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[Physiology](https://durgical.com/en/physiology/) · [Cardiovascular](https://durgical.com/en/physiology/#s-cardio)

# 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](https://durgical.com/en/anatomy/sinuatrial-node/) · [Atrioventricular (AV) node](https://durgical.com/en/anatomy/atrioventricular-node/) · [Left atrium](https://durgical.com/en/anatomy/left-atrium/) · [Pulmonary veins](https://durgical.com/en/anatomy/pulmonary-veins/)

## Key points

- Three mechanisms: abnormal automaticity, triggered activity (early and delayed afterdepolarizations), reentry.
- Reentry needs: two pathways, unidirectional block, and a path length longer than conduction velocity × refractory period (wavelength).
- Early afterdepolarizations (phase 2–3) come with long QT and bradycardia → torsades de pointes; delayed afterdepolarizations (after phase 3) come with Ca²⁺ overload (digoxin toxicity, catecholamines).
- Atrial fibrillation: triggers from the pulmonary veins + multiple reentry wavelets in a dilated, fibrotic left atrium.
- Slower conduction or a shorter refractory period favour reentry; antiarrhythmics act by slowing conduction or prolonging refractoriness.

## 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 /min **RR** 0.80 s **PR** 0.16 s **QRS** 0.09 s **QT** 0.37 s **QTc** 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 mV **Threshold** −70 mV **Peak** +25 mV **Duration** ≈ 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](https://durgical.com/en/conditions/atrioventricular-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.

## Memory aid

Arrhythmias are a spark (automaticity), an echo (triggered beats) or a racetrack (reentry).

## 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.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/how-arrhythmias-arise/)

## See it in 3D

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

- [Sinoatrial (SA) node](https://durgical.com/en/anatomy/sinuatrial-node/)
- [Atrioventricular (AV) node](https://durgical.com/en/anatomy/atrioventricular-node/)
- [Left atrium](https://durgical.com/en/anatomy/left-atrium/)
- [Pulmonary veins](https://durgical.com/en/anatomy/pulmonary-veins/)

## Related topics

- [The ventricular action potential](https://durgical.com/en/physiology/the-ventricular-action-potential/)
- [The SA node pacemaker potential](https://durgical.com/en/physiology/the-sa-node-pacemaker-potential/)
- [The cardiac conduction system](https://durgical.com/en/physiology/the-cardiac-conduction-system/)
- [ECG basics: waves, intervals and leads](https://durgical.com/en/physiology/ecg-basics-waves-intervals-and-leads/)
- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)

## Related conditions

- [Atrial fibrillation](https://durgical.com/en/conditions/atrial-fibrillation/)
- [Atrioventricular (heart) block](https://durgical.com/en/conditions/atrioventricular-block/)
- [Chagas cardiomyopathy](https://durgical.com/en/conditions/chagas-cardiomyopathy/)
- [Myocardial Infarction (Heart Attack)](https://durgical.com/en/conditions/myocardial-infarction/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)

## In Pharmacology

- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)
- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)
- [Lidocaine](https://durgical.com/en/pharmacology/lidocaine/)

[← All of physiology](https://durgical.com/en/physiology/)

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](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-2-cardiac-muscle-and-electrical-activity) (OpenStax (Rice University), 2022); [Atrial Fibrillation](https://www.ncbi.nlm.nih.gov/books/NBK526072/) (StatPearls (NCBI Bookshelf), 2025); [Chagas Disease](https://www.ncbi.nlm.nih.gov/books/NBK459272/) (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).

## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake

Representative model, for educational purposes only.

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Source: https://durgical.com/en/physiology/how-arrhythmias-arise/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/how-arrhythmias-arise/