Abstract

THE HEMOSTATIC GOALS for anticoagulation during cardiac surgery are to prevent clotting to allow for cannulation and initiation of cardiopulmonary bypass (CPB), inhibit thrombin generation during CPB, and reverse anticoagulation in a safe and complete manner.1 “Adequate anticoagulation” for CPB is traditionally determined by the activated coagulation time (ACT), a whole blood hemostatic activation test that is influenced by multiple causes.1–4 Heparin resistance has been frequently reported in the literature, often because of a variety of causes.5–15 The definition commonly used for heparin resistance is an ACT of <480 seconds after the addition of 500 U/kg of heparin.5–9 Unfortunately, the terminology used for heparin resistance is a misnomer; in fact, what is observed is an alteration in heparin dose-responsiveness, with a shift of the heparin response curve. Patients actually increase their ACT in response to heparin but not in a linear fashion.8 True heparin resistance is potentially associated with a homozygous antithrombin deficiency, a syndrome that is most likely incompatible with life. Therefore, it is proposed that the term “heparin resistance” be replaced with “altered heparin responsiveness,” especially because the ACT is used to determine this clinical syndrome.

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