Myocardial protection

Methods of Myocardial Protection

Myocardium need vs. Surgical demand!

Surgeon wants:

  1. rapid induction, maintenance and easy reversal of cardiac arrest
  2. relaxed heart to allow for mobilization and traction
  3. a preferably bloodless and unobscured field
  4. sufficient time for adequate correction of cardiac or coronary defects

Achieved by: Diastolic arrest + minimal coronary perfusion with blood + tolerate myocardial ischaemia.

Myocardium wants:

  • intact cell machinery, rapid restoration of metabolism and function
  • avoidance of ischaemia
  • delay harmful effects of ischaemia

Achieved by: Electromechanical diastolic arrest to lower metabolic demands of the myocardium by the following methods:

  1. Cardioplegia
    • Composition: Blood, Crystalloid (Guru meta-analysis 2006 – no difference in MI/death)
    • Electrolytes: Extracellular (high K/Mg/HCO3), Intracellular  (low K)
    • Timing: Intermittent, Continuous, Hot-shot
    • Route: Coronary artery (antegrade), Coronary sinus (retrograde)
    • Temperature: Cold 4-10 C, Warm
  2. Hypothermia
    • Topical: Ice slush, cold saline, cold jacket
    • Global: CPB machine with heater-cooler
  3. Unloading
    • CPB
  4.  Additives
    • see below
  5. Conditioning:
    • Volatile anaesthetics – anaesthetic pre-conditioning mimicking ischaemic preconditioning. Minor episodes of ischaemia protecting from later severe ischaemic episode. (Symons 2006 meta-analysis)

How to recognise optimal protection

Observe the heart carefully during surgery. If optimal, heart reverts to sinus after cross-clamp removal.

If suboptimal:

  • Difficulty weaning off CPB – Need for IABP, inotropic support
  • Dysrhythmias; VF – internal cardioversion
  • ECG changes
  • Raised cardiac enzymes/proteins
  • Low cardiac output
  • Long-term: myocardial fibrosis, chronic heart failure, low EF

Cardioplegia solutions

High concentration of K+ is pre-requisite.

Cardioplegia additives

  1. Beta-blockade – lowers O2 consumption, sympathetic tone, cell membrane stabilisation
  2. Glucose-insulin-K+ – Insulin Cardioplegia Trial 2002 showed no benefit
  3. Anti-inflammatory – anti-oxidants (glutathione) to scavenge ischaemic free radicals
  4. Neutrophil adhesion blockers – monoclonal Ab in trials, but not in clinical use
  5. Complement inhibitors – reduce neutrophil migration, but PRIMO-CABG 2004 showed no benefit
  6. Na/H exchange inhibition – H+ accumulates from lactic acid, normally removed by Na+/H+ exchanger increasing intracellular Na+. Ischaemia means no ATP, so Na+/K+ pump does not work to remove Na+, instead Na/Ca pump drives Na out and increases intracellular Ca which causes injury. Inhibition of Na/H pump stops increase of intracellular Na and hence stops Na/Ca pump increasing intracellular Ca. GUARDIAN trial showed no benefit except in patients undergoing CABG, EXPEDITION trial showed some benefit, but increased mortality from CVA. ESCAMI showed no benefit.
  7. NO/L-arginine – experimental animal models.

Cardioplegia temperature

  • Cold
  • Warm

Re-do surgery cardioplegia

Uses retrograde cardioplegia because:

  • Antegrade unlikely to reach myocardium supplied by LIMA
  • Temporary graft occlusion to prevent flow from proximal grafts and LIMA
  • Antegrade can cause distal thromboembolism

Components

St Thomas 2: NaCl 110.0 mM, NaHCO3 10.0 mM, KCl 16.0 mM, MgCl2 16.0 mM, CaCl2 1.2 mM, pH 7.8