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Patient-specific susceptibility to the nadir oxygen delivery on cardiopulmonary bypass.

Created on 23 Oct 2025

Authors

Martina Anguissola, Alessandro Barbaria, Roberto Ferrari, Ekaterina Baryshnikova, Giovanna Landi, Marco Ranucci

Published in

European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery. Oct 22, 2025. Epub Oct 22, 2025.

Abstract

Maintaining a nadir oxygen delivery ≥ 280 mL/min/m2 during cardiopulmonary bypass is a pillar of the goal-directed perfusion strategy in cardiac surgery. However, there are patients who develop a cardiac surgery associated acute kidney injury despite an adequate oxygen delivery and others who do not develop an acute kidney injury despite a low oxygen delivery. The present study aims to determine the independent factors associated with these 2 conditions. Methods: Post-hoc analysis of 2 previously published series.
the population size was 1,030 patients. Inability to maintain the target oxygen delivery was found in 35% of the patients, and the independent determinants were female gender, low creatinine clearance, low preoperative hematocrit and non-elective surgery. Acute kidney injury was found in 18.3% of the total patient population. Within the patients with a nadir oxygen delivery < 280 mL/min/m2 73% did not develop an acute kidney injury. These patients were younger, with a lower baseline serum creatinine, shorter cardiopulmonary bypass and lower peak lactate. Within the patients with a nadir oxygen delivery ≥ 280 mL/min/m2 13% developed an acute kidney injury: these patients were older, with a lower baseline hematocrit, land onger cardiopulmonary bypass.
preoperative anemia is the main determinant of a failing goal directed perfusion. In younger patients at short cardiopulmonary bypass may be possible to reduce the target oxygen delivery. Acute kidney injury in patients with a nadir oxygen delivery ≥ 280 mL/min/m2 is a relatively rare condition whose mechanisms remain to be elucidated.

PMID:
41124609
Bibliographic data and abstract were imported from PubMed on 23 Oct 2025.

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