Association Between Intraoperative Hyperoxia and Acute Kidney Injury After Cardiac Surgery: A Retrospective Observational Study

Objective

Optimal oxygen management during cardiac surgery has not been established, and studies on the effects of perioperative hyperoxia on postoperative acute kidney injury (AKI) are scarce. The association between intraoperative hyperoxia and AKI after cardiac surgery involving cardiopulmonary bypass was evaluated for the present study.

Design

Retrospective observational study.

Setting

A tertiary teaching hospital.

Participants

Adult patients who underwent cardiac surgery with cardiopulmonary bypass from November 2006–December 2018.

Interventions

None.

Measurements and Main Results

The area above arterial oxygen partial pressure (PaO ₂) threshold of 300 mmHg (AOT ₃₀₀, mmHg × h) was used as a metric of intraoperative hyperoxia and was associated with postoperative AKI, using the logistic regression analysis. Data also were fitted using the restricted cubic spline model. Sensitivity analyses were conducted using different PaO ₂ thresholds (150, 200, 250, and 350 mmHg). A total of 2,926 patients were analyzed. Intraoperative AOT ₃₀₀ independently was associated with the risk of AKI (odds ratio 1.0009; 95% confidence interval 1.0002-1.0015). A PaO ₂ increment of 100 mmHg above PaO ₂ 300 mmHg for an hour was associated with an increased risk of AKI by 9.4% (1.0009 ¹⁰⁰ ≈ 1.094). In the spline model, the log-odds of AKI increased as AOT ₃₀₀ increased. In the sensitivity analyses, AOT ₂₅₀ and AOT ₃₅₀ also significantly were associated with the risk of AKI, whereas AOT ₁₅₀ and AOT ₂₀₀ were not. As the PaO ₂ threshold increased from 150 to 350 mmHg, the odds ratio gradually increased.

Conclusions

Intraoperative hyperoxia significantly was associated with the risk of AKI after cardiac surgery involving cardiopulmonary bypass.