VENTRICULAR-FIBRILLATION VOLTAGE AS A MONITOR OF THE EFFECTIVENESS OFCARDIOPULMONARY-RESUSCITATION

Ventricular fibrillation (VF) voltage was previously identified as a p redictor of the success of cardiopulmonary resuscitation. In the prese nt study we investigated the mechanism by which VF voltage predicts th e success of cardiac resuscitation in a well-established rodent model of cardiac arrest. After 4 minutes of untreated VF, precordial compres sion was initiated and maintained for 6 minutes. Increases in coronary perfusion pressure during precordial compression were associated with concomitant increases in VF voltage (r = 0.61, p = 0.013). Significan tly greater coronary perfusion pressure (24 vs 17 mm Hg) and VF voltag e (0.17 vs 0.12 mV) were observed in resuscitated animals. To obviate electrical artifacts produced by precordial compression, boluses of ox ygenated blood were injected into the ascending aorta in another 5 ani mals as an alternative method of cardiac resuscitation. This restored myocardial perfusion before defibrillation. Increases in M voltage fro m 0.04 mV to 0.47 mV during aortic infusions were again correlated wit h coronary perfusion pressure (r = 0.62, p < 0.01) and predicted the s uccess of cardiac resuscitation. Greater VF voltages after initiation of cardiac resuscitation were associated with increases in myocardial creatine phosphate, from 0.23 to 0.70 mmol/kg wet weight, and signific ant decreases in lactate content, from 22.8 to 13.9 mmol/kg wet weight . Increases in creatine phosphate were highly correlated with increase s in VF voltage (r = 0.99, p < 0.01). Accordingly, increases in M volt age during cardiac resuscitation reflect increases in myocardial perfu sion and favorable changes in myocardial energy metabolism. As such, V F voltage, like coronary perfusion pressure, serves as a quantitative predictor of the success of cardiopulmonary resuscitation.