• Cerebral effects of CPB
    • Cerebral death, non-fatal CVA, coma, encephalopathy, delirium, opthalmic abnormalities. Occur in 5-20%
    • Increasing age with associated co-morbidities predisposes to cerebral injury following CPB eg hypertension, DM, carotid stenosis, neurological disease
    • Risk of stroke is 1-5% and this increases chance of death from CABG to 20%
    • Neurological injury
      • Type 1 (3%)
        • Cerebral deaths, non-fatal CVA, TIA
      • Type 2 (3%)
        • New intellectual deterioration at discharge or seizures
    • Biochemical markers of injury
      • Neurone specific endolase
      • Creatine phosphokinase
      • S-100 beta protein (glial cell derived)
    • Mechanisms and prevention of cerebral injury
      • Patient factors
        • Age
        • Male
        • Existing poor ventricular function
        • Thrombus
        • DM
        • Previous CVA
        • Carotid stenosis
        • Atherosclerosis
        • Genetic factors
      • Procedural factors
        • Embolism
        • Valve surgery
        • Cerebral hypoperfusion
        • Long CPB time >2hrs
        • Hyperglycaemia
        • Poor temp control
        • SIRS
    • Pharmacological protection results thus far have disappointed. After neuronal injury, glutamate binds to NMDA receptors which causes a cascade of intracellular responses and ultimately neuronal death. Remacemibe (NMDA receptor antagonist) did show a small benefit.
    • Genetic factors play a role eg the APOE4 gene
    • Rewarming should be done carefully and gradually as rapid rewarming can cause gas to come out of solution
    • Standard CPB is non pulsatile at 2-2.4L/min/m² and studies have shown no benefit in using pulsatile flow
    • Membrane oxygenators and arterial filters have reduced micro-emboli load. Roller pumps cause spallation whereas centrifugal pumps do not
    • Heparinising the circuit to ACT >400s +/- FFP or ATIII concentrate is used.
    • Inflammation due to complement, coagulation and kallikrenin systems activate neutrophils which release free radicals causing cellular damage, capillary leak and SIRS.
    • Acid base management
      • Alpha stat management
        • No correction made for patients temperature. If undergoing moderate hypothermia, alpha stat has better outcomes as auto regulation is better maintained
      • PH stat management
        • Temperature correction is used and normocapnoea is maintained during hypothermia by the addition of CO₂. Used in paeds and has better outcome during deep hypothermic circulatory arrest (DHCA).
    • Determinants of CBF
      • MAP
        • Combined CV and neuro outcomes better if arterial pressure is higher (80-100mmHg) during CPB. 50mmHg is likely to be the minimal tolerable level
      • CO₂
        • CO₂ reactivity is preserved during CPB so is important to maintain during CPB
      • Temp & haematocrit
        • Normally there is cerebral metabolism-flow coupling. A fall in temp from 37 to 27 reduces CMR by 50%. Metabolism coupling fails below 22 degrees.
        • Haemodilution can improve CBF but over dilution leads to inadequate oxygen delivery.
    • CEACCP
      Link:ceaccp.oxfordjournals.org/content/3/4/115.full.pdf