The artificial surface of the bypass circuit is a powerful thrombotic stimulus which is not completely suppressed by heparin anticoagulation. Thrombus is produced and increases progressively during cardiopulmonary bypass, consuming clotting factors, activating platelets, and stimulating fibrinolysis. The activation of coagulation and fibrinolysis is also part of the systemic inflammatory response to cardiopulmonary bypass which includes activation of complement and leukocytes. Attempts to reduce hemostatic activation include improvements in oxygenators (membrane rather than bubble) and the biocompatibility of the materials used in the circuit, the search for drugs that are more effective than heparin in suppressing thrombus formation (e.g. hirudin), and the use of antifibrinolytic agents. Epsilon-aminocaproic acid has been used before and after bypass to reduce bleeding, but has a tendency to produce thrombosis. This is the major concern with all such agents—balancing the risk of thrombosis of grafts and in other vascular beds against that of prolonged bleeding. Tranexamic acid and aprotinin are used before and during bypass to reduce postoperative bleeding. Full risk-benefit analyses are not yet available and thus precise regimens are not defined, with the exception of the use of aprotinin in reoperation.
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