide complexes (fusion beats)

  • Morphology changes beat to beat

  • Much faster than typical AF (which rarely >180 bpm without accessory pathway).

Danger

• Giving AV nodal blockers (adenosine, diltiazem, verapamil, beta-blockers, digoxin, amiodarone) → blocks AV node → all conduction forced down accessory pathway → ventricular fibrillation.

Management

• Avoid AV nodal blockers.

• If unstable → synchronized cardioversion.

• If stable → procainamide or electrical cardioversion.

• Refer for EP ablation.

4. Prolonged QT Syndrome

ECG Clues

• QTc >500 ms = ↑ risk of torsades de pointes.

• Especially visible in precordial leads (e.g., V2).

Causes

• Congenital channelopathies

• Electrolyte abnormalities (↓K, ↓Mg, ↓Ca)

• Medications (QT-prolonging drugs: antiarrhythmics, macrolides, fluoroquinolones, antipsychotics, etc.)

Risk

• Syncope often mistaken for seizure (myoclonic jerks during hypoperfusion).

• Can deteriorate into torsades → VF → sudden death.

Management

• Identify/remove offending drug or electrolyte imbalance.

• IV magnesium if torsades.

• Beta-blockers or AICD depending on congenital/acquired cause.

Summary: ECG Red Flags in Syncope

Always check for:

1. Ischemia/MI

2. Arrhythmias/AV block

3. Hypertrophic Cardiomyopathy – High voltage + deep narrow Q waves (esp. lateral leads)

4. Brugada Syndrome – RBBB-like pattern + ST elevation in V1–V2

5. WPW – Short PR + delta wave; AF with changing morphologies and extreme rates

6. Prolonged QT – QTc >500 ms, risk of torsades.