Canonical Question
Antiarrhythmic
Master answer
| CLASS | ACTION | ELECTRO- PHYSIOLOGY | DRUGS | THERAPEUTIC INDICATIONS |
|---|---|---|---|---|
| I. Na – Channel Blockers | ||||
| Ia | Intermediate dissociation | ↓ phase 0 ↓↓ conduction v ↑ repolarisation ↑ APD | Quinidine Disopyramide Procainamide | Atrial and ventricular arrhythmias esp. post MI |
| Ib | Fast dissociation | ↔,↓ phase 0 ↓ conduction v ↓ repolarisation ↓ APD | lignocaine phenytoin tocainide, mexilitine | Ventricular arrhythmias post MI, digoxin induced arrhythmias |
| Ic | Slow dissociation | ↓↓↓↓ phase 0 ↓↓↓↓ conduction v ± repolarisation ↔ APD | flecainide ecainide, lorcainide | Refractory arrhythmias |
| II. β – Blockers | ||||
| ↓ SA firing – ↓ rate, conduction | propranalol* atenolol, esmolol | Rate control in AF, AT, Flutter and VT | ||
| III. K – Channel Blockers | ||||
| Delay phase 3 (repol) ↑ APD ↑ ERP | amiodarone bretylium, sotalol^ | AF / Flutter termination | ||
| IV. Ca – Channel Blockers | ||||
| ↓ AV conduction ↑ PR interval ↓ rate/conduction | verapamil diltiazem | SVT and AF or Flutter | ||
| OTHERS (Some call this Class V) | ||||
| Blocks Na+/K+ ATPase → ↑Ca2+, ↓K+, ↑Ach | ↑ contractility ↓ AV conduction | Digoxin | AF rate control Heart Failure | |
| Opens K+ channels via adenosine receptors | Hyperpolarizes myocardium ↓ AV conduction ↓ SA firing | Adenosine# Ibutilide | Terminate SVT or reveal underlying rhythm in tachycardias | |
| Stimulates Na+/K+ATPase | Membrane stabilization | Magnesium | VF / Torsades de pointes | |
| Notes | * Propranalol also has Na blocking activity ^ l-sotalol has beta blocking and class III activities; d-sotalol is a pure class III agent. Commercially available sotalol is a racemic (equal part) mixture. # Amiodarone – blocks Na, Ca, K channels, and exhibits beta blockade. | |||
The effect on the myocardial action potential of each class is:

| Class Ia | Class Ib | Class Ic | Class II | Class III | Class IV | |
|---|---|---|---|---|---|---|
| Depolarisation rate (phase 0) | ↓ | ↔ or ↓ | ↓↓↓↓ | ↔ | ↔ | ↓↓↑↔± ↔ |
| Conduction velocity | ↓↓ | ↓ | ↓↓↓↓ | ↓ | ↓ | ↔ |
| Effective Refractory Period | ↑↑↑↑ | ↓ | ↑ | ↓ | ↑↑↑↑ | ↔ |
| Action potential duration | ↑ | ↓ | ↔ or ↑ | ↑ | ↑↑↑↑ | ↓ |
| Automaticity | ↓ | ↓ | ↓ | ↓ | ↓ | ↔ |
| P-R duration | ↔ | ↔ | ↑ | ↔ or ↑ | ↑ | ↔ or ↑ |
| QRS duration | ↑ | ↔ | ↑↑↑↑ | ↔ | ↑ | ↔ |
| QTc duration | ↑ | ↔ or ↓ | ↑ | ↓ | ↑↑↑↑ | ↔ |
Sotalol Effects
- l-sotalol has beta blocking and class III activities
- d-sotalol is a pure class III agent
- Commercially available sotalol is a racemic (equal part) mixture.
- Class III Effects (K – channel blocking)
- Blocking of outward K+ channels slows cardiac repolarisation, which increases the cardiac refractory period.
- Delay phase 3 (repol), ↓ AV conduction,
- ↑↑↑↑ APD, ↑↑↑↑ ERP
- ↑↑↑↑ QTc
- ↓ automaticity
- ↓ ectopy
- ↓ defibrillation energy requirement
- May ↑ inotropy
- Class II Effects (β – Blocker)
- Antagonizes β1 & β2 receptors
- ↓ SA firing – ↓ heart rate, conduction
- can prolong the QT interval.
- can cause polymorphic ventricular tachycardia (Torsades de Pointes)
- recommended to be initiated in the inpatient setting to monitor the QT interval after each dose
- can cause severe bradycardia necessitating drug discontinuation

Gladwin / Sakurai / JC 2020
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2008B Q13 | Classify antiarrhythmic drugs, including their mechanisms of action, and give an example of one drug from each group. | historical_member | — |