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The utilization of cardiopulmonary bypass (CPB) offers a dichotomy in the need for complete anticoagulation in preparation for and while on CPB and for hemostasis at the end of CPB. The surgical process itself stimulates the release of thrombogenic substances such as tissue factor. Furthermore, blood has a natural tendency to clot when it encounters foreign surfaces and in addition, the presence of a foreign substance incites an inflammatory response that further increases the propensity of the blood to clot. Because of this, the blood circulating through the cardiopulmonary bypass circuit is at high risk for clotting if special anticoagulation strategies are not employed. Such strategies include but are not limited to anticoagulation of the patient’s blood and the bypass circuit priming solution prior to placement of cannulas in the patient, as well as the use of heparin bonded bypass circuits. Patients are generally kept anticoagulated for the duration of the bypass period. At the completion of the bypass period, the heparin effect is reversed, usually with protamine. This is done to achieve hemostasis in an effort to stave off or limit postoperative bleeding. In this chapter, we will review anticoagulation in preparation for and during CPB and strategies to achieve hemostasis after the bypass period.


Anticoagulation is necessary in order to avoid the formation of thrombus in the CPB circuit and prevent acute disseminated intravascular coagulation while on bypass. Unfractionated heparin is most commonly used for anticoagulation in preparation for CPB and while on CPB. Heparin is a large sulfated glycosaminoglycan polymer, which is negatively charged at physiologic pH. Because of its polarity and size, it stays primarily in the intravascular space. Peak onset of action is approximately 1–3 minutes after administration invtravascularly and its elimination half-life is 1–1.5 hour. Heparin is excreted via the kidneys and is also metabolized by the reticuloendothelial system. Its anticoagulation effect is via a special pentasaccharide sequence on the molecule that binds to antithrombin III and potentiates its inhibitor effect primarily on thrombin and factor Xa and to a lesser extent on IXa, XIa, and XIIa as well. The end result is a disruption of both the intrinsic and common pathways of plasma coagulation.

Dosing for heparin is generally by weight or by dose–response titration. As for the weight-based method, most places use 300–400 U/kg in preparation for going on bypass. Keep in mind that for morbidly obese patients it may be better to dose to ideal body weight initially and give additional heparin if needed. The dose response curve is generated by measuring the activated clotting time (ACT) before and after a specific dose of heparin (e.g., 200 U/kg). A line is drawn between the two results and via extrapolation; the dose of heparin needed to achieve the desired ACT is acquired. With this strategy, the CPB priming solution also needs to have a heparin concentration (3–4 units/mL) similar to that of the ...

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