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.