What is the mechanism of ventricular fibrillation?

Mechanism of Ventricular Fibrillation

Ventricular fibrillation (VF) is characterized by uncoordinated electrical activity with chaotic, rapid ventricular activation resulting in ineffective cardiac contraction and hemodynamic collapse. 1

Pathophysiological Mechanisms

Initiation and Substrate

• Reentry: The primary mechanism of VF involves reentrant circuits requiring:
  • A trigger (often a premature ventricular contraction)
  • A substrate to sustain the arrhythmia 1
• Structural substrate: Myocardial fibrosis, scarring (from prior MI), or patchy fibrosis in cardiomyopathy creates heterogeneous conduction pathways 1
• Functional substrate: Ion channel dysfunction or electrolyte abnormalities can create electrical heterogeneity even in structurally normal hearts

Maintenance Mechanisms

1. Rotors: Three-dimensional rotational circuits (spiral waves) that:

   • Activate the ventricles at extremely high frequencies (>550 activations/minute)
   • May drift throughout the heart or remain relatively stationary 2
   • Generate wave fronts that break up at varying distances, creating complex patterns

2. Wave Break: The high-frequency electrical waves emanating from rotors encounter tissue with varying refractory periods, causing wave fragmentation and creation of daughter wavelets 2

3. Multiple Wavelet Hypothesis: Multiple independent wavelets propagate through the ventricles simultaneously, colliding and creating new wavefronts in a self-sustaining process

Electrophysiological Features

• Rapid rate: Ventricular activation at >300 beats per minute
• Irregular R-R intervals: Completely chaotic ventricular activation
• ECG characteristics: Irregular, rapid oscillations varying in amplitude, shape, and timing 1
• Loss of coordinated contraction: Results in immediate hemodynamic collapse

Contributing Factors

Autonomic Influences

• Sympathetic activation: Increases risk of VF through:
  • Enhanced automaticity
  • Shortened refractory periods
  • Increased heterogeneity of repolarization 1
  • Elevated catecholamine levels make VT harder to terminate and more likely to degenerate into VF

Ischemia and Reperfusion

• Ischemia: Creates:

  • Heterogeneous conduction
  • Abnormal automaticity from injury currents between infarcted/ischemic tissue and healthy myocardium 1
  • Partial repolarization of resting membrane potential

• Reperfusion: Paradoxically can trigger VF through:

  • Calcium overload
  • Free radical generation
  • Washout of protective metabolites 3

Progression and Evolution

VF is not static but evolves through distinct phases:

1. Early phase: More organized with larger amplitude
2. Transition phase: Progressive disorganization
3. Late phase: Completely chaotic, low amplitude activity
4. Terminal phase: Asystole if not treated 3

Clinical Implications

• VF requires immediate defibrillation, as the likelihood of successful termination decreases with time
• In prolonged VF (>7.5 minutes), immediate countershock is less effective than providing brief myocardial perfusion with CPR and epinephrine before defibrillation 4
• Self-terminating VF is extremely rare but can occur when chaotic rhythm organizes into more monomorphic ventricular tachycardia before termination 5
• VF recurrence after successful defibrillation is common (50-80%) and associated with worse outcomes 3

Understanding these mechanisms has led to targeted therapies including catheter ablation of VF rotor substrate in certain cases, and guides the timing of defibrillation relative to CPR in prolonged cardiac arrest scenarios.