Abstract 11713: Association Between Early Post-Resuscitation Oxygen Exposure and Lung Injury After Cardiac Arrest
Preclinical data link oxygen exposure (FiO2) to acute lung injury presumably through oxidative stress, but clinical data is lacking. Early changes in lung dynamic compliance and oxygenation weakly predict clinical outcome in ARDS patients and reflect the severity of lung injury. We examined whether oxygen exposure in the initial 24h after resuscitation was associated with worsening dynamic compliance or oxygen diffusion in blood. Consecutive cardiac arrest (CA) patients, who survived at least 24h requiring mechanical ventilation and for whom complete data were available within 6h of arrest, were selected from the University of Pittsburgh CA database. Factors associated with dynamic compliance were explored using linear regression. The 130 patients included had a mean age of 60.2±16.1 years, 57.7% suffered out-of-hospital CA, 40% presented in ventricular fibrillation, and survival to discharge was 43.8%. Oxygen exposure, based on the sum of hourly FiO2 for the first 24h post-CA, was weakly associated (p=0.025) with change in dynamic compliance at 24h (Table 1), but not with changes in SOFA respiratory (SOFA-R) score, which reflects oxygen diffusion. Oxygen exposure was also not associated with secondary outcome measures including survival, discharge cerebral performance categories or modified Rankin Scale scores or with changes in SOFA cardiovascular scores at 24h, but was strongly associated (p<0.001) with initial SOFA-R and first measured PaO2. Compliance changes were inversely associated with the initial SOFA-R (p=0.022). Once we controlled for initial SOFA-R, the relationship between oxygen exposure and compliance was no longer significant (Table 1; p=0.157). Oxygen exposure was not independently associated with worsened post-arrest oxygen diffusion or respiratory compliance after controlling for early oxygenation deficits. These data suggest that post-CA oxygen exposure is a marker for oxygen requirements rather than a direct pulmonary toxin.
- © 2012 by American Heart Association, Inc.