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Anticoagulation is mandatory for any form of extra-corporeal circulation to prevent activation of the coagulation system through contact between blood and artificial surfaces and through blood stasis. The absence of sufficient anticoagulation is likely to result in clot formation within minutes of aortic cannulation and commencement of CPB, with detrimental consequences for the patient. This chapter briefly outlines the history of heparin before discussing its pharmacology, intraoperative hemostasis monitoring, the management of heparin resistance and Heparin Induced Thrombocytopenia (HIT) and the outlook for anticoagulation on CPB.
Perioperative management of hemostasis and coagulopathy is a complex, time-sensitive task for the anesthesiologist. The combination of anticoagulant medications and possible inherent bleeding disorders makes the ability to diagnose potential causes and risks of bleeding and guide therapy critically important. Point-of-care testing is an essential tool that has been used in clinical practice for decades and provides rapid results at the bedside. This chapter details recent advances in the monitoring of coagulation and hemostasis to assist the practitioner in guiding therapy, reduce the administration of unnecessary blood products, and improve patient outcomes
This chapter describes the coagulation pathway, the pharmacology of heparin, monitoring of anticoagulation status, problems associated with heparin usage, alternatives to heparin, the reversal of anticoagulation following termination of cardiopulmonary bypass (CPB) and the prevention and management of bleeding. Unfractionated heparin (UFH) remains the standard anticoagulant for CBP for several reasons. Activated clotting time (ACT) is a functional assay of heparin anticoagulation and is the most widely employed test. Thrombocytopenia can occur after CPB due to dilution of blood volume with the extracorporeal circuit volume and platelet consumption or sequestration. Platelet function impairment is considered to be the main hemostatic defect during CPB. The synthetic antifibrinolytic agents ε-aminocaparoic acid (EACA) and tranexamic acid (TA) bind to lysine binding sites in both plasminogen and plasmin and produce a structural change. This prevents the conversion of plasminogen to plasmin and also prevents the activation of plasmin.