Cardiac Action Potential
A. Fast-response cells (Atrial muscle, Ventricular muscle, His–Purkinje)
Phases
Phase 0 → Fast Na⁺ influx → rapid upstroke
Phase 1 → Transient K⁺ out
Phase 2 → Ca²⁺ plateau (L-type)
Phase 3 → K⁺ repolarisation
Phase 4 → Stable resting potential
Key point:
Conduction velocity depends on the Phase 0 slope
Anything that blocks Na⁺ channels slows conduction → promotes re-entry block or termination
Drugs acting here
Class I (flecainide, lidocaine)
Class III (amiodarone via phase 3)
B. Slow-response cells (SA node, AV node)
Phases (No phase 1 or 2)
Phase 0 → Ca²⁺ influx (slow)
Phase 4 → Spontaneous depolarisation (automaticity)
Key point:
Rate depends on slope of Phase 4
AV nodal delay is physiological protection
Drugs acting here
β-blockers
Verapamil / diltiazem
Digoxin (↑ vagal tone)
Arrhythmias arise from:
1️⃣ Re-entry (circuits)
2️⃣ Automaticity (pacemaker misfire)
3️⃣ Triggered activity (after-depolarisations)
1. Re-entry (common). Classic examples
Atrial flutter (macro-reentry)
AVNRT
AVRT (WPW)
Scar-related VT (post-MI)
Many cases of AF (micro-reentry)
Drugs:
Flecainide, amiodarone
Ablation (definitive)
2. ↑ d automaticity: Cells fire faster than they should. Phase 4 slope becomes steeper. Triggered by sympathetic tone. Examples
Sinus tachycardia
Ectopic atrial tachycardia
Junctional tachycardia
Drugs:
β-blockers
Ivabradine (sinus node)
Caution: Automatic tachycardias do not terminate with cardioversion
3. Triggered activity (excitability problem). This is about after-depolarisations. Causes Prolonged QT or Bradycardia. Example
Torsades de pointes
Digoxin-induced VT
Catecholamine-mediated arrhythmias
Drug
Magnesium
β-blockers
Treat cause (Digoxin Fab if toxic)
Drugs for arrhythmia
β-blockers
↓ automaticity
↓ AV nodal conduction
Digoxin
↑ vagal tone → AV node
No effect on re-entry circuits
Flecainide
Slows fast Na⁺ conduction
Excellent for re-entry
Dangerous in scarred myocardium
Amiodarone
Hits all three mechanisms
Effective but toxic (lung, liver, and thyroid) + vortex keratopathy