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From the *University of California, San Diego, Sulpizio Cardiovascular Center, LaJolla, CA, †Heart and Diabetes Centre NRW, Ruhr-University Bochum, Bad Oeynhausen, Germany; and ‡Department of Anesthesiology, Queen Fabiola Children’s University Hospital, Brussels, Belgium. Address reprint requests to Sonia Nhieu, MD, University of California, San Diego, Department of Anesthesiology, Thornton Hospital, 9300 Campus Point Drive #7770, LaJolla, CA 92023-7770. E-mail: snhieu@ucsd.edu Cardiac Anesthesia Fellow. UNFRACTIONATED HEPARIN (UFH) is the most widely used intravenous drug in the United States with as many as 60% of hospitalized patients receiving this agent. The incidence of heparin-induced thrombocytopenia (HIT) is approximately 2% of patients who receive UFH. HIT syndrome type II (HIT-II) is an immune-mediated reaction in which serum antibodies against heparin-platelet factor 4 (HPF4) complexes are produced in patients who receive heparin therapy. The reaction typically develops 5 to 10 days after exposure and leads to a decrease in platelet count of 50% or more and a paradoxical hypercoagulable state. No ideal method of anticoagulation exists for patients with HIT. In non-surgical patients requiring anticoagulation and medical management of HIT, approved therapies in the United States are limited to argatroban and lepirudin. Recommendations for anticoagulation for patients with HIT requiring cardiac surgery include delaying surgery until HIT antibodies are negative, administering platelet inhibitors in addition to heparin, or using an alternative anticoagulation strategy. Unfortunately, many patients, especially those requiring cardiac surgery, cannot delay the operation, and an alternative to heparin for intraoperative anticoagulation must be used. The use of cardiopulmonary bypass (CPB) further complicates the situation because of the higher levels of anticoagulation required. Use of bivalirudin for anticoagulation in patients with HIT undergoing cardiac surgery has increased and, in a few small studies, has demonstrated a similar safety and efficacy profile compared to UFH. Bivalirudin is a synthetic, direct thrombin inhibitor made up of twenty amino acids and is approved for patients undergoing percutaneous coronary intervention. Its elimination is predominantly dependent on thrombin active site-mediated proteolytic cleavage, resulting in a short half-life of 25 minutes. Approximately 20% of the drug is excreted unchanged by the kidney, leading to a doubling of the half-life in patients with severe renal impairment. The drug’s safety profile appears unchanged, even with respect to hemorrhagic complications, in patients with moderate impairment of renal function. However, in dialysis-dependent patients, the half-life increases markedly to approximately 3 to 5 hours. While the