Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity

BACKGROUND: Blood transfusion is used to treat acute anemia with the goal of increasing blood oxygen-carrying capacity as determined by hematocrit (Hct) and oxygen delivery (DO₂). However, increasing Hct also increases blood viscosity, which may thus lower DO₂ if the arterial circulation is a rigid hydraulic system as the resistance to blood flow will increase. The net effect of transfusion on DO₂ in this system can be analyzed by using the relationship between Hct and systemic blood viscosity of circulating blood at the posttransfusion Hct to calculate DO₂ and comparing this value with pretransfusion DO₂. We hypothesized that increasing Hct would increase DO₂ and tested our hypothesis by mathematically modeling DO₂ in the circulation. METHODS: Calculations were made assuming a normal cardiac output (5 L/min) with degrees of anemia ranging from 5% to 80% Hct deficit. We analyzed the effects of transfusing 0.5 or more units of 300 cc of packed red blood cells (PRBCs) at an Hct of 65% and calculated microcirculatory DO₂ after accounting for increased blood viscosity and assuming no change in blood pressure. Our model accounts for O2 diffusion out of the circulation before blood arriving to the nutritional circulation and for changes in blood flow velocity. The immediate posttransfusion DO₂ was also compared with DO₂ after the transient increase in volume due to transfusion has subsided. RESULTS: Blood transfusion of up to 3 units of PRBCs increased DO₂ when Hct (or hemoglobin) was 60% lower than normal, but did not increase DO₂ when administered before this threshold. CONCLUSIONS: After accounting for the effect of increasing blood viscosity on blood flow owing to increasing Hct, we found in a mathematical simulation of DO₂ that transfusion of up to 3 units of PRBCs does not increase DO₂, unless anemia is the result of an Hct deficit greater than 60%. Observations that transfusions occasionally result in clinical improvement suggest that other mechanisms possibly related to increased blood viscosity may compensate for the absence of increase in DO₂.