Dysrhythmias result from abnormalities in:
• Automaticity • Triggered activity • Conduction
Successful treatment requires understanding the cardiac action potential.
Two major cell types:
• Phase 0 – Na+ influx • Phase 1 – Early repolarization • Phase 2 – Ca2+ plateau • Phase 3 – K+ repolarization • Phase 4 – Resting potential
• Phase 0 – Ca2+ influx • Phase 3 – K+ repolarization • Phase 4 – Spontaneous depolarization
Drugs modify specific ion currents within these phases.
Block Phase 0 depolarization in fast-response cells.
Subclasses:
• Class IA – Moderate Na block + QT prolongation
• Class IB – Mild Na block (shortens QT)
• Class IC – Strong Na block (no QT change)
Used for rhythm control.
Suppress sympathetic stimulation.
Primarily used for rate control.
Goal: • Restore and maintain sinus rhythm
Agents:
• Class I drugs • Class III drugs
Higher proarrhythmic risk.
All antiarrhythmics can worsen arrhythmias.
Most notable:
• QT prolongation → torsades de pointes • Class IC drugs in structural heart disease
Never treat ECG without treating the patient.
Atrial Fibrillation:
SVT (AVNRT/AVRT):
Ventricular Tachycardia:
Bradycardia:
✔ Rate control is often safer than rhythm control ✔ QT prolongation increases torsades risk ✔ Class IC drugs contraindicated in structural heart disease ✔ Amiodarone is effective but toxic ✔ Treat the patient, not just the ECG
Related:
→ Beta-Blockers → Non-DHP Calcium Channel Blockers → Return to Cardiovascular Modules