Abstract 93: A Percutaneous Left Ventricular Assist Device Improves Survival in a Porcine Model of Cardiac Arrest and Resuscitation
Introduction: Manual chest compressions usually result in 20-30% of normal vital organ blood flow. Hence, improving circulation during cardiopulmonary resuscitation (CPR) may increase the number of successfully resuscitated patients.
Hypothesis: Optimizing intra- and post-CPR hemodynamics by using a percutaneous intravascular left-ventricular-assist device (LVAD) instead of chest compressions increases the rate of return of spontaneous circulation (ROSC).
Methods: Seven pigs were instrumented with an LVAD (Impella 2.5, Abiomed, Danvers, MA) and a pulmonary artery catheter to measure mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), mean pulmonary artery pressure (MPAP) and pulmonary capillary wedge pressure (PCWCP). Data from previous experiments (Derwall et al. Shock 2010) using conventional CPR with a piston driven chest compressor served as control (n=8).
In both groups CA was electrically induced and left untreated for 10 minutes before CPR was attempted, either by activating the LVAD at the highest possible flow, or performing chest compressions at a rate of 100/min. After two injections of 1mg adrenaline and a total of 6 minutes CPR, defibrillation was attempted. Hemodynamic values were recorded for 120 minutes before animals were weaned from the respirator.
Results: On average, the LVAD delivered 1.3 ± 0.1 L/min during CPR (34 % of baseline CO) resulting in an increase in MAP from 18 ± 10 mmHg after 10 minutes of CA to 35 ± 2 mmHg before defibrillation (see Figure ; * indicates p<0.05 for MAP at 10 vs. 16 min). MAP, HR, MPAP and PCWP did not differ before CA or after 120 minutes following CPR. While all animals (n=7) in the LVAD group presented with ROSC following CPR, only 50% (n=4) of the animals in the chest compressions group could be successfully resuscitated (p=0.035).
Conclusion: Using a percutaneous LVAD instead of conventional chest compressions did not significantly alter post-CPR hemodynamics, but improved the rate of ROSC in this model.
- © 2012 by American Heart Association, Inc.