Arrhythmia Mechanisms and Electrophysiology

Cardiac arrhythmias arise when the orderly generation and spread of the cardiac impulse is disturbed. Their mechanisms fall into a small number of conceptual categories — abnormal impulse formation, abnormal conduction, and combinations of the two — that together explain disorders ranging from atrial fibrillation to ventricular tachycardia. Knowing these mechanisms is the basis for understanding why arrhythmias occur and how they are targeted by ablation and surgical interruption.

Definition

Arrhythmia mechanisms are the electrophysiological processes — disturbances of impulse formation (enhanced or abnormal automaticity, triggered activity) and of impulse conduction (reentry, block) — that produce abnormal cardiac rhythms.

Scope

This entry covers the electrophysiological substrate of arrhythmia: the cardiac action potential and ion channels, automaticity and triggered activity, reentry and the conditions that sustain it, and the structural and electrical remodelling that perpetuates rhythms such as atrial fibrillation. It is a reference and educational topic and offers no individualised antiarrhythmic or procedural advice.

Core questions

• What ionic currents shape the cardiac action potential and its regional differences?
• How do enhanced automaticity and triggered activity differ as mechanisms of abnormal impulse formation?
• What conditions of conduction and refractoriness permit reentry to initiate and sustain?
• How does electrical and structural remodelling perpetuate arrhythmias such as atrial fibrillation?

Key concepts

• Cardiac action potential and ion channels
• Automaticity
• Triggered activity and afterdepolarisations
• Reentry and unidirectional block
• Refractoriness and conduction velocity
• Electrical and structural remodelling

Key theories

Reentry

Self-sustaining circulation of an impulse around an anatomical or functional obstacle, requiring unidirectional block and conduction slow enough that recovered tissue can be re-excited; the dominant mechanism of many sustained tachyarrhythmias.

Triggered activity

Impulse initiation arising from afterdepolarisations — early afterdepolarisations during repolarisation and delayed afterdepolarisations driven by calcium overload — that reach threshold and fire.

Remodelling in atrial fibrillation

The concept that atrial fibrillation alters atrial electrophysiology and structure in ways that shorten refractoriness and promote further fibrillation, captured in the idea that "atrial fibrillation begets atrial fibrillation."

Mechanisms

Normal rhythm depends on pacemaker automaticity in the sinoatrial node and orderly conduction through the atrioventricular node and His–Purkinje system. Arrhythmias arise when this is perturbed in one of three ways. Abnormal impulse formation includes enhanced or ectopic automaticity and triggered activity from early or delayed afterdepolarisations, the latter often reflecting calcium overload. Abnormal impulse conduction permits reentry, in which an impulse circulates through a pathway with unidirectional block and sufficiently slow conduction to re-excite recovered tissue. Ischaemia and infarction create heterogeneous conduction and refractoriness that favour ventricular reentry, while atrial fibrillation illustrates how the arrhythmia itself remodels the atria to sustain disordered activation.

Clinical relevance

These mechanisms explain why arrhythmias appear after ischaemia, surgery, or chamber dilatation, and they provide the conceptual basis for ablation and surgical lesion sets that interrupt reentrant circuits. The entry describes mechanism and is not a guide to selecting antiarrhythmic therapy or procedures for an individual patient.

Evidence & guidelines

The mechanistic framework here is drawn from experimental electrophysiology and authoritative reviews rather than from treatment guidelines; clinical management of specific arrhythmias is addressed in dedicated cardiology and electrophysiology guidance outside this entry.

History

The reentry concept dates to early-twentieth-century studies of circulating excitation, and the distinction between automaticity, triggered activity, and reentry was clarified through mid- and late-twentieth-century cellular electrophysiology. Janse and Wit's comprehensive review of ischaemic ventricular arrhythmia and Nattel's synthesis of atrial fibrillation mechanisms exemplify the modern mechanistic understanding.

Key figures

• Michiel Janse
• Andrew Wit
• Stanley Nattel
• Gordon Moe

Seminal works

• janse-wit-1989
• nattel-2002

Frequently asked questions

What are the main mechanisms of cardiac arrhythmia?

They are grouped into disorders of impulse formation (enhanced or abnormal automaticity and triggered activity) and disorders of impulse conduction (chiefly reentry), with many arrhythmias combining elements of both.

Why does atrial fibrillation tend to persist once it starts?

Atrial fibrillation induces electrical and structural remodelling that shortens atrial refractoriness and alters conduction, creating a substrate that makes further fibrillation more likely — the idea that atrial fibrillation begets atrial fibrillation.