Coagulation changes to systemic acidosis and bicarbonate correction in swine

As part of our overall interest in the mechanisms and treatment related to the development of the lethal triad of hypothermia, acidosis, and coagulopathy seen in trauma patients, the purpose of this study was to determine whether acidosis, inducible either by HCl infusion or hemorrhage/hypoventilation, leads to coagulopathy, and if correction of the acidosis will alleviate this coagulopathy.

In two separate experiments, acidosis was induced in anesthetized swine by (1) HCl infusion (n = 10) or (2) hemorrhage/hypoventilation (n = 8). Arterial blood samples were taken before HCl infusion or hemorrhage (arterial pH 7.4), after HCl infusion or hemorrhage (pH 7.1), and after bicarbonate infusion to return pH to 7.4. Arterial pH and blood gases were measured every 15 minutes.

Acidosis (arterial pH 7.1) led to a hypocoagulation as measured by several coagulation parameters. In both experiments, acidosis was associated with a significant decrease in the maximum strength of the clot and the rate at which the clot formed. There was a significant decrease in endogenous thrombin potential and maximum thrombin concentration after acidosis in both groups (thrombin generation assay). However, the activated clotting time, prothrombin time, and activated partial thromboplastin time were significantly elevated only in the HCl-infused group. Fibrinogen concentration and platelet count were significantly reduced in both groups after acidosis. The hypocoagulation that was induced by either hemorrhage/hypoventilation or HCl infusion was not immediately corrected after returning pH to 7.4 with bicarbonate injection.

These data suggest that acidosis induced by HCl infusion or by hemorrhage/hypoventilation leads to hypocoagulation. Simple correction of the arterial pH with bicarbonate is not sufficient to correct this coagulopathy.