Learning Objective
By the end of this section, learners should be able to explain the mechanism of action of Class II antiarrhythmic drugs and describe their effects on pacemaker activity and clinical use in supraventricular tachyarrhythmias and post–myocardial infarction prophylaxis.
CLASS II: BETA BLOCKERS
Class II antiarrhythmic drugs act by blocking β₁-adrenergic receptors, thereby preventing sympathetic stimulation of the heart that would normally increase intracellular cAMP levels.
Mechanism of Action
- ↓ β-receptor activation → ↓ cAMP
- ↓ SA node automaticity
- ↓ AV nodal conduction
- ↓ slope of Phase 4 depolarization in pacemaker cells
- Slowing of spontaneous diastolic depolarization → ↓ heart rate
Drugs
- Propranolol (nonselective β-blocker)
- Cardioselective β₁-blockers:
- Atenolol
- Metoprolol
- Esmolol (short-acting, IV)
Clinical Uses
- Post–myocardial infarction prophylaxis
- Supraventricular tachyarrhythmias (SVTs)
- Acute SVTs (Esmolol IV)
NOTE: Class I Drug Dissociation Rate (“Slow CAB”)
| Class | Dissociation Rate from Na⁺ Channel |
|---|---|
| IC | Slowest |
| IA | Intermediate |
| IB | Fastest |
CLINICAL CORRELATE: Long QT Syndrome
A hereditary disorder caused by mutations in cardiac potassium channels, resulting in delayed repolarization and increased risk of ventricular arrhythmias.
Drugs That May Induce Torsade de Pointes
- Potassium-channel blockers
- Class IA
- Class III
- Antipsychotics (e.g., thioridazine)
- Tricyclic antidepressants
Activity
Management of Torsade de Pointes
- Correct hypokalemia
- Correct hypomagnesemia
- Discontinue QT-prolonging medications
