Abstract 2047: The Importance of Oxygen during Cardiopulmonary Resuscitation (CPR) to Optimize Return of Spontaneous Circulation
Recent CPR work has stressed the importance of good quality chest compressions without interruption and a de-emphasis on minute-ventilation in order to improve cardiac arrest resuscitation rates. However, when ventilation is coupled with chest compression, the optimal oxygen concentration during CPR is not known. Reoxygenation is associated with increased reactive oxygen species production. Previous studies have shown that ventilation with high oxygen concentration after CPR is associated with worse neurologic outcome. We tested the hypothesis that initial ventilation during CPR without oxygen (100% N2) improves resuscitation success.
Methods: Sprague-Dawley rats were anesthetized with ketamine/xylazine (IP), intubated and ventilated with room air. A KCl bolus (0.04 mg/g) was given (IV) to induce asystolic cardiac arrest and ventilation was stopped. At 6 minutes, CPR was started with an automated chest compressor at a rate of 200 –240/min and epinephrine (0.01 mg/kg) was given 1 minute later. During CPR, the ventilation rate was 50% of baseline with one of three oxygen concentrations
0% O2 (100% N2)
21% O2, or
The prescribed oxygen concentration was continued for 2 minutes after return of spontaneous circulation (ROSC) and then all animals were switched to 100% oxygen for 1 hour prior to extubation. Blood gases were measured at 2 min and 1 hr after ROSC. Group comparisons were done using Fisher’s exact test and ANOVA.
Results: ROSC was achieved in 1/10 (100% N2), 9/11 (21% O2) and 10/12 (100% O2, p<0.001). ROSC times after starting CPR were 115±29 sec in the 21% O2 group and 95±11 sec in the 100% O2 group (mean ± SEM, p = 0.5). Aortic end-diastolic pressure before ROSC was not different among groups. 100% oxygen ventilation in the first two minutes resulted in higher PaO2 at ROSC 2 min (109±44 mm vs. Hg 33±8 mm Hg, p<0.001). Survival to 72 hours was 0/1 (100% N2), 7/9 (21% O2) and 8/10 (100% O2) with a low neurologic deficit score in both O2 groups (NDS range 5–25).
Conclusions: In a mild cardiac arrest model with generally good neurologic recovery, initial CPR ventilation with no O2 had no benefit and did not allow for ROSC. The potential harmful effects of high concentration O2 ventilation are likely mitigated by the low myocardial oxygen delivery of CPR.
This research has received full or partial funding support from the American Heart Association, AHA Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania & West Virginia).