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Coronary Artery Bypass Graft (CABG)
Patients undergoing CABG are initially in a state of imbalance toward hypercoagulable state. The exposure of the patient's blood to the cardiopulmonary bypass (CPB) circuitry diminishes the hypercoagulable state and proceeds into an imbalanced hypocoagulable phase. Exposure to negatively-charged CPB surfaces invariably leads to the activation of platelets and the intrinsic pathway, while the tissue traumatized by surgery exposes TF to the blood stream, leading to activation of the extrinsic pathway. In addition, exposing the blood to artificial surfaces, the accompanying flow turbulence, the effect of the oxidation by the CPB pump further leads to platelet activation and damage. All this leads to consumption of coagulation proteins and platelets, and together with the dilutional coagulopathy results in approximately 50% reduction in platelet number and coagulation factors, shifting the balance from a hypercoagulable to hypocoagulable state. Also, in 5-7% of patients undergoing CPB cardiac procedures the endothelium reacts to the trauma of surgery by releasing high levels of TPA, which in the presence of a hypocoagulable state, leads to primary fibrinolysis. Accordingly, as we treat the patient to achieve a restoration of normal hemostasis and recovery of vascular integrity with blood products and/or pharmaceutical agents, we shift the hypocoagulable state to normal or beyond to a hypercoagulable state. The CPB circuit activates the hemostasis process, introduces emboli, and even microscopic debris that further activates these elements once circulating in the patient's vasculature. Once the patient reaches the post-protamine stage, a restoration of his initial "normal" hemostasis - an imbalance towards hypercoagulability -- is reinstated.
Case Study
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