The most common electrophysiologic mechanisms leading to SCD are tachyarrhythmias such as ventricular fibrillation (VF) or ventricular tachycardia (VT). Interruption of tachyarrhythmias, using either an automatic external defibrillator (AED) or an implantable cardioverter defibrillator (ICD), has been shown to be an effective treatment for VF and VT.[4] The implantable defibrillator has become the central therapeutic factor in the prevention and treatment of sudden cardiac death. Patients with tachyarrhythmias, especially VT, carry the best overall prognosis among patients with sudden cardiac arrest (SCA).
There are multiple factors at the organ (eg imbalance of autonomic tone), tissue (eg reentry, wave break, and action potential duration alternans), cellular (eg triggered activity, and automaticity) and subcellular (abnormal activation or deactivation of ion channels) level involved in generation of VT or VF in different conditions. An anatomical or a functional block in the course of impulse propagation may create a circuit with the wave front circling around it and resulting in VT. Other mechanisms such as wave break and collisions are involved in generating VF from VT. While at the tissue level the above-mentioned reentry and wave break mechanisms are the most important known mechanisms of VT and VF, at the cellular level increased excitation or decreased repolarization reserve of cardiomyocytes may result in ectopic activity (eg automaticity, triggered activity), contributing to VT and VF initiation.