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  • Bleeding and the need for blood products frequently complicate both elective and emergency cardiac surgery. Innumerable surgical database analyses undertaken in recent years have demonstrated the deleterious effects of blood and blood component transfusion in cardiac surgery patients. Further complicating medical decision making, there are also data demonstrating the deleterious consequences of the agents designed to minimize the need for those very transfusions. Conversely, there are other studies which highlight the negative effects of failing to transfuse. This chapter will examine the causes, prevention, and management of perioperative bleeding in cardiac surgery. Additionally, since most cardiac surgical emergencies are associated with increased bleeding these too will be reviewed.


Hemostasis during and after cardiac surgery begins with surgical control of active bleeding sites. Unfortunately, control of bleeding in cardiac surgery is far more complicated than the mere application of suture to a bleeding vessel. Rather, the effects of hypothermia and hemodilution perturb the entire coagulation system, which balances clot formation and clot degradation. Anticoagulation required for cardiopulmonary bypass (CPB) coupled with the activation of the coagulation, fibrinolytic, and inflammatory systems further disrupts hemostatic mechanisms.1,2


Primary hemostasis occurs when the subendothelial layer of a bleeding vessel is exposed to injury. The endothelial cell of the normal vessel wall is antithrombogenic. However, the subendothelial layer is replete with thrombogenic tissue factor (TF) to initiate coagulation (Figure 16–1). Platelets adhere to subendothelial collagen-von Willebrand factor (vWF) via their glycoprotein (GP) Ib receptors to begin the local clot formation. Fibrinogen links adjacent platelets through their GP IIb/IIIa receptors and a clot is born.

Figure 16–1.
Graphic Jump Location

The coagulation pathway. The extrinsic pathway consists of tissue factor (TF) and FVIIa. The intrinsic pathway develops from factors FXIIa, FXIa, FIXa, and FVIIIa. The common pathway to fibrin involves FXa, FVa, and thrombin. Factor FXIIIa links fibrin. Thrombin activates platelets (PLT). Regulation of the clotting cascade is provided by tissue factor pathway inhibitor (TFPI) which inhibits the tissue factor VIIa complex. Activated protein C (APC) inactivates factors FVa and FVIIIa. Lastly antithrombin (AT) inhibits thrombin. (Redrawn from: Mackman N. The role of tissue factor and factor VIIa in hemostasis. Anesth Analg. 2009;108(5):1447-1452, with permission.)


Coagulation follows through activation of the well-known coagulation cascades and is limited and regulated by various proteins and mechanisms (Figure 16–2). Tissue factor and factor VIIa through the extrinsic pathway activate factor X leading to the generation of thrombin and then the conversion of fibrinogen to fibrin via the common pathway. The intrinsic pathway follows from the activation of factors XII, IX, and XI and results in activation of factor X and finally generation of thrombin through the common pathway. Various inhibitory proteins moderate the clotting cascade. Tissue factor pathway inhibitor (TFPI) inhibits the initiation of the extrinsic pathway, protein C and protein S inactivate factor VIIIa and factor Va. Antithrombin ...

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