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Heparin resistance during cardiac surgery is defined as the inability of an adequate heparin dose to increase the activated clotting time (ACT) to the desired level. Failure to attain the target ACT raises concerns that the patient is not fully anticoagulated and initiating cardiopulmonary bypass may result in excessive activation of the hemostatic system. Although antithrombin deficiency has generally been thought to be the primary mechanism of heparin resistance, the reasons for heparin resistance are both complex and multifactorial. Furthermore, the ACT is not specific to heparin’s anticoagulant effect and is affected by multiple variables that are commonly present during cardiac surgery. Due to these many variables, it remains unclear whether decreased heparin responsiveness as measured by the ACT represents inadequate anticoagulation. Nevertheless, many clinicians choose a target ACT to assess anticoagulation, and interventions aimed at achieving the target ACT are routinely performed in the setting of heparin resistance. Treatments for heparin resistance/alterations in heparin responsiveness include additional heparin or antithrombin supplementation. In this review, we discuss the variability of heparin potency, heparin responsiveness as measured by the ACT, and the current management of heparin resistance.