Experimental studies have revealed that a wide variety of different pathophysiological mechanisms may induce ventricular fibrillation (VF) and cardiac arrest during acute myocardial ischaemia or infarction. Distinct phases of enhanced vulnerability (the amount of current required to stimulate ectopic activity in the heart following application of an extra stimulus) to VF follow coronary occlusion and correspond to 'pre-hospital', 'in-hospital' and 'out-of-hospital' periods of arrhythmogenesis. Electrophysiological evidence suggests very early (phase 1a) VF results from multiple re-entrant excitation within the ischaemic zone. Slowed and fragmented conduction and inhomogeneities in refractoriness rapidly develop which mapping studies show to occur in association with development of spatial inhomogeneities in residual blood flow distribution and metabolism. Onset of VF may be triggered by adrenergic mechanisms or influenced by peripheral metabolic responses. Automatic mechanisms (spontaneous pacemaker activity) may induce later VF or VF on reperfusion or trigger re-entry. Findings indicate no single therapeutic approach to be likely to protect against all forms of cardiac arrest.
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