# Antiarrhythmic Drugs by Vaughan Williams Class

> Antiarrhythmic drugs for NEET-PG Medicine covering Vaughan Williams class I to IV mechanisms, indications, key toxicities and the ECG effect of each class.

- Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/antiarrhythmic-drugs-vaughan-williams
- Exam / course: NEET-PG · Subject: Medicine
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-08
- Last updated: 2026-10-08
- Reference basis: KD Tripathi Essentials of Medical Pharmacology; Katzung's Basic and Clinical Pharmacology; Harrison's Principles of Internal Medicine
- How to cite: "Antiarrhythmic Drugs by Vaughan Williams Class", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/antiarrhythmic-drugs-vaughan-williams

## Direct answer

Antiarrhythmic drugs are classified by the Vaughan Williams scheme into four classes by their main electrophysiological action: sodium channel blockade (class I), beta-blockade (class II), potassium channel blockade that prolongs repolarisation (class III) and calcium channel blockade (class IV). Each class has a characteristic ECG effect and a signature toxicity that examiners test. Amiodarone, which acts across several classes, carries pulmonary, thyroid and hepatic toxicity.

## What you must remember

- **Class IA:** quinidine, procainamide and disopyramide prolong the action potential, QRS and QT; quinidine causes cinchonism and procainamide a lupus-like syndrome.
- **Class IB:** lidocaine, mexiletine and phenytoin shorten the action potential with little QRS change; lidocaine toxicity is CNS, including seizures.
- **Class IC:** flecainide and propafenone widen the QRS markedly with little QT change; avoid after myocardial infarction because of the CAST findings.
- **Class II:** beta-blockers such as propranolol, metoprolol and esmolol slow sinus and AV nodal conduction and prolong the PR interval.
- **Class III:** amiodarone, sotalol, dofetilide and ibutilide prolong repolarisation; sotalol and dofetilide carry a torsades risk.
- **Class IV:** verapamil and diltiazem slow AV nodal conduction; avoid them in pre-excited atrial fibrillation and in reduced ejection fraction.
- **Amiodarone:** pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal microdeposits and photosensitivity, with a long half-life that prolongs these risks.
- **Outside the scheme:** digoxin and adenosine, often grouped as class V; digoxin causes yellow-green visual halos and is worsened by hypokalaemia.

## A wide complex tachycardia in a young athlete

A 26-year-old footballer presents with a fast irregular palpitation near 200 beats per minute. The ECG shows a wide complex irregular tachycardia with an accessory pathway pattern.

1. **Recognise the pattern:** the correct approach recognises pre-excited atrial fibrillation.
2. **Avoid AV nodal blockers:** the reflex answer of verapamil or digoxin can push the ventricular rate even faster when an accessory pathway conducts from the fibrillating atria, so adenosine, digoxin, verapamil, diltiazem and beta-blockers are avoided.
3. **Choose the drug for a stable patient:** procainamide or ibutilide is used.
4. **Cardiovert if unstable:** synchronised DC cardioversion is used if the patient is unstable.

The second case shows a different drug logic. A 60-year-old man with a previous myocardial infarction and an ejection fraction of 35 per cent has frequent ventricular ectopics. Flecainide is the wrong choice, because the CAST experience showed harm with class IC agents in post-infarction patients with asymptomatic ventricular ectopy. A beta-blocker or amiodarone is preferred instead.

In both cases the same question organises the answer: what is the substrate, and what does the drug do to the pathway it is meant to affect?

## Where the examiner tests the ECG

Examiners rarely ask for the class in isolation, so the interval change usually decides the answer.

- **Trap:** reading a prolonged QRS as a class III effect. — **Correct:** a prolonged QRS points to class IA or IC, a shortened QT with little QRS change to class IB, a prolonged PR to class II or IV, and a prolonged QT to class III.
- **Trap:** assuming quinidine and lidocaine toxicity look the same. — **Correct:** quinidine and procainamide cause torsades, while lidocaine toxicity presents as CNS symptoms and seizures.
- **Trap:** treating verapamil with a beta-blocker as harmless. — **Correct:** the combination can produce profound bradycardia or heart block.
- **Trap:** classing digoxin as one of the four Vaughan Williams classes. — **Correct:** digoxin and adenosine sit outside the classic four classes, so a stem asking which agents lie outside the four classes expects digoxin and adenosine.

Interaction questions follow the same pattern: digoxin levels rise with amiodarone, and hypokalaemia worsens digoxin toxicity. Amiodarone spans several classes, which explains both its breadth and its long-lasting toxicity.

## Frequently asked questions

### Which Vaughan Williams class prolongs the QT interval?

Class III agents such as amiodarone, sotalol and dofetilide prolong the QT interval by blocking potassium channels, and class IA agents do so too. Class IB agents shorten the QT, while class IC agents change it little.

### Why are AV nodal blockers avoided in pre-excited atrial fibrillation?

Verapamil, diltiazem, digoxin and adenosine block the AV node and push conduction down the accessory pathway, which can accelerate the ventricular rate towards ventricular fibrillation. Procainamide or ibutilide is preferred in a stable patient.

### What are the main toxicities of amiodarone?

Amiodarone toxicity includes pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal microdeposits and photosensitivity with blue-grey skin discolouration. Its very long half-life means these effects persist for weeks to months after the drug is stopped.

### What is the characteristic toxicity of procainamide?

Procainamide causes a drug-induced lupus-like syndrome, agranulocytosis with prolonged use, and QT prolongation that can progress to torsades. Monitoring the blood count and the QTc is therefore part of safe prescribing.