Cardiopulmonary Bypass Flashcards
Hemolysis on CPB: causes
Causes:
- mechanical shear stress and turbulence
- contact with non-endothelial surfaces and air
- pressure gradients for venous drainage (vacuum assist)
- cardiotomy suction use (pump suckers)
CPB effect on WBCs
WBC activation by contact with non-endothelial surfaces
- Activation leads to pro-inflammatory and pro-coagulant states (but can also lead to coagulopathy)
- Activated neutrophils release cytotoxic enzymes and free radials; migrate outside vessels leading to tissue edema and cellular dysfunction
- Activated monocytes promote thrombin generation via tissue factor
CPB effect on platelets
- Can decrease platelet count by 30-50% due to hemodilution, platelet adhesion to the circuit, mechanical disruption, shear stress, sequestration in tissues
- Qualitative defects: excessive activation leading to blunted response to stimulation
- Protamine can activate platelets leading to aggregation, sequestration, and thrombocytopenia
CPB effect on endothelial cells
- Activated within minutes of going on CPB
- Up-regulate anticoagulant and fibrinolytic pathways
- Can cause a consumptive coagulopathy (this is why we give an antifibrinolytic)
What causes fibrinolysis on CPB?
- release of tPA
- fibrin formation that is not fully suppressed by systemic heparinization
What are the components of the contact system?
- Factor XII (activated by contact with non-endothelial surfaces in the CPB circuit) –> converted to FXIIa –> activates coagulation cascade, fibrinolysis, etc.
- Factor XI
- Kallikrein
- High-molecular weight kininogen
What is the complement system and how is it activated during cardiac surgery?
Cytotoxic immune system that initiate and amplify the inflammatory response. Activates platelets and can contribute to CPB coagulopathy.
- During CPB: “alternate” (antigen-antibody independent) pathway
- Heparin-protamine complexes: “classic” pathway
What is the end result of the coagulation cascade?
Fibrin clot formation
What is the intrinsic pathway?
Blood exposed to foreign material in the CPB circuit –> activation of Factor XII –> formation of activated Factor Xa
What is the extrinsic pathway?
Endothelial disruption exposes blood to tissue factor –> TF complexes with Factor VIIa to activate FXa.
What is the common pathway?
The extrinsic and intrinsic pathways converge at FXa. Includes factors V, X, II and fibrinogen.
What does PT and aPTT measure?
PT/INR: extrinsic pathway
- Factor VII + common pathway
aPTT: intrinsic pathway
- Factors XII, XI, IX, VIII + common pathway
Common pathway:
- Factors V, X, II, fibrinogen
Risk factors for post-op myocardial dysfunction
- Pre-operative LV dysfunction
- Acute ischemia
- Advanced age
- X-clamp time
- Total CPB time
- Perioperative bleeding
- Dilated cardiac chambers
Incidence of prolonged mechanical ventilation after cardiac surgery
7.5-10%
- Defined as intubation >72 hrs post-op
- Associated with increased mortality
Pathophysiology of lung injury on CPB
- Neutrophils/pro-inflammatory mediators (neutrophils adhere to pulmonary endothelium and release proteolytic enzymes/ROS)
- Ischemic injury (lungs are only supplied by bronchial arteries during CPB; no PA blood flow)
- Reperfusion injury
- Atelectasis 2/2 prolonged apnea
- Pulmonary capillary membrane damage = edema
