Arrhythmias and Electrophysiology
This domain tests rhythm recognition under time pressure, acute management algorithms, anticoagulation decisions in atrial fibrillation, and the inherited channelopathies that cause sudden death in structurally normal hearts.
Acute tachycardia
- Unstable tachycardia with a pulse: synchronised cardioversion.
- Regular narrow-complex: vagal manoeuvres, then adenosine 6 mg, then 12 mg.
- Irregular narrow-complex: atrial fibrillation until proven otherwise; control rate with a beta-blocker or diltiazem.
- Stable wide-complex: procainamide or amiodarone; avoid verapamil if the rhythm could be ventricular.
Atrial fibrillation
- Anticoagulate by CHA2DS2-VASc: score 2 or more in men and 3 or more in women is a clear indication; DOACs are preferred over warfarin except with mechanical valves or moderate-severe mitral stenosis.
- Rate control targets resting heart rate below 110 beats per minute with a lenient strategy.
- Catheter ablation is first-line for symptomatic paroxysmal AF in selected patients, especially with heart failure.
Key syndromes
- WPW with pre-excited AF: avoid AV nodal blockers; use procainamide or ibutilide and cardioversion if unstable.
- Torsades de pointes: intravenous magnesium, correct potassium, stop QT-prolonging drugs, pace or use isoproterenol.
- Brugada type 1: coved ST elevation 2 mm or more in V1-V2 with T inversion.
- Long QT: avoid QT-prolonging drugs, beta-blockade, consider ICD in high-risk patients.
Pacing indications
- Complete heart block, Mobitz II, symptomatic sinus node dysfunction, and alternating bundle branch block are Class I indications.
Worked example
A 68-year-old with palpitations has an irregular tachycardia at 140, CHA2DS2-VASc of 4, and no structural disease. He is electrically cardioverted if unstable; otherwise rate control with metoprolol, start apixaban, and refer for ablation if symptomatic.
Traps
- Adenosine is contraindicated in pre-excited AF and severe asthma.
- Amiodarone prolongs the QT and interacts with warfarin and digoxin.
- Digoxin toxicity is potentiated by hypokalaemia and renal impairment.