How arrhythmias are tested on Step 1
Expect an ECG description (sawtooth flutter waves, irregularly irregular rhythm, delta wave, twisting QRS) and questions on mechanism, emergency treatment, or a drug's ion-channel target and toxicity.
Any tachycardia with hypotension, altered mental status, ischemic chest pain, or acute heart failure needs synchronized cardioversion. Pulseless VT and VF need defibrillation. Drug choices apply to stable patients.
Mechanisms
Reentry needs two pathways with different conduction and refractory properties plus a unidirectional block.
Recognizing the major rhythms
Classify first by QRS width and regularity.
| Rhythm | ECG | Key point |
|---|---|---|
| Atrial fibrillation | Irregularly irregular, no P waves | Stroke risk; rate or rhythm control |
| Atrial flutter | Sawtooth flutter waves, often 2:1 (rate ~150) | Macro-reentry around the tricuspid annulus; ablation curative |
| AVNRT | Regular narrow, ~150–250, P waves hidden | Vagal maneuvers, adenosine |
| WPW (AVRT) | Short PR, delta wave, wide QRS at baseline | Procainamide if AF with WPW; ablation |
| Ventricular tachycardia | Wide regular complexes | Often after MI; amiodarone or cardioversion |
| Torsades de pointes | Polymorphic VT twisting around baseline; long QT | IV magnesium; correct K⁺; stop QT drugs |
| Ventricular fibrillation | Chaotic, no QRS | Defibrillate; most common cause of sudden cardiac death |
Multifocal atrial tachycardia (≥ 3 P-wave shapes, irregular) is associated with COPD.
| AV block | ECG | Level | Management |
|---|---|---|---|
| First-degree | PR > 200 ms, every P conducts | AV node | Usually none |
| Mobitz I (Wenckebach) | PR lengthens until a beat drops | AV node | Often benign; inferior MI, drugs |
| Mobitz II | Constant PR, sudden dropped QRS | His–Purkinje | Pacemaker (can progress to complete block) |
| Third-degree | P waves and QRS independent | Any | Pacemaker; Lyme carditis can be reversible |
Atropine helps nodal blocks but not infranodal (Mobitz II, many third-degree) blocks.
Antiarrhythmic drugs
The Vaughan Williams classes map onto the phases of the cardiac action potential.
| Class | Mechanism | Examples | Key toxicity |
|---|---|---|---|
| IA | Moderate Na⁺ block; ↑ AP duration | Quinidine, procainamide | QT prolongation; drug-induced lupus (procainamide); cinchonism (quinidine) |
| IB | Weak Na⁺ block; ↓ AP duration; ischemic tissue | Lidocaine, mexiletine | CNS effects (seizures) |
| IC | Strong Na⁺ block | Flecainide, propafenone | Proarrhythmic after MI or in structural disease |
| II | β blockade; ↓ phase 4 slope in nodes | Metoprolol, esmolol | Bradycardia, AV block |
| III | K⁺ block; ↑ AP duration and QT | Amiodarone, sotalol, dofetilide | Torsades; amiodarone: lung fibrosis, thyroid, liver, corneal deposits |
| IV | Ca²⁺ channel block in nodes | Verapamil, diltiazem | Bradycardia, constipation, heart failure |
| Other | Adenosine (↑ K⁺ out, AV block); digoxin (vagal); magnesium | — | Adenosine: flushing, chest pain, sense of doom |
Amiodarone has class I–IV actions; check thyroid, liver, and pulmonary function at baseline and during therapy.
Clinical application
WPW is a classic trap.
A 24-year-old with a known delta wave on prior ECGs presents with an irregular wide-complex tachycardia at 240/min. Blood pressure is stable. Why should verapamil be avoided, and what is appropriate?
- Irregular wide complexes in a patient with WPW suggest atrial fibrillation conducting down the accessory pathway.
- Blocking the AV node with verapamil, diltiazem, digoxin, or adenosine removes the competing route, sending even more impulses down the accessory pathway.
- This can accelerate the ventricular rate into ventricular fibrillation.
Answer. Use procainamide (or synchronized cardioversion if unstable); avoid AV nodal blockers. Definitive treatment is catheter ablation of the accessory pathway.