Na and coauthors [5] reported signi cant variations to heparin responsiveness in an observational study of pa- tients with known, stabilized infectious endocarditis. Garvin and associates [6] also reported observed varia- tions in heparin response in patients having CPB. In a retrospective institutional database review of 3,880 pa- tients, these investigators found wide variation in the heparin bolus dose required to obtain a target ACT. The initial unfractionated heparin bolus dose did not correlate well with the rst post-heparin ACT (r2 0.03). The route and timing of the initial administration of unfractionated heparin has a direct impact on the ability to obtain a therapeutic ACT. A small randomized trial done by Grima and colleagues [7] found that intermittent doses of unfractionated heparin administered before CPB (100 IU/kg for 3 doses) maintained adequate levels of anticoagulation during CPB better than a single bolus dose of 300 IU/kg. Intermittent pre-CPB heparin treat- ment resulted in lower mean decreases in factor VIII, brinogen, antithrombin III, and platelet count than if a large bolus dose were administered. In a prospective nonrandomized trial performed by Neema and col- leagues [8], 6 of the 100 patients who received 300 IU/kg of unfractionated heparin before CPB had a resultant post-heparin ACT less than 350 seconds. Other patho- logic disturbances such as thrombocytosis may limit the effectiveness of weight-based heparin bolus administration. Owing to the heterogeneity of the pharmacodynamic response to unfractionated heparin, the utilization of ex vivo heparin dose-response technologies was studied as a more accurate prediction of initial heparin dosing. Although ex vivo heparin dose-response technologies may identify patients who have a reduced sensitivity to conventional doses of heparin, these tests have limited ability to calculate correctly an optimal initial unfractio- nated heparin bolus dose. 