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Ventricular fibrillation: Mechanisms of initiation and maintenance

Journal

ANNUAL REVIEW OF PHYSIOLOGY
Volume 62, Issue -, Pages 25-50

Publisher

ANNUAL REVIEWS
DOI: 10.1146/annurev.physiol.62.1.25

Keywords

sudden death; cardiac turbulence; ventricles; phase singularities; wavebreaks; vortex-like reentry; rotors; spiral waves; scroll waves; fibrillatory conduction

Categories

Funding

  1. NHLBI NIH HHS [R01-HL60843, P01-HL39707] Funding Source: Medline
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL039707, R01HL060843] Funding Source: NIH RePORTER

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Ventricular fibrillation (VF) is the major immediate cause of sudden cardiac death. Traditionally, VF has been defined as turbulent cardiac electrical activity, which implies a large amount of irregularity in the electrical waves that underlie ventricular excitation. During VF, the heart rate is too high (> 550 excitations/minute) to allow adequate pumping of blood. In the electrocardiogram (ECG), ventricular complexes that are ever-changing in frequency, contour, and amplitude characterize VE This article reviews prevailing theories for the initiation and maintenance of VF, as well as its spatio-temporal organization. Particular attention is given to recent experiments and computer simulations suggesting that VF may be explained in terms of highly periodic three-dimensional rotors that activate the ventricles at exceedingly high frequency. Such rotors may show at least two different behaviors: (a) At one extreme, they may drift throughout the heart at high speeds producing beat-to-beat changes in the activation sequence. (b) At the other extreme, rotors may be relatively stationary, activating the ventricles at such high frequencies that the wave fronts emanating from them breakup at varying distances, resulting in complex spatio-temporal. patterns of fibrillatory conduction. In either case, the recorded ECG patterns are indistinguishable from VE The data discussed have paved the way for a better understanding of the mechanisms of VF in the normal, as well as the diseased, human heart.

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