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Red blood cell transfusion does not increase oxygen consumption in critically ill septic patients

Published by National Institutes of Health | U.S. Department of Health & Human Services | Metadata Last Checked: September 07, 2025 | Last Modified: 2025-09-06
Background Red blood cell (RBC) transfusion is commonly used to increase oxygen transport in patients with sepsis. However it does not consistently increase oxygen uptake at either the whole-body level, as calculated by the Fick method, or within individual organs, as assessed by gastric intra-mucosal pH. Aim This study evaluates the hemodynamic and oxygen utilization effects of hemoglobin infusion on critically ill septic patients. Methods Fifteen septic patients undergoing mechanical ventilation whose hemoglobin was <10 g% were eligible. Ten patients (APACHE II: 25.5 ± 7.6) received an infusion of 1 unit of packed RBC over 1 h while sedated and paralyzed. The remaining five control patients (APACHE II: 24.3 ± 6.0) received a 5% albumin solution (500 ml) over 1 h. Hemodynamic data, gastric tonometry and calorimetry were obtained prior to and immediately after RBC transfusion or 5% albumin infusion. Results Transfusion of RBC was associated with an improvement in left ventricular systolic work index (38.6 ± 12.6 to 41.1 ± 13.0 g/min/m2; P = 0.04). In the control group there was no significant change in the left ventricular systolic work index (37.2 ± 14.3 to 42.2 ± 18.9 g/min/m2). An increase in pulmonary vascular resistance index (203 ± 58 to 238 ± 49 dyne/cm5/m2; P = 0.04) was also observed, while no change was produced by colloid infusion (237 ± 87.8 to 226.4 ± 57.8 dyne/cm5/m2). Oxygen utilization did not increase either by Fick equation or by indirect calorimetry in either group. Gastric intramucosal pH increased only in the control group but did not reach statistical significance. Conclusion Hemoglobin increase does not improve either global or regional oxygen utilization in anemic septic patients. Furthermore, RBC transfusion may hamper right ventricular ejection by increasing the pulmonary vascular resistance index.

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