Alterations in Coagulation Induced by Hypothermia and Acidosis in Swine1

Although clinical coagulopathy is associated with acidosis and hypothermia, the underlying mechanisms by which these factors alter the coagulation process remains unclear. The primary purpose of this study was to investigate the contributory effects of acidosis and hypothermia to the development of coagulopathy. Twentyfour pigs were randomly divided into control (pH 7.4, 39°C), acidotic (pH 7.1, 39°C), hypothermic (pH 7.4, 32°C), and combined acidotic-hypothermic (pH 7.1, 32°C) groups (n=6/group). Acidosis and hypothermia were introduced by infusion of 0.2M HCl and using a blanket with circulating cold water (4°C), respectively. Measurements were compared before (pre) and 10 min after the induction of acidosis and hypothermia (post). Development of coagulopathy was defined as a significant increase in splenic bleeding time in vivo. Coagulopathy developed shortly after the induction of acidosis and/or hypothermia. Splenic bleeding time was prolonged by 41%, 57%, and 72% in acidotic, hypothermic, and the combined groups (p<0.05, pre vs post in each group), respectively. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis caused both a delay in the onset of thrombin generation and an impairment in thrombin generation rate. The reaction time (latency time for initial clot formation) of the thromboelastogram (TEG) was prolonged in the hypothermia and the combined groups, but not in the acidotic group. The α-angle (the rapidity of fibrin build up and cross linking) of the TEG was reduced in the acidosis and combined groups, but not in the hypothermia group. We conclude that acidosis and hypothermia cause coagulopathy via different mechanisms.