Abstract 190: Potential Mechanism for Improved Neurological Survival After Cardiac Arrest After Treatment with Active Compression-Decompression Cardiopulmonary Resuscitation Combined with Augmentation of Negative Intrathoracic Pressure

Abstract

Objective: Active compression decompression (ACD) CPR with augmentation of negative intrathoracic pressure using an impedance threshold device (ITD) has been previously shown to enhance refilling of the heart and improve neurologically intact survival when compared with standard (S) CPR. To study the neuroprotective effects of ACD CPR + ITD, we tested the hypothesis that this new approach improves brain perfusion by reducing intracranial pressure (ICP) during the decompression phase of CPR, thereby lowering resistance to forward flow. Methods: Following 8.5 minutes of untreated ventricular fibrillation in 9 anesthetized (100 ug/kg/min propofol) female farm pigs (29.2 ± 1.3 kg), ACD CPR + ITD or SCPR was initiated in random order for 5 minutes followed by 5 additional minutes of CPR with the alternate method. Results: Cerebral perfusion pressures (mmHg) were improved with ACD CPR + ITD (21.9 ± 1.2) versus SCPR (8.9 ± 0.8, p<0.0001). The effects of the CPR on the absolute ICP values and the rate of ICP change during the decompression phase are shown in Table 1. Mean carotid blood flow (ml/min) in the ACD CPR + ITD group was also higher (12.0 ± 2.2 versus 8.0 ± 1.5, p=0.008). Conclusions: The increase in cerebral perfusion pressures and carotid blood flow observed with ACD CPR + ITD was associated with lower diastolic ICP values and a more rapid decrease in ICP during the decompression phase of CPR compared with SCPR. These findings support a dual mechanism for neuroprotection with ACD CPR + ITD: increased forward brain flow and decreased intracerebral resistance, allowing more time for cerebral perfusion.