Initiation of Ventricular Fibrillation Outside Hospital

The mechanism of arrhythmias following acute infarction, whether enhanced auto-maticity or re-entry or both, appears to vary depending on the time after coronary occlusion. Early after myocardial infarction, ventricular fibrillation may result from re-entrant excitation. During the later stages of infarction enhanced automaticity may precipitate ventricular fibrillation. Janse et al. have suggested that, within the first 15 minutes following experimental coronary occlusion, the premature beat is initiated by injury currents [1]. By its prematurity this beat increases the differences in conduction velocity and refractory periods of ischemic and non-ischemic tissue in the border zone and creates the conditions where micro re-entry can exist. It is probable that minute differences in the way the premature beat is conducted may decide whether or not re-entry succeeds.