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Antiarrhythmics

Medicines that slow, convert or prevent abnormal heart rhythms by acting on ion channels, beta receptors or the AV node. Most can also cause arrhythmias.

Updated

What they are

A mixed group sorted by the Vaughan Williams classes: class I blocks sodium channels (IA quinidine, procainamide, disopyramide; IB lidocaine, mexiletine; IC flecainide, propafenone), class II are beta blockers, class III blocks potassium channels and lengthens repolarisation (amiodarone, sotalol, dofetilide, ibutilide, dronedarone) and class IV are the non-dihydropyridine calcium channel blockers (verapamil, diltiazem). Adenosine and digoxin act on the AV node outside the four classes.

Mechanism of action

Sodium channel blockers slow the upstroke of the action potential and conduction (wider QRS); IA drugs also lengthen repolarisation, IB drugs act mostly on depolarised or ischaemic tissue, and IC drugs slow conduction the most. Potassium channel (IKr, hERG) blockers lengthen the action potential and refractory period (longer QT). Beta blockers and calcium channel blockers slow the sinus node and AV conduction. Adenosine opens potassium channels in the AV node through A1 receptors and blocks it for seconds.

Target: Cardiac sodium (Nav1.5), potassium (hERG/IKr) and L-type calcium channels, beta-1 receptors, adenosine A1 receptors

Drugs in this class

Others in the class

  • Dronedarone
  • Dofetilide
  • Ibutilide
  • Mexiletine
  • Disopyramide
  • Vernakalant

Test yourself

Think of the answer, then tap the question to see it.

Which Vaughan Williams class do flecainide and propafenone belong to, and what is their main ECG effect?

Class IC: strong sodium channel block that slows conduction and widens the QRS, with little effect on repolarisation.

Which two classes most often prolong the QT and cause torsades de pointes?

Class IA (quinidine, procainamide, disopyramide) and class III (sotalol, dofetilide, ibutilide; amiodarone less often).

Why are class IC drugs avoided after a myocardial infarction?

In the CAST trial they increased deaths and arrests in post-infarction patients, through proarrhythmia in scarred myocardium.

Why is an AV nodal blocker given with a class I drug in atrial flutter?

Slowing the flutter rate can let the AV node conduct every beat (1:1), so the ventricular rate can rise sharply.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: DailyMed - AMIODARONE HYDROCHLORIDE tablet (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - FLECAINIDE ACETATE tablet (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - PROPAFENONE HYDROCHLORIDE tablet, film coated (DailyMed (U.S. National Library of Medicine), 2026).

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Representative model, for educational purposes only.