Hypothermia-induced coagulopathy during hemorrhagic shock

A porcine model of hemorrhagic shock was used to study the effect of hypoth ermia on hemodynamic, metabolic, and coagulation parameters. The model was designed to simulate the events of severe blunt injury with hemorrhage occu rring initially, to a systolic blood pressure of 30 mm Hg, followed by simu ltaneous hemorrhage and crystalloid volume replacement, followed by cessati on of hemorrhage and blood replacement. Half of the animals were rendered h ypothermic by external application of ice, and half remained normothermic, There was seven pigs in each group. Two deaths occurred in each during the hemorrhage phase. The hypothermic pigs demonstrated larger reduction in car diac output than normothermic pigs. Volume replacement in the normothermic group restored cardiac output to baseline values. In the hypothermic group, cardiac output remained depressed despite volume replacement. Prothrombin times and partial thromboplastin times showed significantly more prolongati on in the hypothermic group. Furthermore, this was not corrected by replace ment of shed blood in the hypothermic group, as was seen in the normothermi c group. We conclude that when shock and hypothermia occur together, their deleterious effect on hemodynamic and coagulation parameters are additive. The effects of hypothermia persist despite the arrest of hemorrhage and vol ume replacement. Thus, it is necessary to aggressively address both shock a nd hypothermia when they occur simultaneously.