Abstract
BackgroundThe microvascular reperfusion injury after retransfusion has not been completely characterized. Specifically, the question of heterogeneity among different microvascular beds needs to be addressed. In addition, the identification of anaerobic metabolism is elusive. The venoarterial PCO2 to arteriovenous oxygen content difference ratio (Pv-aCO2/Ca-vO2) might be a surrogate for respiratory quotient, but this has not been validated. Therefore, our goal was to characterize sublingual and intestinal (mucosal and serosal) microvascular injury after blood resuscitation in hemorrhagic shock and its relation with O2 and CO2 metabolism.MethodsAnesthetized and mechanically ventilated sheep were assigned to stepwise bleeding and blood retransfusion (n = 10) and sham (n = 7) groups. We performed analysis of expired gases, arterial and mixed venous blood gases, and intestinal and sublingual videomicroscopy.ResultsIn the bleeding group during the last step of hemorrhage, and compared to the sham group, there were decreases in oxygen consumption (3.7 [2.8–4.6] vs. 6.8 [5.8–8.0] mL min−1 kg−1, P < 0.001) and increases in respiratory quotient (0.96 [0.91–1.06] vs. 0.72 [0.69–0.77], P < 0.001). Retransfusion normalized these variables. The Pv-aCO2/Ca-vO2 increased in the last step of bleeding (2.4 [2.0–2.8] vs. 1.1 [1.0–1.3], P < 0.001) and remained elevated after retransfusion, compared to the sham group (1.8 [1.5–2.0] vs. 1.1 [0.9–1.3], P < 0.001). Pv-aCO2/Ca-vO2 had a weak correlation with respiratory quotient (Spearman R = 0.42, P < 0.001). All the intestinal and sublingual microcirculatory variables were affected during hemorrhage and improved after retransfusion. The recovery was only complete for intestinal red blood cell velocity and sublingual total and perfused vascular densities.ConclusionsAlthough there were some minor differences, intestinal and sublingual microcirculation behaved similarly. Therefore, sublingual mucosa might be an adequate window to track intestinal microvascular reperfusion injury. Additionally, Pv-aCO2/Ca-vO2 was poorly correlated with respiratory quotient, and its physiologic behavior was different. Thus, it might be a misleading surrogate for anaerobic metabolism.
Highlights
The microvascular reperfusion injury after retransfusion has not been completely characterized
Observational studies found that venoarterial PCO2 difference (Pv-aCO2) to arteriovenous oxygen content difference (Ca-vO2) ratio might be a surrogate for respiratory quotient (RQ) [9, 10]
Each variable was normalized after retransfusion, but at 2′, Cardiac index (CI) and superior mesenteric artery to measure blood flow (SMABF) were higher than baseline
Summary
The microvascular reperfusion injury after retransfusion has not been completely characterized. The restoration of systemic oxygen transport may not prevent the development of multiple organ failure Possible explanations for this phenomenon are the oxygen debt accumulated during shock [1], the reperfusion injury mainly related to oxygen species production [2], and the persistent depression of microvascular perfusion [3]. Observational studies found that venoarterial PCO2 difference (Pv-aCO2) to arteriovenous oxygen content difference (Ca-vO2) ratio might be a surrogate for RQ [9, 10] This assumption relies on Fick’s principle, which states that VCO2 and VO2 can be calculated as the product of cardiac output by the respective venoarterial content difference. Those studies have not compared Pv-aCO2/Ca-vO2 with RQ
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