Ventricular fibrillation (V-fib or VF) is a cardiac condition that consists of a lack of coordination of the contraction of the muscle tissue of the large chambers of the heart that eventually leads to the heart stopping altogether.
Ventricular fibrillation is considered a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease, as evidenced by lack of pulse, blood pressure and respiration, and death will occur.
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly, rather than contracting in unison, and so the ventricles fail to pump blood into the arteries and into systemic circulation. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischemic heart disease. Despite much work, the underlying nature of fibrillation is not completely understood. Most episodes of fibrillation occur in diseased hearts, however others occur in so-called normal hearts. Much work still has to be done to elucidate the mechanisms of ventricular fibrillation.
The condition can often be reversed by the electric discharge of DC current from a defibrillator. Antiarrhythmic agents like amiodarone or lidocaine can help, but, unlike atrial fibrillation, VF rarely reverses spontaneously in large adult mammals. Although a defibrillator is designed to correct the problem, and its effects can be dramatic, it is not always successful.
In patients at high risk of ventricular fibrillation the use of an implantable cardioverter defibrillator has been shown to be beneficial.
The role of re-entry or circus motion was demonstrated separately by Mines and Garrey [Mines GR 1913, Garrey WE 1914]. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue were stimulated at a single point, the subsequent waves of depolarization would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischemic or infarcted myocardium, or underlying scar tissue.
It is possible to think of the advancing wave of depolarization as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance - the propagation velocity - will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarized with continuation of the wavefront.
In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.