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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Hyperoxic ventilation enables hemodilution beyond the critical myocardial hemoglobin concentration.

BACKGROUND: When initiated in anemic hypoxia, hyperoxic ventilation (ventilation with pure O2, FiO2 1.0, HV) reverses hypoxia-induced ECG-changes and enables survival for several hours. The quantification of the HV-induced gain in anemia tolerance and particularly the Hb-equivalent of HV in this situation are unknown. METHODS: Nine anaesthetized pigs were hemodiluted under normoxia (FiO2 0.21) by exchange of whole blood for hydroxyethyl starch (HES) until predefined, ischemia associated ECG-changes occurred (timepoint Hb(crit)). From that time on all animals were ventilated with 100% O2 (FiO2 1.0). In the case of disappearance of the ECG changes with onset of HV, the animals were further hemodiluted until ECG changes reoccurred. RESULTS: HV initiated in anemic hypoxia (Hb 2.3 +/- 0.2 g/dl) improved ECG-readings of all animals, and allowed for a further exchange of 14 +/- 11 ml/kg blood until ECG-changes reoccurred at Hb 1.2 +/- 0.4 g/dl. CONCLUSION: HV initiated in anemic hypoxia creates a margin of safety for myocardial tissue oxygenation and thus further increases anemia tolerance. The Hb equivalent of HV in this situation amounts to approximately 1g/dl.[1]

References

  1. Hyperoxic ventilation enables hemodilution beyond the critical myocardial hemoglobin concentration. Meier, J., Kemming, G., Meisner, F., Pape, A., Habler, O. Eur. J. Med. Res. (2005) [Pubmed]
 
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