Abstract
To use blood lactate (BL) as an end-point metabolic marker for the begin resuscitation of volume replacement in experimental hemorrhagic shock. Group I (n=7) was not bled (Control). Animals in Group II (n=7) were bled to a MAP of 30mmHg in thirty minutes. Hemodynamic and metabolic data were recorded at Baseline, at 30, 60 and 120 minutes after Baseline. The animals were intubated in spontaneous breathing (FIO2=0.21) with halothane. Group I all survived. In Group II all died; no mortality occurred before a BL<10mM/L. Beyond the end-point all animals exhibited severe acidemia, hyperventilation and clinical signs of shock. Without treatment all animals died within 70.43±24.51 min of hypotension shortly after reaching an average level of BL 17.01±3.20mM/L. Swine's breathing room air spontaneously in hemorrhagic shock not treated a blood lactate over 10mM/L results fatal. The predictable outcome of this shock model is expected to produce consistent information based on possible different metabolic and hemodynamic patterns as far as the type of fluid and the timing of resuscitation in near fatal hemorrhagic shock.
Highlights
Animal experiments done in laboratories suffer some limitations when compared to patients in hemorrhagic shock
The removal of blood through a catheter targeted to a given volume or to a mean arterial pressure (MAP) may not simulate a fulminating bleeding that has ceased immediately[1] or a persistent bleeding by an open vessel, a situation known as uncontrolled bleeding[2]
30mmHg exhibited a prompt increase in mean arterial pressure as soon as halothane was reduced from 1 to 0.5%, so that it was possible to remove an additional amount of blood
Summary
Animal experiments done in laboratories suffer some limitations when compared to patients in hemorrhagic shock. The removal of blood through a catheter targeted to a given volume or to a mean arterial pressure (MAP) may not simulate a fulminating bleeding that has ceased immediately[1] or a persistent bleeding by an open vessel, a situation known as uncontrolled bleeding[2]. In spite of these limitations, the use of a model of hemorrhagic shock is valuable, in order to simulate most of the serious acute hemorrhages observed clinically and to induce a low perfusion state for a period long enough to produce hemodynamic and metabolic effects that may lead to the death of the animal. In other words, surviving animals in hemorrhagic shock, driven, either by pressure or by predetermined volume, did not exhibit systematic and reproducible significant changes in base deficit or lactate levels in the blood
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