Fibrillation is a chaotic, turbulent state for the electrical signal fronts in the heart. In the ventricle it is fatal if not treated promptly. The standard treatment is by an electrical shock to reset the cardiac state to a normal one and allow resumption of a normal heart beat.
The fibrillation wave fronts are organized into scroll waves, more or less analogous to a vortex tube in fluid turbulence. The centerline of this 3D rotating object is called a filament, and it is the organizing center of the scroll wave.
The electrical shock, when turned on or off, creates charges at the conductivity discontinuities of the cardiac tissue. These charges are called virtual electrodes. They charge the region near the discontinuity, and give rise to wave fronts that grow through the heart, to effect the defibrillation. There are many theories, or proposed mechanisms, to specify the details of this process. The main experimental data is through signals on the outer surface of the heart, so that simulations are important to attempt to reconstruct the electrical dynamics within the interior of the heart tissue. The primary electrical conduction discontinuities are at the cardiac surface. Secondary discontinuities, and the source of some differences of opinion, are conduction discontinuities at blood vessel walls.
In this lecture, we will present causal mechanisms for the success of the virtual electrodes, partially overlapping, together with simulation and biological evidence for or against some of these.
The role of small blood vessels has been one area of disagreement. To assess the role of small blood vessels accurately, many details of the modeling have been emphasized, including the thickness and electrical properties of the blood vessel walls, the accuracy of the biological data on the vessels, and their distribution though the heart. While all of these factors do contribute to the answer, our main conclusion is that the concentration of the blood vessels on the exterior surface of the heart and their relative wide separation within the interior of the heart is the factor most strongly limiting the significant participation of small blood vessels in the defibrillation process.