Heparin Resistance (HR) during cardiac surgery is defined as the inability of an adequate heparin dose to increase the activated clotting time (act) to the desired level



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Heparin Resistance (HR) during cardiac surgery is defined as the inability of an adequate heparin dose to increase the activated clotting time (ACT) to the desired level. Alternatively, heparin resistance is defined as a decrease in the heparin dose response (HDR). Unfortunately, the heparin dose and ACT goal used to define HR in the literature varies greatly. The definition of HR can greatly impact anticoagulation management as many clinicians alter anticoagulation management strategies to reach the desired ACT.

The chief concern amongst clinicians managing HR is that failure to optimize anticoagulation during cardiopulmonary bypass (CPB) will result in activation of the coagulation system. At best, this will result in consumption of coagulation factors and potentially contributing to a consumptive coagulopathy. At worst, a catastrophic thrombosis will occur in the CPB circuit. Anticoagulation with heparin has long been the anticoagulant of choice for CPB as it is fast in onset and readily reversed. One of the main disadvantages of heparin is that the anticoagulant response varies amongst patients. Because of this, the ACT is routinely performed during cardiac surgery to ensure adequate anticoagulation.

The ACT is a crude test that entails adding a contact activator to a sample of the patient’s blood and measuring the time that is required for the blood to form a fibrin clot. Although administering heparin prolongs the ACT, the ACT is also affected by many other variables routinely seen during CPB. Because the ACT is not specific to heparin, it remains unclear if decreased heparin responsiveness as measured by the ACT is always a reflection of inadequate anticoagulation.

Adding to the complexity of HR is that the mechanism is multifactorial. Traditionally the mechanism of HR has been thought to be related to antithrombin (AT) deficiency. As heparin’s anticoagulant effect is mediated through AT, a deficiency would thus make heparin less effective as an anticoagulant. However, many patients with HR have normal AT levels and/or do not respond with an increase in heparin responsiveness when supplemented with AT. Thus, there must be a non-AT dependent mechanism for HR.



Despite the limitations in our understanding of HR, many clinicians choose to intervene when the target ACT is not achieved. Options for treatment include administering additional heparin and supplementation of AT with either AT concentrate or fresh frozen plasma. Another option for management of HR would be to accept the current ACT and commence CPB without additional treatment. Without a full understanding of HR, the intervention that is chosen may not only be harmful side effects and costly, but lack efficacy. Therefore, a clinician should choose a rational approach to management of HR that takes into consideration all factors related its diagnosis and mechanism.


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