Arrhythmia Mechanisms

The three mechanisms in one sentence

A heart misfires only in three ways. Re-entry: an impulse circles a closed loop and re-excites tissue that has just recovered. Automaticity: a non-pacemaker cell starts firing on its own. Triggered activity: an action potential is immediately followed by a second, abnormal depolarization. Roughly 60-70% of clinical sustained arrhythmias are re-entrant; 20-30% automatic; 5-10% triggered.

Re-entry — the circulating wavefront

Re-entry is the easiest mechanism to picture: an electrical wave gets trapped in a loop. To sustain a loop, three things must coexist:

• Two electrically distinct pathways forming a circuit — slow and fast limbs of the AV node (AVNRT), the bundle of Kent and the AV node (AVRT), or scar-bordered corridors after MI.
• Unidirectional block in one limb so the wave travels only one direction.
• Slow conduction in the surviving limb so that by the time the wave completes the loop, the original tissue has finished its refractory period and can be excited again.

Break any one and the loop dies. That is exactly how ablation works — burn a 4 mm line across the slow limb and the circuit cannot complete. WPW ablation is curative in over 95% of cases. Re-entry typically starts and stops abruptly with a single premature beat that finds the substrate at the right moment.

Automaticity — the rogue pacemaker

Only specialized cells should spontaneously depolarize: SA node, AV junction, His-Purkinje system. Their phase 4 drift comes from the inward funny current (I_f) and sodium-calcium exchange. When ordinary atrial or ventricular cells acquire this property — typically from ischemia, hypokalemia, catecholamine surge, stretch, or hypoxia — they become ectopic pacemakers. If the ectopic rate exceeds the SA node's intrinsic rate (~60-100 bpm), the ectopic focus drives the heart.

Classic examples: accelerated idioventricular rhythm during MI reperfusion (60-110 bpm), focal atrial tachycardia originating near pulmonary vein ostia, and many post-cardiac-surgery atrial tachycardias. These rhythms warm up and cool down rather than starting abruptly — a key clinical clue.

Triggered activity — afterdepolarizations

An action potential triggers a second action potential — same beat, second event. Two flavors:

• Early afterdepolarization (EAD): occurs during phase 2 or 3, when repolarization is abnormally prolonged. L-type calcium channels reactivate, producing an inward current that drives the membrane back up. EADs require a long QT — congenital (KCNQ1, KCNH2 mutations) or acquired (azithromycin, ondansetron, methadone, sotalol, hypokalemia). The arrhythmia they cause is Torsades de Pointes, a polymorphic VT that twists around the baseline. It is pause-dependent — typical onset is a long-short R-R coupling.
• Delayed afterdepolarization (DAD): occurs after full repolarization in calcium-overloaded cells. Spontaneous SR calcium release activates the sodium-calcium exchanger (NCX) in its forward mode, generating an inward current. Digitalis toxicity, catecholamines, ischemia, and the RyR2 mutation of catecholaminergic polymorphic VT (CPVT) all produce DADs.

Worked clinical example

A 22-year-old presents with a third episode of sudden palpitations and dizziness. Baseline ECG shows a short PR interval (100 ms) and a slurred upstroke on the QRS — the delta wave. During tachycardia, the ECG showed a regular narrow-complex tachycardia at 220 bpm that terminated abruptly with 6 mg IV adenosine.

Reasoning: short PR + delta = an accessory pathway (Kent bundle). Adenosine works because it blocks the AV node, breaking the re-entrant circuit. The mechanism is orthodromic AV re-entrant tachycardia — antegrade conduction down the AV node, retrograde up the accessory pathway, a stable loop. Treatment is catheter ablation of the accessory pathway (curative in 95%+). Antegrade conduction down a Kent bundle during atrial fibrillation, however, can deliver 1:1 ventricular response above 250 bpm and degenerate to VF — which is why WPW with AF is treated with procainamide or DC cardioversion, never AV-nodal blockers.

Mechanism vs ECG signature — the lookup table

How to read the mechanism from the surface ECG

Feature	Re-entry	Automaticity	Triggered (EAD)	Triggered (DAD)
Onset	Abrupt, after a PAC/PVC	Gradual warm-up	Pause-dependent (long-short)	Tachycardia-dependent
Termination	Abrupt, adenosine works	Gradual cool-down	Self-limited bursts	Bursts
Classic example	WPW (AVRT), AVNRT, atrial flutter	Focal atrial tach, AIVR	Torsades de Pointes	Digoxin VT, CPVT
Baseline ECG clue	Delta wave (WPW)	Often normal	Long QTc > 500 ms	Often normal at rest
Drugs that abort	Adenosine, vagal maneuvers	Beta blockers, ivabradine	Magnesium 2 g IV	Beta blockers, digoxin-Fab
Curative procedure	Catheter ablation	Focal ablation	Correct QT, ICD if congenital	ICD + beta blocker (CPVT)

Common mistakes

• Giving AV-nodal blockers to WPW with atrial fibrillation. Blocking the AV node funnels all the chaotic atrial impulses through the accessory pathway — 1:1 conduction over 250 bpm and degeneration to VF. Use procainamide or DC cardioversion.
• Treating Torsades like normal VT. Amiodarone prolongs QT and worsens the substrate. Give magnesium 2 g IV, correct potassium, stop the offending drug, consider overdrive pacing.
• Missing the warm-up. A heart rate that climbs from 90 to 160 over a minute is automaticity, not re-entry — do not expect adenosine to terminate it.
• Calling every wide-complex tachycardia "VT." SVT with aberrancy can mimic VT; mechanism analysis (regularity, AV dissociation, fusion beats) refines the diagnosis.
• Ignoring electrolytes. Hypokalemia and hypomagnesemia create the substrate for both EADs and DADs. Replace before chasing exotic diagnoses.