The Viscosity Target in Hemorrhagic Shock

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We read with great interest the article published in a recent issue of Critical Care Medicine by Tanaka et al (1) describing the effect of RBC transfusion on sublingual microcirculation in hemorrhagic shock (HS). The authors explain the improvement in sublingual microcirculation after RBC transfusion as due to one erythrocyte property. Erythrocytes in hypoxic conditions may sense tissue oxygen tension and couple this information with the release of vasodilatory agents such as adenosine triphosphate or nitric oxide (NO), ensuring blood flow to hypoxic tissue. However, this erythrocyte capability is altered by blood storage (2). Fresh blood transfusion improves microcirculation more than stored blood transfusion in experimental HS. There could be another mechanism to explain the improvement in microcirculation by stored RBC transfusion.
Wall shear stress (WSS) is a crucial agonist enabling the endothelium release of NO, ensuring precapillary vasodilation and capillary perfusion. RBC transfusion, by enhancing hematocrit, may increase viscosity, WSS, and NO production (WSS = wall share rate [WSR] × viscosity). In an elegant study of HS in a murine model, Cabrales et al (3) demonstrate that fresh RBCs without oxygen-carrying capacity restore blood viscosity, reinstate microvascular conditions, and enhance systemic hemodynamics. Thus using hyperviscous plasma expander also improves microcirculation variables in experimental HS. Studies describing the effect of hemodilution on microcirculation have suggested that the functional lower limit in the decrease in RBC concentration is mainly determined by the drop in blood viscosity rather than the reduction in oxygen-carrying capacity. Finally, blood viscosity is not affected by blood storage. In the present study, microcirculation improvement after stored blood transfusion is mainly explained by blood viscosity enhancing.
Experimental HS models have shown that the impairment of functional capillary density (FCD) is the main determinant of outcome. During HS, viscosity and WSR decrease leading to WSS and capillary perfusion impairment. The viscosity target consists of sustaining blood viscosity by rapid blood transfusion to avoid capillary collapse, FCD lowering, and maintaining microcirculatory flow until the hemorrhage is controlled. Also, reducing fluid resuscitation avoids viscosity decrease.
The controlled resuscitation strategy trial (4) (fluid restriction in trauma shock) may illustrate the viscosity target. The treated group received less fluid resuscitation and earlier blood transfusion, leading to sustained blood viscosity. Mortality in this group decreased significantly.
As the authors noted, hemoglobinemia could not predict microcirculatory response after blood transfusion. In experimental HS described by Kerger et al (5), 2 hours after withdrawal of 70% blood volume, hemoglobin level decreased to only 8.4 g/dL and 20% of the animals died before transfusion. Hemoglobinemia could not reflect blood loss or predict microcirculatory response after transfusion.
As demonstrated by Wiggers et al (6) in 1945, in experimental HS, delayed blood retransfusion fails to save animals. In experimental studies, the primary advantage of earlier transfusion is to sustain microcirculatory perfusion, which inhibits activation of irreversible shock mediators such as inducible NO synthase. Reducing transfusion delay may then decrease mortality rate.
It seems difficult to guide the transfusion strategy on the hemoglobin level at 8 g/dL as recommended in traumatic HS, especially if blood loss is ongoing.
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