Mitochondrial oxygen tension in critically ill patients receiving red blood cell transfusions: a multicenter
M Baysan1,2,3, B Hilderink4,5, L van Manen4
1Department of Intensive Care Medicine, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.
Purpose:
Currently, there is no marker of efficacy of red blood cell (RBC) transfusion. This study describes the impact of RBC transfusion on mitochondrial oxygen tension (mitoPO2) and mitochondrial oxygen consumption (mitoVO2) in critically ill patients with anemia.
Methods:
Critically ill patients with a hemoglobin concentration < 10 g/dL, for whom a single RBC unit had been ordered, were included. MitoPO2 was measured with the COMET device immediately before RBC transfusion, 0.5 h, 1 h, 3 h, and 24 h after RBC transfusion. MitoVO2 was calculated from dynamic mitoPO2 measurements during cessation of local oxygen supply.
Results:
Sixty-three patients participated, median age 64.0 (interquartile range (IQR) 52.3-72.8) years, median hemoglobin concentration before transfusion 7.4 (IQR 7.1-7.7) g/dL. Median mitoPO2 values were 55.0 (IQR 49.6-63.0) mmHg before RBC transfusion, 51.0 (IQR 41.5-61.2) directly after and 67.3 (IQR 41.6-83.7) at 24 h after RBC transfusion. Median mitoVO2 values were 3.3 (IQR 2.1-5.9) mmHg/s before RBC transfusion, 3.7 (IQR 2.0-5.1) mmHg/s directly after, and 3.1 (IQR 2.5-4.8) mmHg/s 24 h after RBC transfusion. In the higher Hb concentration group (> 7 g/dL), we saw a dissociation of the effect of RBC transfusion on mitoPO2 versus on mitoVO2 values. MitoPO2 and mitoVO2 values were not associated with commonly used parameters of tissue perfusion and oxygenation.
Conclusion:
RBC transfusion did not alter mitoPO2 and mitoVO2 in critically ill patients with anemia. MitoPO2 and mitoVO2 values were not notably associated with Hb concentrations, parameters of severity of illness and markers of tissue perfusion or oxygenation. Given the high baseline value, it cannot be excluded nor confirmed whether RBC can improve low mitoPO2. Trial registration number NCT03092297 (registered 27 March 2017).
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