The Limit of Anemia Tolerance during Hyperoxic Ventilation with Pure Oxygen in Anesthetized Domestic Pigs

Background: During acellular replacement of an acute blood loss,hyperoxic ventilation (HV) increases the amount of O-2 physicallydissolved in the plasma and thereby improves O-2 supply to the tissues.While this effect could be demonstrated for HV with inspiratory O-2fraction (FiO(2)) 0.6, it was unclear whether HV with pure oxygen(FiO(2) 1.0) would have an additional effect on the physiological limitof acute normovolemic anemia. Methods: Seven anesthetized domestic pigswere ventilated with FiO(2) 1.0 and subjected to an isovolemichemodilution protocol. Blood was drawn and replaced by a 6%hydroxyethyl starch (HES) solution (130/0.4) until a sudden decrease oftotal body O-2 consumption (VO2) indicated the onset of O-2 supplydependency (primary endpoint). The corresponding hemoglobin (Hb)concentration was defined as ‘ critical Hb’ (Hb crit). Secondaryendpoints were parameters of myocardial function, central hemodynamics,O-2 transport and tissue oxygenation. Results: HV with FiO(2) 1.0enabled a large blood-for-HES exchange (156 +/- 28% of the circulatingblood volume) until Hb crit was met at 1.3 +/- 0.3 g/dl. Aftertermination of the hemodilution protocol, the contribution of O 2physically dissolved in the plasma to O-2 delivery and VO2 hadsignificantly 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 FiO(2) 1.0 maintains O-2 supply to tissues duringextensive blood-for-HES exchange. In acute situations, where profoundanemia must be tolerated (e.g. bridging an acute blood loss until redblood cells become available for transfusion), O-2 physically dissolvedin the plasma becomes an essential source of oxygen. However,compromised cardiovascular performance might require additionaltreatment