输血后增加红细胞比容同时增加血液粘度并不改善循环氧输送

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Posttransfusion Increase of Hematocrit per se Does Not Improve Circulatory Oxygen Delivery due to Increased Blood Viscosity

背景与目的

输血用于治疗急性贫血目的是使通过血细胞比容(Hct)和氧气输送DO2来确定的血液携氧能力有所增加。然而,增加Hct也会增加血液粘度,因此如果动脉循环是硬化的液压系统,因为血流阻力会增加氧气运输会降低。输血对该系统DO2的最终影响可以通过使用输血后的Hct即输血后的循环血液的Hct与全身血液粘度之间的关系来计算DO2并将其与预输血前的DO2进行比较来分析。我们假设增加Hct会增加DO2并通过数学建模循环中的DO2来测试我们的假设。

方  法

假设正常心输出量(5 L / min),贫血程度为5%至80%的Hct缺失。假设没有血压变化的影响,我们分析了在65%的Hct时输入0.5个或更多单位的300cc包装红细胞(PRBC)的影响,并计算了考虑到输血后增加血液粘度后微循环的DO2。我们的模型在血液到达营养循环以及血流速度变化之前,将O2扩散到循环中。输血即刻后的DO2也同输血完成血管容积增加时的DO2进行比较。

结  果

当Hct(或血红蛋白)比正常值低60%时,多达3个单位的PRBC输血增加了DO2,但在该阈值之前施用时没有增加DO2。

结  论

考虑到由于Hct的增加会使血液粘度变大从而增加对血流的影响,我们发现在DO2的数学模拟中,输高达3单位的PRBC不会增加DO2,除非贫血是由于Hct减少大于60%的结果。输血偶尔会导致临床改善的结果表明其他可能与血液粘度增加有关的机制可能补偿DO2增加的缺乏。

原始文献摘要

Zimmerman, Robert; Tsai, Amy G.; Salazar Vázquez, Beatriz Y.; More.Posttransfusion Increase of Hematocrit per se Does Not Improve Circulatory Oxygen Delivery due to Increased Blood Viscosity.Anesthesia & Analgesia . 24(5):1547-1554, May 2017.

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.

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