Human heart in ventricular fibrillation.
Ventricular fibrillation is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. It is the most commonly identified arrhythmia in cardiac arrest patients.
While there is some activity, the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography.
Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (“flatline”). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain-dead, due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.
Causes of ventricular fibrillation are:
- Abnormal automaticity: In the healthy myocardium, the rhythm of contraction is regulated by sinoatrial node,that acts like a pacemaker and generates the normal sinus rhythm. Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously, separated from the sinoatrial node. The product of a hypoxic myocardium can be hyperirritable myocardial cells and these may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry ventricular arrhythmia. It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.
- Re-entry: The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. 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 was stimulated at a single point, the subsequent waves of depolarisation 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 ischaemic or infarcted myocardium, or underlying scar tissue.