Cardiac Arrhythmias are disturbances in the normal rhythm or rate of the heartbeat.
Anti-arrhythmic drugs are classified based on the Vaughan-Williams classification into four main classes, each with distinct mechanisms of action.
Major Classes of Anti-Arrhythmic Drugs:
1) Class I: Sodium Channel Blockers
Block sodium channels, affecting phase 0 depolarization and slowing conduction velocity.
Subclasses:
A) Class IA
Examples: Quinidine, Procainamide, Disopyramide
MOA: Block fast Na⁺ channels, prolong action potential and refractory period.
Uses: Ventricular and supraventricular arrhythmias.
Side Effects: Proarrhythmia (torsades de pointes), hypotension, GI disturbances.
B) Class IB
Examples: Lidocaine, Mexiletine
MOA: Preferentially block Na⁺ channels in ischemic/depolarized tissue, shortening action potential.
Uses: Acute ventricular arrhythmias, post-MI.
Side Effects: CNS effects (seizures, confusion), allergies.
C) Class IC
Examples: Flecainide, Propafenone
MOA: Strong Na⁺ channel blockade, slowing conduction without prolonging action potential.
Uses: Supraventricular and ventricular arrhythmias.
Side Effects: Proarrhythmia, bradycardia, hypotension.
2) Class II: Beta-Blockers
Reduce sympathetic activity, decreasing heart rate and contractility.
Examples: Propranolol, Metoprolol, Esmolol
MOA: Block β-receptors, reducing AV node conduction and prolonging refractory periods.
Uses: Supraventricular and ventricular arrhythmias, ischemic heart disease, and hypertension.
Side Effects: Bradycardia, fatigue, bronchoconstriction.
3) Class III: Potassium Channel Blockers
Prolong repolarization by blocking potassium channels.
Examples: Amiodarone, Sotalol, Dofetilide
MOA: Prolong action potential and refractory period.
Uses: Ventricular and supraventricular arrhythmias.
Side Effects: QT prolongation, torsades de pointes, thyroid and pulmonary toxicity (amiodarone).
4) Class IV: Calcium Channel Blockers
Block calcium influx, affecting AV node conduction.
Examples: Verapamil, Diltiazem
MOA: Inhibit L-type Ca²⁺ channels, reducing automaticity and heart rate.
Uses: Supraventricular arrhythmias and rate control.
Side Effects: Bradycardia, hypotension, constipation.
5) Other Anti-Arrhythmic Agents
Adenosine:
MOA: Activates A1 receptors, transient AV node blockade.
Uses: Acute SVT termination.
Side Effects: Transient asystole, flushing, chest discomfort.
Digoxin:
MOA: Inhibits Na⁺/K⁺-ATPase, increasing vagal tone and reducing AV conduction.
Uses: Rate control in atrial fibrillation/flutter with heart failure.
Side Effects: Toxicity (nausea, vision changes, arrhythmias).
Clinical Considerations:
Proarrhythmic Risks: Some anti-arrhythmics can induce new or more severe arrhythmias.
Underlying Heart Disease: Drug choice depends on the presence of structural heart disease.
Monitoring: Regular ECGs, electrolyte levels, and assessment for drug-specific toxicities.