Zimmerman Robert, Tsai Amy G, Salazar Vázquez Beatriz Y, Cabrales Pedro, Hofmann Axel, Meier Jens, Shander Aryeh, Spahn Donat R, Friedman Joel M, Tartakovsky Daniel M, Intaglietta Marcos
From the *Departments of Mechanical Engineering; †Bioengineering, University of California, San Diego, La Jolla, California; ‡Department of Experimental Medicine, School of Medicine, Universidad Nacional Autónoma de México, México, DF, México; §Department of Odontology, Universidad Juárez del Estado de Durango, Durango, Dgo, México; ‖School of Surgery, Faculty of Medicine Dentistry and Health Sciences, University of Western Australia, and Centre for Population Health Research, Curtin University, Perth, Western Australia, Australia; ¶Institute of Anesthesiology, University of Zurich and University Hospital Zurich, Zurich, Switzerland; #Clinic of Anesthesiology and Intensive Care, Faculty of Medicine, Kepler University Linz, Austria; **Department of Anesthesiology, Critical Care Medicine, Pain Management and Hyperbaric Medicine at Englewood Hospital & Medical Center, Director TeamHealth Research Institute, Englewood, New Jersey; and ††Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York.
Anesth Analg. 2017 May;124(5):1547-1554. doi: 10.1213/ANE.0000000000002008.
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.
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.
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.
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.
输血用于治疗急性贫血，目标是提高血细胞比容（Hct）和氧输送量（DO2）所决定的血液携氧能力。然而，Hct升高也会增加血液黏度，如果动脉循环是一个刚性液压系统，由于血流阻力增加，这可能会降低DO2。通过利用输血后Hct时循环血液的Hct与全身血液黏度之间的关系来计算DO2，并将该值与输血前的DO2进行比较，可以分析该系统中输血对DO2的净效应。我们假设增加Hct会增加DO2，并通过对循环中的DO2进行数学建模来检验我们的假设。
假设心输出量正常（5升/分钟），血细胞比容缺乏程度为5%至80%，进行计算。我们分析了在血细胞比容为65%时输注0.5单位或更多单位300毫升浓缩红细胞（PRBC）的效果，并在考虑血液黏度增加且假设血压无变化的情况下计算了微循环DO2。我们的模型考虑了血液到达营养循环之前从循环中扩散出的氧气以及血流速度的变化。还将输血后即刻的DO2与输血导致的容量短暂增加消退后的DO2进行了比较。
当Hct（或血红蛋白）比正常水平低60%时，输注多达3单位的PRBC会增加DO2，但在该阈值之前进行输血时不会增加DO2。
在考虑到因Hct升高导致血液黏度增加对血流的影响后，我们在对DO2的数学模拟中发现，输注多达3单位的PRBC不会增加DO2，除非贫血是由Hct缺乏大于60%所致。输血偶尔会导致临床改善的观察结果表明，可能与血液黏度增加相关的其他机制可能会弥补DO2未增加的情况。
