2. Anti-dysrhythmic Drugs

Anti-dysrhythmic Drugs Overview

• Presented by Dr. Declan McKernan

• Contact: declan.mckernan@universityofgalway.ie

• Course: PM309 Cardiovascular Drugs

Learning Outcomes

• Describe targets and mechanisms of action of major classes of anti-dysrhythmic drugs with named examples.

• Compare and contrast mechanisms of action, pharmacokinetics, and side effects of these drugs with named examples.

Mechanisms of Action of Anti-dysrhythmic Drugs

Visual Summary

• Action Potential Patterns:

  • Lengthened, shortened, and unchanged potentials observed with various drug actions.

Classification of Antiarrhythmic Drugs

Table 1: Antiarrhythmic Drug Classification

Targets of Anti-dysrhythmic Drugs

• Class I examples: Flecainide (Na+ blocker)

• Class II examples: Propranolol (b-receptor antagonist)

• Class III examples: D-sotalol (K+ blocker)

• Class IV examples: Verapamil (Ca+ blocker)

Specific Indications for Antiarrhythmic Drugs

Table 2: Drug Indications

• Sinus Tachycardia: Propranolol

• Sinoatrial Reentrant Tachycardia: Verapamil

• AV Nodal Reentrant Tachycardia: IV Verapamil, IV Diltiazem

• Atrial Fibrillation: IV Procainamide, IV Ibutilide

• Ventricular Tachycardia: Lidocaine, IV Procainamide

Class-Specific Drug Mechanisms

Class I Drugs

• Mechanism of Action: Block voltage-sensitive Na+ channels.

• Effects: Decreased automaticity and upstroke velocity, prolonged effective refractory period.

Class IA Drugs

• Mechanism: Moderate block on open Na+ channels; also blocks K+ channels.

• Examples: Quinidine, Procainamide, Disopyramide.

• Side Effects: Diarrhea, nausea, drug interactions (e.g., digoxin).

Class IB Drugs

• Mechanism: Bind to open/inactivated Na+ channels, mild block.

• Examples: Lidocaine, Mexiletine.

• Clinical Use: Emergencies for ventricular arrhythmias only; safe in prolonged QT syndrome.

Class IC Drugs

• Mechanism: Most potent Na+ channel blockers.

• Risk: Can worsen existing arrhythmias; used only in life-threatening situations.

Class II Drugs

• Mechanism: B-adrenergic receptor blockade; decreases sympathetic influence on SA and AV nodes.

• Examples: Propranolol, Atenolol.

• Clinical Uses: Tachycardias induced by physical/emotional stress.

Class III Drugs

• Mechanism: Block K+ channels, prolong plateau, and repolarization.

• Example: Amiodarone (also has Class I, II, IV activities).

Class IV Drugs

• Mechanism: Block Ca2+ channels in nodal tissues to decrease conduction velocity.

• Examples: Verapamil, Diltiazem.

Pharmacokinetics of Antiarrhythmic Drugs

Table 4: Summary of Pharmacokinetic Properties

• Notable Drugs:

  • Amiodarone: 200-400 mg daily; hepatic metabolism; long half-life (~53 days).

  • Digoxin: 0.25 mg; renal elimination; 20-30% bioavailability.

Summary of Drug Classes

• Class I: Block Na+ channels; decrease automaticity and arrhythmia risk.

• Class II: Inhibit sympathetic input at pacemaker cells.

• Class III: Prolong repolarization by blocking K+ channels.

• Class IV: Block Ca2+ channels, impacting conduction in nodal tissues.