• Peri-op myocardial protection
    • Strategies that increase the heart's ability to withstand ischaemic insult
    • If ischaemia is interrupted at appropriate point leads to:
      • Stunning
        • Can be helped with inotropes or calcium
        • Due to cytosolic calcium overload and the development of oxygen free radicals
      • Hibernation
        • Resting muscle that can return to normal function if flow or demand is altered
        • May be due to repeated stunning effects
        • TNF-α implicated, causing disuse atrophy and loss of myofibrils
        • Examined by means of PET & dobutamine stress echo
    • Temperature
      • Hypothermia offers myocardial protection
      • Reduces O₂ consumption from 80ml/100g/min to 0.3ml/100g/min at 22ᵒC
      • Venting the heart reduces wall tension which has a beneficial effect
    • Cardioplegia
      • Blood based better at preserving myocyte and endothelial function
      • Blood delivers nutrients, buffering capacity and ability to scavnage free radicals
      • Low temp may predispose to reperfusion injury but has good protective properties
      • Some advocate warm plegia with cold maintenance
    • Pharmcotherapy
      • β-blockers
        • Increased rate of CVA however
        • May benefit select high risk groups
      • α2 agonists
      • Statins
      • GKI infusions in NON-diabetics
    • Ischaemic preconditioning
      • Exposure to physical or pharmacological stimulus reduces subsequent injury from ischaemia
      • Broadly classified
        • Ischameic preconditioning (IPC)
        • Anaesthetc preconditioning (APC)
        • Remote ischaemic preconditioning (RIPC)
      • IPC
        • Early - 15 mins to several hours
          • Adenosine may activate phospholoipase C
          • Increase in protein kinase C
          • This phosphorylates mitochondrial ATP-sensitive K⁺ channels
          • Opening these channels prevents calcium overload
          • Protects against infarction but not stunning
        • Late 12hrs - 4 days
          • Alterations in myocardial cell structure
          • Protects against infarction and stunning
          • Synthesis of myocardial protection factors
            • COX-2
            • Nitric oxide synthase
            • Causes reduced apoptosis
      • APC
        • All volatiles seem to have cardioprotective effects
        • Also have negative inotropic and chonotropic effets that benefit myocardial O₂ balance
        • Have effect that mimics IPC
        • Maximal effect at 1.5-2 MAC but 0.25 effective
        • May also have hepatic, neuronal and renal preconditioning effects
        • Xenon, adenosine, nicorandil and noradrenaline have properties similar
      • RIPC
        • Inducing distant ischaemia to obtain a myocardial protective effect (eg. 5 minutes of renal artery occlusion before coronary reperfusion decreases infarct size)
        • Also likely to involve adenosine
    • CEACCP
      Link:ceaccp.oxfordjournals.org/content/9/3/97.full.pdf