Cardiology > Antiarrhythmic Drugs

Background

Antiarrhythmic drugs are pharmacological agents that modify the electrical activity of the heart to suppress or prevent abnormal rhythms (arrhythmias). They act on ion channels, autonomic tone, or nodal tissue to restore and maintain sinus rhythm, control ventricular rate, or terminate arrhythmic episodes.

They are used to manage supraventricular and ventricular arrhythmias, improve symptoms, prevent recurrence, and reduce the risk of arrhythmia-related complications such as stroke or sudden cardiac death.

Classification/Types (Vaughan–Williams System)

Class I – Sodium Channel Blockers

• IA: Quinidine, procainamide, disopyramide

  • Moderate Na⁺ block, prolong repolarization (↑QT).

• IB: Lidocaine, mexiletine

  • Mild Na⁺ block, shorten repolarization (↓QT).

• IC: Flecainide, propafenone

  • Strong Na⁺ block, minimal effect on repolarization.

Class II – Beta-Adrenergic Blockers

• Examples: Metoprolol, propranolol, esmolol, carvedilol.

• Reduce sympathetic stimulation, slow AV conduction, and decrease automaticity.

Class III – Potassium Channel Blockers

• Examples: Amiodarone, sotalol, dofetilide, ibutilide.

• Prolong repolarization and refractory period (↑QT).

Class IV – Calcium Channel Blockers (non-dihydropyridine)

• Examples: Verapamil, diltiazem.

• Slow conduction through AV node, reduce automaticity.

Other Important Agents

• Adenosine: AV nodal blocker for paroxysmal supraventricular tachycardia (PSVT).

• Digoxin: Enhances vagal tone, slows AV conduction (mainly in atrial fibrillation with heart failure).

• Ivabradine: Inhibits funny current (If), reducing sinus node rate.

Clinical Rationale

Arrhythmias arise from abnormal impulse formation (enhanced automaticity, triggered activity) or abnormal impulse conduction (reentry circuits, conduction block). Antiarrhythmics act by modifying ion channel activity or autonomic inputs, altering conduction velocity, refractoriness, or pacemaker activity to suppress arrhythmias.

Indications

• Atrial fibrillation/flutter: Rhythm control (amiodarone, sotalol, flecainide) or rate control (beta-blockers, diltiazem, digoxin).

• Supraventricular tachycardia (SVT): Adenosine, verapamil, beta-blockers, Class IC drugs in select patients.

• Ventricular arrhythmias: Amiodarone, lidocaine, mexiletine, sotalol.

• Prevention of sudden cardiac death in select high-risk patients (ICD generally preferred, but amiodarone may be used).

• Wolff-Parkinson-White syndrome: Procainamide, flecainide; avoid AV nodal blockers.

Contraindications

• Class IC: Avoid in structural heart disease (post-MI, cardiomyopathy) due to proarrhythmia risk.

• Beta-blockers/CCBs: Contraindicated in severe bradycardia, AV block, or acute decompensated heart failure.

• Amiodarone: Contraindicated in iodine allergy, severe thyroid or pulmonary disease.

• Sotalol/dofetilide: Avoid in prolonged QT or severe renal dysfunction.

Physical Exam Findings Correlated

Vital Signs

• Tachycardia (SVT, AF with RVR, VT).

• Bradycardia or hypotension as side effects.

General Appearance

• Palpitations, dizziness, syncope, or fatigue associated with arrhythmias.

Cardiovascular System

• Irregularly irregular pulse in atrial fibrillation.

• Sustained rapid or wide-complex tachycardia in ventricular arrhythmias.

Neurological System

• Syncope, confusion, or seizure-like activity during arrhythmic episodes.

Advantages

• Effective acute and chronic control of arrhythmias.

• Symptom relief and improved quality of life.

• Some agents (e.g., amiodarone) effective in both supraventricular and ventricular arrhythmias.

Limitations

• Proarrhythmia risk (torsades de pointes, VT).

• Narrow therapeutic windows.

• Frequent need for monitoring (e.g., amiodarone toxicity surveillance, INR with warfarin if combined).

• Limited mortality benefit compared with device therapy (ICDs).

Complications and Adverse Effects

• Class IA: QT prolongation, torsades de pointes, lupus-like syndrome (procainamide).

• Class IB: CNS toxicity (confusion, seizures).

• Class IC: Proarrhythmia in structural heart disease, blurred vision, dizziness.

• Beta-blockers: Bradycardia, bronchospasm, fatigue.

• Amiodarone: Pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal deposits, skin discoloration.

• Sotalol/dofetilide: QT prolongation, torsades de pointes.

• CCBs (verapamil, diltiazem): Bradycardia, hypotension, constipation.

• Adenosine: Transient flushing, chest discomfort, bronchospasm.

• Digoxin: Narrow therapeutic index; toxicity includes GI upset, visual disturbances (yellow vision), arrhythmias.

Follow-Up and Clinical Decision-Making

• Baseline and periodic ECG: To monitor QT interval, QRS width, and bradyarrhythmia risk.

• Organ function monitoring: Thyroid, liver, lung (for amiodarone), renal function (for sotalol/dofetilide).

• Therapeutic drug levels: Digoxin.

• Adjunct therapy: Anticoagulation in atrial fibrillation for stroke prevention.

• Escalation: Consider catheter ablation or device implantation if drug therapy fails or is contraindicated.