Abstract 205: The Effect of Chest Compressions on ETCO 2 Levels During Out-of-Hospital Cardiac Arrest

Abstract

Background Previous investigations have suggested that end-tidal CO2 (EtCO2) values are proportional to cardiac output over a wide range of flow rates, including very low flow rates. Cardiopulmonary resuscitation (CPR) is an integral part of therapy that provides circulatory support for cardiac arrest patients. Therefore, we hypothesize that during cardiac arrest, EtCO2 levels are higher during periods when chest compressions are being performed compared to periods without chest compressions. Objective Compare EtCO2 values during periods of CPR with and without chest compressions in out-of-hospital cardiac arrest (OHCA) patients. Methods Recordings from 128 OHCA patients with both capnogram and chest compression waveforms were collected from 2008 to 2010 in two EMS agencies in Oregon and Texas. Recordings were manually reviewed to select segments recorded during cardiac arrest. An automated technique separated the intervals with chest compressions (27 hours) and intervals without chest compressions (15 hours). For each patient, the average EtCO2 values in the intervals with and without chest compressions were calculated and compared to determine the impact of chest compressions on the EtCO2 levels. Results The table below summarizes the results. For 112 patients the mean EtCO2 value was higher in intervals with chest compressions compared to those without chest compressions. For the other 16 patients, there was a small decrease in EtCO2 values during chest compressions. A paired t-test shows that the mean EtCO2 values with chest compressions (27.1 ± 13.1 mmHg) and without chest compressions (22.2 ± 12.1 mmHg) are significantly different (p < 0.0001). Conclusion For most OHCA patients, chest compressions increased the EtCO2 level, which may reflect an improvement in cardiac output. Monitoring EtCO2 during CPR could provide valuable feedback on the quality of CPR. Further study is required to determine factors that increase the EtCO2 during chest compression.