During cell-free volume replacement, hyperoxic ventilation with Fio2 0.6 generates a readily usable plasmatic oxygen reserve and thereby increases the tolerance toward acute normovolemic anemia.

In this present experimental study the infusion of a PEG-modified LEH provided adequate tissue oxygenation, hemodynamic stability, and a prolongation of survival time after critical anemia. However, these effects were sustained for only a short period of time.

Background: During acellular replacement of an acute blood loss, hyperoxic ventilation (HV) increases the amount of O₂ physically dissolved in the plasma and thereby improves O₂ supply to the tissues. While this effect could be demonstrated for HV with inspiratory O₂ fraction (FiO₂) 0.6, it was unclear whether HV with pure oxygen (FiO₂ 1.0) would have an additional effect on the physiological limit of acute normovolemic anemia. Methods: Seven anesthetized domestic pigs were ventilated with FiO₂ 1.0 and subjected to an isovolemic hemodilution protocol. Blood was drawn and replaced by a 6% hydroxyethyl starch (HES) solution (130/0.4) until a sudden decrease of total body O₂ consumption (VO₂) indicated the onset of O₂ supply dependency (primary endpoint). The corresponding hemoglobin (Hb) concentration was defined as ‘critical Hb' (Hb_crit). Secondary endpoints were parameters of myocardial function, central hemodynamics, O₂ transport and tissue oxygenation. Results: HV with FiO₂ 1.0 enabled a large blood-for-HES exchange (156 ± 28% of the circulating blood volume) until Hb_crit was met at 1.3 ± 0.3 g/dl. After termination of the hemodilution protocol, the contribution of O₂ physically dissolved in the plasma to O₂ delivery and VO₂ had significantly increased from 11.7 ± 2 to 44.2 ± 9.7% and from 29.1 ± 4.2 to 66.2 ± 11.7%, respectively. However, at Hb_crit, cardiovascular performance was found to have severely deteriorated. Conclusion: HV with FiO₂ 1.0 maintains O₂ supply to tissues during extensive blood-for-HES exchange. In acute situations, where profound anemia must be tolerated (e.g. bridging an acute blood loss until red blood cells become available for transfusion), O₂ physically dissolved in the plasma becomes an essential source of oxygen. However, compromised cardiovascular performance might require additional treatment.