Renal Veno-Arterial Carbon Dioxide Gap Fails to Detect Renal Medulla Microcirculatory Changes in a Large Animal Model of Sepsis-Associated Acute Kidney Injury.

The difference in carbon dioxide partial pressure between arterial and mixed venous blood has been recognized as a marker of the adequacy of cardiac output. However, the extent to which the global partial pressure of carbon dioxide (pCO 2 ) gap accurately reflects regional organ blood flow and whether it maintains its predictive value in assessing hypoperfusion and microcirculatory dysfunction associated with sepsis, remains to be elucidated. During this experimental study, 12 anaesthetized, mechanically ventilated and instrumented (renal artery flow probe, renal vein catheter and laser Doppler probe placed directly in the renal medulla) pigs were randomized into two groups-systemic infection group (0.5 g/kg of autologous feces intraperitoneally) and sepsis group (1 g/kg of autologous feces intraperitoneally), characterized by the development of sepsis-associated acute kidney injury (SA-AKI). Over a period of 36 hours, sequential direct assessment of renal medulla microcirculatory changes was performed. The collected data were then coupled with both regional and systemic pCO 2 gap, as well as with other hemodynamic variables. The development of SA-AKI was found to be strongly and negatively associated with renal blood flow and microcirculatory dysfunction. Importantly, neither regional nor systemic pCO 2 gap reflected the microcirculatory failure and exhibited a weak to moderate association with renal blood flow. Furthermore, only a poor correlation was observed between systemic and regional gaps. The present study does not support the hypothesis that the regional pCO 2 gap can be adopted as a direct surrogate marker of hypoperfusion in SA-AKI. Carbon dioxide-derived indices should be interpreted with caution in patients with sepsis.