Background and Goal of Study: The most effective rate of fluid resuscitation in haemorrhagic shock is unknown. We performed a randomized crossover pilot study in a healthy volunteer model of compensated haemorrhagic shock. Following venesection of 15ml.kg-1 of blood, participants were randomized to 20mL.kg-1 of crystalloid over 10 minutes (FAST treatment) or 30 minutes (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.

Materials and Methods: We performed a randomized crossover pilot study in a healthy volunteer model of compensated haemorrhagic shock. Following venesection of 15ml.kg-1 of blood, participants were randomized to 20mL.kg-1 of crystalloid over 10 minutes (FAST treatment) or 30 minutes (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.

Results and Discussion: Nine normotensive healthy adult volunteers participated. No significant differences were observed in DO2, and biochemical variables under the SLOW and FAST treatments. Estimated blood volume at baseline was 5.1L. Blood volume was reduced by 16% following venesection, with a corresponding 5% reduction in cardiac index (CI) (p< 0.001). Immediately following resuscitation under the FAST and SLOW treatments, mean (SD) blood volume increased by 720mL (210mL) and 920mL (223mL), respectively (P< 0.03), corresponding to 54% (7%) and 69% (16%) of the infused volume. This blood volume expansion attenuated with time, to 24% and 25% of the infused volume 30 minutes post-infusion. During fluid resuscitation, blood pressure was higher under FAST treatment, however CI paradoxically decreased in most participants, a finding not observed under SLOW treatment.

Conclusions: No significant differences in DO2 were observed between FAST or SLOW fluid resuscitation treatments. Under both treatments, 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%. Myocardial performance was impaired during FAST fluid resuscitation.

Comparative evaluation of fast or slow crystalloid resuscitation on oxygen delivery in a human model of haemorrhagic shock