Arrhythmia Physiology
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🔑 Key Points
- →Normal automaticity: SA node > AV node > Purkinje (hierarchy of rates)
- →Enhanced automaticity: Faster Phase 4 depolarization in normal pacemaker cells
- →Abnormal automaticity: Phase 4 depolarization in cells that normally lack it (e.g., working myocardium at −50 to −60mV)
- →Phase 4 ionic basis: If (funny current) activates + IK (delayed rectifier K⁺) decays after Phase 3 → net inward current; late ICa,T near threshold
- →Phase 0 upstroke: Fast Na⁺ channels (Purkinje/atrial) or L-type Ca²⁺ (SA/AV node)
- →Characteristic 'warm-up' at onset and 'cool-down' at termination — distinguishes from reentry
- →Can cause VT: Idiopathic VT from Purkinje fibers, some RVOT VT, ischemia-related VT
| Feature | 🎯Automaticity | 🔄Reentry | ⚡EADs | 💥DADs |
|---|---|---|---|---|
| Mechanism | Spontaneous Phase 4 depolarization (If↑ + IK decay) in pacemaker cells or ischemic myocardium; Phase 0 via fast Na⁺ (Purkinje) or L-type Ca²⁺ (SA/AV node) | Circular electrical pathway with unidirectional block and slow conduction | Abnormal depolarization during Phase 2-3 (before full repolarization) reaching threshold | Abnormal depolarization during Phase 4 (after full repolarization) from Ca²⁺ overload reaching threshold |
| Timing | Phase 4 (diastolic depolarization) | N/A (circuit-based) | Phase 2-3 (during repolarization) | Phase 4 (after repolarization complete) |
| Rate Dependence | Variable | Can be any rate | Bradycardia-dependent (slow rates → longer APD → more EADs) | Tachycardia-dependent (fast rates → more Ca²⁺ loading → more DADs) |
| Onset | Gradual "warm-up" period | Sudden onset (often triggered by PAC/PVC) | Often preceded by pauses or bradycardia | Often follows rapid pacing or catecholamine surge |
| Termination | Gradual "cool-down" | Sudden (adenosine, cardioversion, vagal) | Increasing heart rate, Mg²⁺, correcting QT | Slowing rate, reducing Ca²⁺ load, β-blockers |
| Response to Pacing | Can overdrive suppress temporarily | Can entrain and terminate | Overdrive pacing suppresses (→ rate shortens APD) | Rapid pacing can induce or worsen |
| Ionic Mechanism | If (funny current), declining IK, T-type Ca²⁺ | N/A (conduction-based) | Reactivation of L-type Ca²⁺ or late Na⁺ current during prolonged APD | Spontaneous SR Ca²⁺ release → NCX generates inward current |
| Key Conditions | Ischemia, electrolyte disturbance, catecholamines, digoxin toxicity | Accessory pathways (WPW), AV nodal dual pathways, scar tissue | Long QT syndrome, hypokalemia, hypomagnesemia, Class IA/III drugs, bradycardia | Digoxin toxicity, catecholamine excess, heart failure, CPVT, hypercalcemia |
| Classic Arrhythmias | AIVR, ectopic atrial tachycardia, junctional tachycardia, idiopathic VT (rare) | AVNRT, AVRT (WPW), AFL, scar VT | Torsades de Pointes, drug-induced polymorphic VT | Digoxin-induced VT, CPVT, some reperfusion VT |
Important Concepts
Enhanced Normal Automaticity
Increased rate of Phase 4 depolarization in cells with normal pacemaker function (SA node, AV junction, Purkinje). Caused by increased sympathetic tone, fever, hyperthyroidism, ischemia. Example: Sinus tachycardia, accelerated junctional rhythm.
Abnormal Automaticity
Development of Phase 4 depolarization in cells that don't normally have it (atrial or ventricular myocytes). Occurs when resting membrane potential is reduced (less negative, -50 to -60mV) due to ischemia, infarction, or electrolyte abnormalities. Can cause VT in ischemic tissue.
Automaticity-Mediated VT
VT can arise from enhanced Purkinje fiber automaticity (post-MI, idiopathic) or abnormal automaticity in ischemic ventricular myocardium. Characterized by warm-up/cool-down, cannot be entrained like reentry. AIVR (rate 60-100) is classic example post-reperfusion.