Antiarrhythmics Pharmacology Summary
Cardiac Conduction Phases:
Phase 0 - Ventricular Depolarization:
• Na+ channels open leading to a rapid Na+ influx initiating contraction of ventricles.
Phase I - Initial Repolarization:
• Na+ channels close
• Transient K+ efflux moving back to resting membrane potential.
Phase 2 - Plateau Phase
• Ca++ channels open leading to slow Ca++ influx to balance out K+ efflux
• Delays ventricular repolarization
Phase 3 - Ventricular Repolarization:
• Ca2+ channels close
• K* efflux increases out of cells allowing ventricles to relax.
Phase 4 - True Resting Membrane Potential:
• K+ channels remain open to maintain a negative resting potential.
• Atrial depolarization occurs initiating contraction of atrial muscles.
Vaughan Williams Classification:
CLASS 1 - Sodium Channel Blockers:
• MOA: Block fast Na+ channels to reduce speed of ion conduction
• ↓ slope of phase 0 to decrease rate and magnitude of depolarization
• Divided into 3 categories based on Na+ channel blocking effects and AP duration:
- CLASS 1A: Moderate Blockade, Intermediate Action, ↑ EFR & AP duration
- CLASS 1B: Weak Blockade, Fast Action, ↓ EFR & AP duration
- CLASS 1C: Strong Blockade, Slow Action, ←→ EFR & AP duration
CLASS 2 - Beta Blockers:
• MOA: Inhibit B.adrenergic activation (↓ cAMP and Ca++ current) causing ↓SA node and AV node activity (rate control)
• ↓ slope of phase 4 to slow depolarization
• ↑ PR interval to prolong AV node repolarization
CLASS 3 - Potassium Channel Blockers:
• MOA: Block K+ channels (primarily) and block alpha & beta adrenergic receptors, and Ca & Na channels.
- ↑ duration of phase 2 (↑ERP & ↑AP Duration)
- ↑ QT interval (delays time repolarization)
CLASS 4 - Calcium Channel Blockers:
• MOA: Block slow Ca++ channels to prevent Ca++ influx into cells (rate control).
- ↓ slope of phase 0 and 4 to ↑ ERP (slow conduction velocity)
- ↑ PR interval to prolong AV node repolarization
- ↓ contraction force (negative inotropy)
ACCP Cardiology PRN @accpcardprn
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