How arrhythmias arise !

Mechanism
Exam priority: medium

Abnormal heart rhythms come from cells that fire on their own, beats that trigger extra beats, or a signal that loops in a circle.

Updated 2026-11-01

Also called: Reentry, Triggered activity, Abnormal automaticity

See it in 3D: Sinoatrial (SA) node · Atrioventricular (AV) node · Left atrium · Pulmonary veins

What it is

Arrhythmias arise from disorders of impulse formation (abnormal or enhanced automaticity, triggered activity) or of impulse conduction (block and reentry). Reentry needs a circuit, a one-way block and slow enough conduction that tissue ahead has recovered. Ischemia, electrolyte changes, scar and stretch create these conditions.

How it works, step by step

A premature beat reaches a branch point in the conducting tissue.
One path is still refractory and blocks the impulse; the other conducts slowly.
The impulse travels down the slow path and arrives at the far end of the blocked path.
If that tissue has recovered, it conducts the impulse backward (retrograde).
The impulse re-enters the start of the circuit and repeats, producing a sustained tachycardia.

Electrocardiogram: a normal beat in lead II

HR 75 /minRR 0.80 sPR 0.16 sQRS 0.09 sQT 0.37 sQTc 0.41 s

Tap a wave (P, QRS, T, U), an interval (PR, ST, QT) or the RR.

ECG trace (lead II)
Small box: 0.04 s · 0.1 mV
Big box: 0.20 s · 0.5 mV
Selected part

A normal beat as reference: arrhythmias change the P–QRS relationship, the rate or the QRS width.

Action potential

Rest −90 mVThreshold −70 mVPeak +25 mVDuration ≈ 280 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

Mainly Na⁺
Mainly K⁺
Mainly Ca²⁺
Rest
Threshold
ARP: absolute refractory period
RRP: relative refractory period

Illustrative model drawn by Durgical from typical values; each cell type has its own time scale and values are approximate, not for clinical decisions.

Mechanisms with examples

Mechanism	What happens	Example
Enhanced or abnormal automaticity	Non-pacemaker cells develop phase 4 depolarization	Accelerated idioventricular rhythm in ischemia, ectopic atrial tachycardia
Early afterdepolarization	Re-depolarization during a long plateau	Torsades de pointes in long QT
Delayed afterdepolarization	Ca²⁺ overload causes depolarization after repolarization	Digoxin toxicity arrhythmias
Reentry	An impulse circles back into recovered tissue	AV nodal reentry, atrial flutter, ventricular tachycardia around a scar
Conduction block	Impulses fail to pass	AV block, bundle branch block

Clinical notes

Chagas cardiomyopathy (endemic in parts of Colombia) leaves patchy fibrosis that supports ventricular reentry, AV block and sudden death.
Hypokalemia and hypomagnesemia prolong repolarization and favour early afterdepolarizations.

Test yourself

Think of the answer, then tap the question to see it.

What three conditions are needed for reentry?

Two pathways forming a circuit, a unidirectional block in one of them, and conduction slow enough (or a circuit long enough) that tissue ahead has recovered when the impulse arrives.

Why does digoxin toxicity cause delayed afterdepolarizations?

Inhibiting the Na⁺/K⁺ pump raises intracellular Na⁺, which reduces Ca²⁺ exit by the Na⁺/Ca²⁺ exchanger; Ca²⁺ overload causes spontaneous SR release and depolarizing currents after repolarization.

Why are long QT and bradycardia risk factors for torsades de pointes?

A long plateau gives L-type Ca²⁺ channels time to reactivate, producing early afterdepolarizations that can trigger polymorphic ventricular tachycardia.

Why does a drug that prolongs the refractory period terminate some reentrant tachycardias?

The returning impulse meets tissue that is still refractory, so the circuit is broken.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Pharmacology

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 19.2 Cardiac Muscle and Electrical Activity (OpenStax (Rice University), 2022); Atrial Fibrillation (StatPearls (NCBI Bookshelf), 2025); Chagas Disease (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 13). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.