What causes cardiac fibrillation?

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Last updated: August 15, 2025 • View editorial policy

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Mechanisms of Cardiac Fibrillation

Cardiac fibrillation occurs due to a combination of structural abnormalities, electrical remodeling, and triggering factors that create an arrhythmogenic substrate in the heart tissue, leading to chaotic electrical activity that disrupts normal cardiac contraction.

Atrial Fibrillation Mechanisms

Structural Factors

  • Atrial fibrosis is a common feature in both experimental and human AF, making the atria more sensitive to profibrotic signaling than ventricles 1
  • Structural changes including inflammation, hypertrophy, and myocyte loss create heterogeneous conduction pathways 1, 2
  • Atrial dilation, increased wall stress, and altered architecture increase susceptibility to AF 1
  • Even in patients with paroxysmal AF without recognized structural heart disease, atrial biopsies reveal inflammatory infiltrates and fibrosis 1

Electrical Abnormalities

  • Electrical remodeling is characterized by progressive shortening of atrial effective refractory periods, supporting the concept that "atrial fibrillation begets atrial fibrillation" 1
  • Ion channel dysfunction alters impulse formation and propagation 1
  • Impaired electrical coupling between myocytes fosters three-dimensional conduction abnormalities (breakthroughs) that maintain AF 1
  • Abnormal calcium handling contributes to arrhythmogenesis:
    • High atrial rates elevate diastolic calcium and intracellular calcium storage 1
    • Altered calcium homeostasis persists after restoration of normal sinus rhythm, making AF recurrence more likely 1

Autonomic Influences

  • Changes in sympathetic or parasympathetic tone alter atrial action potential and refractory periods 1
  • Approximately one-third of patients with paroxysmal AF present with well-defined adrenergic or vagal triggers 1
  • Ganglionated plexi, sympathetic hyperinnervation, and nerve sprouting contribute to AF in some patients 1
  • Vagal stimulation shortens atrial refractory periods, potentiating initiation and maintenance of AF 1

Ventricular Fibrillation Mechanisms

While the question primarily addresses fibrillation generally, it's important to note that ventricular fibrillation shares some mechanisms with atrial fibrillation but has distinct characteristics:

  • Ventricular fibrillation can occur in structurally normal hearts (primary electrical disease) but carries high recurrence risk 3
  • Structural heart disease, myocardial ischemia, and cardiomyopathies are common predisposing factors
  • Electrolyte abnormalities (particularly hypokalemia, hypomagnesemia, or hypocalcemia) increase QTc prolongation and risk of torsade de pointes, which can degenerate into ventricular fibrillation 4

Pathophysiological Cycle

A vicious cycle exists between fibrillation and heart failure:

  • AF can lead to tachycardiomyopathy, a reversible cause of heart failure 1
  • Heart failure promotes atrial structural and electrical changes through:
    • Hemodynamic and mechanical mechanisms
    • Neurohormonal activation including the renin-angiotensin-aldosterone system (RAAS) 1
    • Volume retention, increased ventricular filling pressures, and functional mitral regurgitation 1
    • Alterations in calcium handling and calcium overload 1

Risk Factors and Triggers

Several conditions increase susceptibility to fibrillation:

  • Cardiovascular conditions: hypertension, coronary artery disease, valvular heart disease, cardiomyopathies 2
  • Systemic factors: hyperthyroidism, sleep apnea, obesity, diabetes, chronic kidney disease 2
  • Acute triggers: alcohol intake, surgery, myocardial infarction, pericarditis, pulmonary conditions 2
  • Genetic factors: mutations in ion-channel genes and common genetic variants (particularly on chromosome 4q25) 1

Clinical Implications

Understanding these mechanisms has important treatment implications:

  • Rhythm control strategies aim to reverse electrical remodeling
  • Rate control addresses the hemodynamic consequences of irregular rhythm
  • Upstream therapy targets structural remodeling through RAAS inhibition
  • Catheter ablation targets triggers (particularly pulmonary vein isolation) and substrate modification

Pitfalls and Caveats

  • The distinction between cause and effect can be challenging—fibrillation both results from and causes structural and electrical changes
  • Not all patients with similar risk factors develop fibrillation, suggesting individual susceptibility factors
  • Treating only rate or rhythm without addressing underlying structural abnormalities may lead to treatment failure
  • Electrolyte abnormalities must be corrected before antiarrhythmic therapy to avoid proarrhythmic effects 4

Understanding these complex mechanisms is essential for developing personalized prevention and treatment strategies for cardiac fibrillation.

References

1
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

2
Guideline

Atrial Fibrillation Causes and Risk Factors

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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