Pathophysiological effects of CPB on haemostasis

Pathophysiological effects of CPB on haemostasis

1) Denaturing Of Plasma Proteins

· Bubble oxygenators & cardiotomy suction —> air-blood interface —> modify coagulation factors —> coagulation factor defects

2) Deposition on extracorporeal surface

· Platelets & coagulation factors (esp fibrinogen) deposit on the extracorporeal surface:

Plasma proteins adhere to solid surface —> platelets adhere to absorbed proteins

3) Fibrinolysis

· Plasma proteins adhere to solid surface —> activation of thrombin —> thrombin stimulates endothelium —> release t-PA —> fibrinolysis

· fibrin breakdown products usually clear one hour post CPB

· rare patients exhibit marked fibrinolysis —> bleeding from clot lysis + interference with polymerisation of newly formed fibrin

· success of antifibrinolytic drugs in decreasing postop bleeding

4) DIC [consumptive coagulopathy]

· inadequate heparinisation —> active coagulation in extracorporeal circuit —> factor consumption —> secondary fibrinolysis

· extremely rare

5) Whole body inflammatory response associayed with CPB

· vascular endothelium provides a non thrombogenic surface due to their synthesis of prostoglandins and peptides; unlike all other cells & extracorporeal circuit surfaces which initiate coagulation

· massive activation stimulus of CPB make large doses of heparin essential

· heparin inhibits factor X & thrombin; in the final steps of the coagulation cascade —> therefore during CPB the initial steps of this cascade are are inhibited —> see activation of various white cells + endothelial cells, platelets, kallikrein, kinin, fibrinolytic & coagulation cascades —> whole body inflammatory response

6) Platelets

· cardiotomy suction exposes platelets to air-blood & tissue-blood interfaces —> platelet activation

· the amount of blood aspirated by cardiotomy sucker directly correlates with platelet loss

· filters also provide a surface for platelets to aggregate

· CPB activates platelets by an unknown mechanism

· Rheological factors such as shear stresses,turbulance and stagnant flow areas have less effect on platelets than red cells

· The most most platelet destructive areas in CPB are the oxygenator & cardiotomy suction

· Large surface area of synthetic surface of membrane oxygenators accounts for rapid decline in platelet count

· However bubble oxygenators have a greater effect in reducing platelet numbers

· Dilution is responsible for most of the thrombocytopenia during CPB, platelet adhesion, aggregation & destruction is responsible for the remainder

· hypothermia also causes thrombocytopenia by a reversible sequestration of platelets in the portal circulation

7) Hypothermia

· temperature dependent enzymatic processes determine sequential activation of coagulation factors

^·many enzymatic reaction attenuate 7% for each decrease of 1^o C

^·therefore, fibrin formation may likewise be retarded

· see this effect in prolongation of ACT at cooler temperatures

· this effect is especially relevant if inadequately rewarmed