HEMOSTATIC CHANGES IN THE PULMONARY BLOOD DURING CARDIOPULMONARY BYPASS

Pulmonary injury may result from the use of cardiopulmonary bypass (CP B). We investigated changes in the haemostatic system in the pulmonary vein during CPB compared with blood that circulated through the bypas s circuit. Paired samples were taken from the pulmonary vein and centr al venous pressure (CVP) line during the peri-operative period from te n patients. Plasma levels of factor VII (P < 0.001), prekallikrein (P < 0.05), antithrombin III (P < 0.001) and heparin cofactor II (P < 0.0 05) were decreased in the pulmonary vein after 20 min of bypass compar ed with pre-operative levels. In the pulmonary vein there was a signif icant increase in neutrophil expressed CD11b (P < 0.001), neutrophil e lastase: alpha(1)-antitrypsin complexes (P < 0.001), endothelin-1(P < 0.001) and thrombin-antithrombin complexes (P < 0.001) by the end of b ypass compared with pre-operative levels. There was no significant cha nge in monocyte expressed CD11b, factor XII or C1-esterase inhibitor i n the pulmonary vein for the study period. None of these variables wer e significantly different in the pulmonary vein compared with CVP line . In the pulmonary vein plasma levels of activated factor VII decrease d following heparin administration (P < 0.001) in the majority of pati ents which was coincidental to an increase (P < 0.001) in tissue facto r pathway inhibitor (TFPI). This increase in TFPI was significantly hi gher in the pulmonary vein compared with CVP line (P < 0.05) There was a decrease in neutrophil count by 20 min on CPB in both the pulmonary vein and CVP line (P < 0.001) and this did not return to pre-operativ e levels in the pulmonary vein. Soluble thrombomodulin levels decrease d by 20 min on CPB in the CVP line (P < 0.05) but tended to increase i n the pulmonary vein, although this was not statistically significant. In conclusion we found evidence of thrombin generation and possible e ndothelial damage together with increased neutrophil activation and ad hesion molecule expression in the pulmonary vein during CPB which may play an important role in the development of post-CPB pulmonary injury .