O2delivery and CO2production during cardiopulmonary bypass as determinants of acute kidney injury: Time for a goal-directed perfusion management?

Abstract

Introduction: Acute kidney injury (AKI) is common after cardiac operations. There are different risk factors or determinants of AKI, and some are related to cardiopulmonary bypass (CPB). In this study, we explored the association between metabolic parameters (oxygen delivery (DO2) and carbon dioxide production (VCO2)) during CPB with postoperative AKI.Methods: We conducted a retrospective analysis of prospectively collected data at two different institutions. The study population included 359 adult patients. The DO2and VCO2levels of each patient were monitored during CPB. Outcome variables were related to kidney function (peak postoperative serum creatinine increase and AKI stage 1 or 2). The experimental hypothesis was that nadir DO2values and nadir DO2/VCO2ratios during CPB would be independent predictors of AKI. Multivariable logistic regression models were built to detect the independent predictors of AKI and any kind of kidney function damage.Results: A nadir DO2level < 262 mL/minute/m2and a nadir DO2/VCO2ratio < 5.3 were independently associated with AKI within a model including EuroSCORE and CPB duration. Patients with nadir DO2levels and nadir DO2/VCO2ratios below the identified cutoff values during CPB had a significantly higher rate of AKI stage 2 (odds ratios 3.1 and 2.9, respectively). The negative predictive power of both variables exceeded 90%. The most accurate predictor of AKI stage 2 postoperative status was the nadir DO2level.Conclusions: The nadir DO2level during CPB is independently associated with postoperative AKI. The measurement of VCO2-related variables does not add accuracy to the AKI prediction. Since DO2during CPB is a modifiable factor (through pump flow adjustments), this study generates the hypothesis that goal-directed perfusion management aimed at maintaining the DO2level above the identified critical value might limit the incidence of postoperative AKI. © 2011 de Somer et al.; licensee BioMed Central Ltd.