Posttransfusion Increase of Hematocrit per se Does Not Improve Circulatory Oxygen Delivery due to Increased Blood Viscosity.
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.
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.
Robert
R
Zimmerman
Amy G
AG
Tsai
Beatriz Y
BY
Salazar Vázquez
Pedro
P
Cabrales
Axel
A
Hofmann
Jens
J
Meier
Aryeh
A
Shander
Donat R
DR
Spahn
Joel M
JM
Friedman
Daniel M
DM
Tartakovsky
Marcos
M
Intaglietta
D000465:Algorithms; D000740:Anemia / Q000097:blood / Q000628:therapy; D001783:Blood Flow Velocity; D001803:Blood Transfusion / Q000379:methods*; D001809:Blood Viscosity; D004058:Diffusion; D006400:Hematocrit; D006801:Humans; D008962:Models, Theoretical; D010100:Oxygen / Q000008:administration & dosage*; D010101:Oxygen Consumption
D010100:Oxygen