However, ACT devices vary considerably in their measurement platforms, activators, sample volumes, and sensitivities to external elements such as hemodilution, hypothermia, and concomitant drug therapies [23, 24]. It appears that arterial versus venous blood sampling and a wait period as long as 15 minutes do not signi cantly affect the ACT result [25, 26]. Currently there are many instruments and platforms available that purport to measure ACT values. To ratio- nally utilize an ACT device for patients undergoing CPB, it is important to understand how the testing platform works, the therapeutic target that corresponds to a his- torical ACT of 480 seconds, and how well the results correlate with anti-Xa activity. In an early study of hep- arin monitoring and ACT threshold values, it was noted that the two most commonly used ACT devices correlated with each other, yet there was signi cant bias with one of the instruments [27]. Another observational study showed that many ACT tests correlated poorly with heparin level as assessed by anti-Xa plasma activity [28]. Patteril and associates [29] demonstrated that after switching their cohort population to a newer ACT device, the new instrument yielded a lower mean ACT value compared with temporal controls (557 versus 618 sec- onds, p < 0.05), and a higher dose of unfractionated heparin was needed to achieve a minimum ACT of 480 seconds [29]. A certain level of validation has been per- formed for other ACT instruments as well [30]. Tests that use a maximal degree of activation of the blood sample by using multiple or more potent activators produce shorter clotting times relative to the standard ACT with a single activator [11]. The tests that utilize a maximally activated sample also report less variability in clotting times and are less susceptible to prolongation by hypothermia and artifacts [10]. 