title: Hyperoxic ventilation at the critical haematocrit.
abstract: OBJECTIVE
  During normovolaemic haemodilution arterial O(2)-content decreases exponentially. Nevertheless, tissue oxygenation is first maintained initially by increased organ perfusion and O(2)-extraction. As soon as these compensatory mechanisms are exhausted, myocardial ischaemia and tissue hypoxia occur at an individual 'critical' haematocrit (Hct) value. This study was conducted in order to assess whether tissue hypoxia at the critical Hct is reversed by hyperoxic ventilation with 100% O(2).
  
  
  METHODS
  Eighteen anaesthetized pigs were ventilated with room air and were hemodiluted by 1:1 exchange of blood with 6% pentastarch to their individual critical Hct (onset of myocardial ischaemia; significant ECG changes). At the critical Hct, hyperoxic ventilation was initiated. In nine complete datasets, global O(2) delivery and consumption, local tissue O(2) partial pressure (tpO(2)) (MDO-Electrode, Eschweiler, Kiel, Germany) and organ blood flow (microsphere method) in skeletal muscle were analyzed at baseline, after haemodilution to the critical Hct and after 15 min of hyperoxic ventilation.
  
  
  RESULTS
  At the critical Hct (7.2+/-1.2%), tpO(2) was reduced from 23+/-3 to 10+/-2 Torr with 50% of all values in the hypoxic range (<10 Torr, all P<0.05). During hyperoxic ventilation, contribution of physically dissolved O(2) to the O(2) delivery and O(2) consumption increased by 400 and 563% (P<0.05) and instantly restored tpO(2) to 18+/-2 Torr, (hypoxic values 25%, P<0.05).
  
  
  CONCLUSIONS
  Hyperoxic ventilation reversed tissue hypoxia at the critical Hct due to preferential utilization of plasma O(2) and allowed temporary preservation of tissue oxygenation. During haemodilution, hyperoxic ventilation might offer an effective bridge until red cells are ready for transfusion.
authors.affiliation: Institute for Surgical Research, Klinikum Grosshadern, Ludwig-Maximilians-University Munich, Marchioninistr 15, 81366 München, Germany. gregor.kemming@icf.med.uni-muenchen.de
authors.forename: G I
authors.initials: GI
authors.lastname: Kemming
authors.forename: F G
authors.initials: FG
authors.lastname: Meisner
authors.forename: M
authors.initials: M
authors.lastname: Kleen
authors.forename: J M
authors.initials: JM
authors.lastname: Meier
authors.forename: J
authors.initials: J
authors.lastname: Tillmanns
authors.forename: J W
authors.initials: JW
authors.lastname: Hutter
authors.forename: C J
authors.initials: CJ
authors.lastname: Wojtczyk
authors.forename: K B
authors.initials: KB
authors.lastname: Packert
authors.forename: D
authors.initials: D
authors.lastname: Bottino
authors.forename: O P
authors.initials: OP
authors.lastname: Habler
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D003326:Coronary Circulation; D004562:Electrocardiography; D006400:Hematocrit; D006438:Hemodilution / Q000009:adverse effects; D006439:Hemodynamics; D018496:Hyperoxia; D018482:Muscle, Skeletal / Q000378:metabolism; D017202:Myocardial Ischemia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D010102:Oxygen Inhalation Therapy; D010313:Partial Pressure; D013552:Swine; D014661:Vasoconstriction
chemical_list: D010100:Oxygen