A Mechanistic Analysis of Possible Blood Transfusion Failure to Increase Circulatory Oxygen Delivery in Anemic Patients

Abstract

The effects of changing hematocrit (Hct) on the rate of circulatory oxygen ( \(\hbox {O}_2\) ) delivery were modeled analytically to describe transfusion of 0.5–3.0 units of packed red blood cells (pRBC, 300 mL/unit, 60% Hct) to anemic patients. In our model, Hct affects \(\hbox {O}_2\) delivery to the microcirculation by changing blood \(\hbox {O}_2\) carrying capacity and blood viscosity, which in turn affects blood flow velocity and, therefore, \(\hbox {O}_2\) delivery. Changing blood velocity impacts the \(\hbox {O}_2\) delivery by affecting the oxygen diffusive losses as blood transits through the arteriolar vasculature. An increase in Hct has two opposite effects: it increases the blood \(\hbox {O}_2\) carrying capacity and decreases the flow velocity. This suggests the existence of an optimal Hct that maximizes \(\hbox {O}_2\) delivery. Our results show that maximal \(\hbox {O}_2\) delivery occurs in the anemic range, where \(\text {Hct} < 39\) %. Optimal blood management is associated with transfusing enough units up to reaching maximal \(\hbox {O}_2\) delivery. Although somewhat complex to implement, this practice would result in both substantial blood savings and improved \(\hbox {O}_2\) delivery.

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