Abstract 4597: The Potential Mechanism of the Detrimental Effect of Defibrillation Prior to CPR after Prolonged Cardiac Arrest
Defibrillation is no longer universally recommended as an initial intervention for reversal of ventricular fibrillation (VF) after prolonged and untreated cardiac arrest. In the present study, we sought to examine this issue in an animal model in which prolonged untreated VF was induced. Our focus was on left ventricular (LV) size and its role in prioritizing either chest compression or initial defibrillation. The success of initial defibrillation after prolonged VF is contingent on LV size and specifically ventricular volumes. VF was electrically induced in 32 domestic male pigs weighing 40±3 kg, and remained untreated for an extraordinarily long 15 minutes. Animals were then randomized to initial defibrillation or chest compression. Defibrillation was with biphasic 120 J. Echocardiograms were obtained immediately before starting chest compression in both groups. Chest compression was performed for 5 minutes prior to defibrillation. CPR was continued until return of spontaneous circulation (ROSC), or for 15 minutes. Mean aortic pressure, right atrial pressure and coronary perfusion pressure (CPP) were continuously measured. LV dimensions were assessed by echocardiographic methods. When chest compression was the initial intervention, 9 of 16 animals achieved ROSC, but no animal which was initially defibrillated had ROSC (p<0.001). CPP during CPR at 1 minute after a shock was significantly decreased in comparison to chest compression only (9 ± 3 vs 15 < 8 (p < 0.04)) and at 5 minutes, 16 ± 5 vs 22± 7 (p < 0.03). LV volumes reduced immediately after defibrillation and prior to start of chest compression (18 ± 2 vs 14 ± 1; p < 0.02). When defibrillation is attempted after prolonged cardiac arrest and prior to chest compression the LV becomes contracted as it does in a strong heart and the effectiveness of precordial compression is accordingly decreased.