Attenuating the defibrillation dosage decreases postresuscitation myocardial dysfunction in a swine model of pediatric ventricular fibrillation.

Recognition and treatment of ventricular fibrillation (VF) are underappreciated pediatric problems. Ventricular fibrillation occurs in 5% to 22% of pediatric out-of-hospital cardiac arrests and is the initial documented rhythm in 10% of pediatric in-hospital cardiac arrests (1–4). Automated external defibrillators (AEDs) designed for adults are often the first defibrillators available for out-of-hospital cardiac arrests. Recognizing that some adult AEDs now have diagnostic algorithms that are accurate in children, recent international guidelines recommend that “For children 1 to 8 yrs of age the rescuer should use a pediatric dose-attenuator system if one is available. If the rescuer provides CPR to a child in cardiac arrest and does not have an AED with a pediatric attenuator system, the rescuer should use a standard AED” (5). A specific biphasic pediatric defibrillation dose was not stipulated. Notably, the standard weight-based dosing strategy for pediatric defibrillation that varies with each child’s weight cannot be set in AEDs (5). New commercially available technology has enabled the delivery of a pediatric dose, approximately one fourth to one third (50–86 J) of the standard adult energy output of the AED (6–10). This attenuated (i.e., pediatric) dosing strategy is effective in pediatric piglet models of VF (6, 8–10) and in children (7). In an earlier study comparing pediatric-dose and adult-dose defibrillation in piglets, we found worse postresuscitation myocardial dysfunction and 24-hr neurologic outcome in the adult-dose group but no difference in 24-hr survival between groups (8). We undertook the present study, substantially extending the sample size of our previous work, to more clearly determine whether the postresuscitation dysfunction, survival, and neurologic outcomes of the two groups differ. Because postresuscitation myocardial dysfunction occurs commonly after successful resuscitation from cardiac arrest and is known to be a major cause of death in the postresuscitation phase, our primary end point was left ventricular function 4 hrs after defibrillation. Secondary end points included postresuscitation myocardial damage (i.e., abnormal plasma troponin levels), return of spontaneous circulation (ROSC), survival to 24 hrs, and 24-hr neurologic outcome. We hypothesized that adult defibrillation doses would result in worse postshock myocardial function and greater myocardial damage.