Brain death has damaging effects on the cellular and subcellular level of the myocardium.49 Myocardial preservation, therefore, begins with proper donor management and manipulation of the deranged neurohormonal milieu consequent to brain death. As early as 1954 it was noted that subendocardial hemorrhage occurs subsequent to brain death,50 and that EKG changes simulating myo-cardial ischemia occur in patients dying from intracranial hemorrhage, status epilepticus, meningoencephalitis, or traumatic brain herniation.51 Neuroendocrine changes consequent to anoxic brain death are marked by an initial hypertensive response due to catecholamine release, followed by progressive vasomotor tone collapse. Free triiodothyronine (T3), thyroxine (T4), cortisol, and insulin, TSH, and ADH decrease significantly within a few hours of the onset of brain death. Myocardial ATP, creatine phosphate, glycogen stores subsequently decrease and myocardial lactate increases. The rates of glucose, pyruvate, and palmitate metabolism as energy substrates are markedly reduced following brain death. Diabetes insipidus, thyroid dysfunction, and an altered HPA (hypothalamic-pituitary-adrenal) axis are factors which are felt to contribute to myofilament ATP unre-sponsiveness.52-54 Hormonal supplementation with triiodothyronine (T3), cortisol, and insulin has been found to augment the hemodynamic status of donor hearts and improve postop graft function.53 However, it should be noted that T3 supplementation may need to be given to both the donor and the recipient in order to have optimal effect.
Was this article helpful?