Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity

Robert Zimmerman, Amy G. Tsai, Beatriz Y. Salazar Vázquez, Pedro Cabrales, Axel Hofmann, Jens Meier, Aryeh Shander, Donat R. Spahn, Joel M. Friedman, Daniel M. Tartakovsky, Marcos Intaglietta

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1547-1554
Number of pages8
JournalAnesthesia and Analgesia
Volume124
Issue number5
DOIs
StatePublished - 2017

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Blood Viscosity
Hematocrit
Oxygen
Anemia
Erythrocytes
Blood Transfusion
Blood Flow Velocity
Blood Circulation
Conservation of Natural Resources
Cardiac Output
Hemoglobins
Blood Pressure

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Zimmerman, R., Tsai, A. G., Salazar Vázquez, B. Y., Cabrales, P., Hofmann, A., Meier, J., ... Intaglietta, M. (2017). Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity. Anesthesia and Analgesia, 124(5), 1547-1554. https://doi.org/10.1213/ANE.0000000000002008

Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity. / 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.

In: Anesthesia and Analgesia, Vol. 124, No. 5, 2017, p. 1547-1554.

Research output: Contribution to journalArticle

Zimmerman, R, Tsai, AG, Salazar Vázquez, BY, Cabrales, P, Hofmann, A, Meier, J, Shander, A, Spahn, DR, Friedman, JM, Tartakovsky, DM & Intaglietta, M 2017, 'Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity', Anesthesia and Analgesia, vol. 124, no. 5, pp. 1547-1554. https://doi.org/10.1213/ANE.0000000000002008
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. / Posttransfusion increase of hematocrit per se does not improve circulatory oxygen delivery due to increased blood viscosity. In: Anesthesia and Analgesia. 2017 ; Vol. 124, No. 5. pp. 1547-1554.
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abstract = "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.",
author = "Robert Zimmerman and Tsai, {Amy G.} and {Salazar V{\'a}zquez}, {Beatriz Y.} and Pedro Cabrales and Axel Hofmann and Jens Meier and Aryeh Shander and Spahn, {Donat R.} and Friedman, {Joel M.} and Tartakovsky, {Daniel M.} and Marcos Intaglietta",
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AU - Zimmerman, Robert

AU - Tsai, Amy G.

AU - Salazar Vázquez, Beatriz Y.

AU - Cabrales, Pedro

AU - Hofmann, Axel

AU - Meier, Jens

AU - Shander, Aryeh

AU - Spahn, Donat R.

AU - Friedman, Joel M.

AU - Tartakovsky, Daniel M.

AU - Intaglietta, Marcos

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N2 - 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.

AB - 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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