• Loretta Ho, Lawrence Lau, Leonid Churilov, Bernhard Riedel, Larry McNicol, Robert G Hahn, and Laurence Weinberg.
• *Department of Anaesthesia, Austin Hospital, University of Melbourne, Heidelberg, Victoria, Australia †Department of Surgery, Austin Hospital, University of Melbourne, Heidelberg, Victoria, Australia ‡The Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, Melbourne, Victoria, Australia §Department of Anaesthesia, Peter MacCallum Cancer Centre, University of Melbourne, Melbourne, Victoria, Australia ||Department of Anaesthesia, Austin Hospital, Heidelberg, Victoria, Australia ¶Department of Surgery and Anaesthesia Perioperative Pain Medicine Unit, University of Melbourne, Melbourne, Victoria, Australia **Södertälje Hospital, Linköping University, Linköping, Sweden ††Karolinska Institutet, Stockholm, Sweden ‡‡Department of Anaesthesia, Austin Hospital, Heidelberg, Victoria, Australia §§Department of Surgery and Anaesthesia Perioperative Pain Medicine Unit, University of Melbourne, Melbourne, Victoria, Australia.
• Shock. 2016 Aug 1; 46 (2): 149-57.

IntroductionThe most effective rate of fluid resuscitation in haemorrhagic shock is unknown.MethodsWe performed a randomized crossover pilot study in a healthy volunteer model of compensated haemorrhagic shock. Following venesection of 15 mL/kg of blood, participants were randomized to 20 mL/kg of crystalloid over 10 min (FAST treatment) or 30 min (SLOW treatment). The primary end point was oxygen delivery (DO2). Secondary end points included pressure and flow-based haemodynamic variables, blood volume expansion, and clinical biochemistry.ResultsNine normotensive healthy adult volunteers participated. No significant differences were observed in DO2 and biochemical variables between the SLOW and FAST groups. Blood volume was reduced by 16% following venesection, with a corresponding 5% reduction in cardiac index (CI) (P < 0.001). Immediately following resuscitation the increase in blood volume corresponded to 54% of the infused volume under FAST treatment and 69% of the infused volume under SLOW treatment (P = 0.03). This blood volume expansion attenuated with time to 24% and 25% of the infused volume 30 min postinfusion. During fluid resuscitation, blood pressure was higher under FAST treatment. However, CI paradoxically decreased in most participants during the resuscitation phase; a finding not observed under SLOW treatment.ConclusionFAST or SLOW fluid resuscitation had no significant impact on DO2 between treatment groups. In both groups, changes in CI and blood pressure did not reflect the magnitude of intravascular blood volume deficit. Crystalloid resuscitation expanded intravascular blood volume by approximately 25%.

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