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.