Fine-Mapping the Association of Acute Kidney Injury With Mean Arterial and Central Venous Pressures During Coronary Artery Bypass Surgery.

BACKGROUND

Prior studies identified thresholds for mean arterial pressure (MAP <65 mm Hg) and central venous pressure (CVP >12 mm Hg) beyond which risk for cardiac surgery-associated acute kidney injury (AKI) increases. Optimal hemodynamic targets-that is, where active protection from AKI is observed-are unclear; however, current guidelines suggest maintaining MAP >65 and CVP 8 to 12. The aim of this study was to identify hemodynamic ranges associated with both increased and decreased risk of AKI by evaluating narrow ranges of MAP, CVP, and joint exposure to MAP and CVP concurrently.

METHODS

In a retrospective cohort study of adults undergoing coronary artery bypass surgery, we fine-mapped the association between AKI and the total number of minutes spent in each of the following narrow hemodynamic ranges: 14 MAP ranges in increments of 5 mm Hg (45-115), 10 CVP ranges in increments of 2 mm Hg (0-20), and 70 joint MAP/CVP ranges. Separate multivariable regression models estimated adjusted odds ratios (aOR) for each range including adjustments for correlations and multiple comparisons across ranges. Joint MAP/CVP ranges were grouped into 5 hemodynamic zones based on contiguity of the ranges and similarity of ORs observed across ranges in a color-coded heatmap. The 5 MAP/CVP zones were included in a single regression model to assess risk for AKI associated with time spent in each hemodynamic zone, independent of time spent in other zones.

RESULTS

In 1199 participants, incidence of AKI was 28%. For every 5-minute spent in each hemodynamic range, risk of AKI was significantly increased in MAP range 45 to 50 (aOR 1.18; P = .002), 50 to 55 (aOR 1.13; P = .001), and 55 to 60 mm Hg (aOR 1.06; P = .001); and significantly decreased in MAP range 90 to 95 mm Hg (aOR 0.85; P <.001). Risk of AKI was significantly increased in CVP range 16 to 18 mm Hg (aOR 1.07; P = .002) and significantly decreased in CVP range 4 to 6 mm Hg (aOR 0.97; P = .025). In joint analyses, both MAP and CVP contributed to AKI risk estimates; risk decreased as CVP decreased within every MAP range and was significantly lower for joint ranges of CVP <8 and MAP >75. In analyses containing all 5 MAP/CVP hemodynamic zones, risk estimates suggested protection from AKI in zone 1 (high MAP/low CVP) and increased risk of AKI in zones 3 to 5 (low MAP/high CVP).

CONCLUSIONS

Fine-mapping identified narrow ranges of MAP, CVP, and joint MAP/CVP associated with both AKI risk and protection. This report is among the first to characterize the association between joint MAP/CVP and AKI. Contrary to current guidelines, there was no evidence for protection associated with MAP 65 to 75 or CVP 8 to 12 mm Hg.