• H Gässler, T Stenzl, E Calzia, L Lampl, M Georgieff, P Radermacher, and S Hafner.
• 1Department of Anaesthesiology and Intensive Care Medicine, Armed Forces Medical Centre, Ulm, Germany 2Institute APV, Ulm University, Ulm, Germany 3Department of Anaesthesiology and Intensive Care Medicine, Ulm University, Ulm, Germany.
• Shock. 2015 Oct 1;44 Suppl 2:3.

IntroductionHaemorrhagic shock (HS) increases mortality after severe trauma, due to tissue hypoxia-induced multiple organ failure. Hyperoxia, i.e. pure O2 breathing, can improve haemodynamics and organ function, but may worsen lung function due to oxidative stress. Therefore, we tested the hypothesis whether hyperoxia would attenuate organ dysfunction after haemorrhage.MethodsAfter 3 hours of HS (withdrawal of ∼30% of calculated blood volume and subsequent titration of mean arterial pressure (MAP) to ∼40mmHg), anaesthetized and mechanically ventilated pigs were randomly assigned to 12 hours of hyperoxia or ventilation at an FiO2 to maintain haemoglobin O2 saturation > 95% ("normoxia") (n = 9 each) together with resuscitation comprising blood re-transfusion and i.v. noradrenaline to restore MAP to pre-shock values. From 12-23 hours of resuscitation normoxia was applied in both groups. Systemic and regional haemodynamics, blood gas analysis, acid-base status, metabolism and renal function were assessed before and at the end of HS and at 12 and 23 hours after HS.ResultsHyperoxia significantly increased the PaO2/FiO2 at 12 hours post-HS. None of the other parameters of haemodynamics, gas exchange, metabolism and renal function showed any inter-group difference.ConclusionIn our model of non-lethal haemorrhage and resuscitation, hyperoxia did not attenuate any parameter of circulatory failure or organ dysfunction. However, hyperoxia appeared to be safe with respect to oxidative stress and/or lung injury.Acknowledgement: Supported by German Department of Defence (AZ E/U2AD/CF523/DF556).

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