Acute
critically ill patients experience a rapid decline in plasma free
thyroid hormone levels (free
triiodothyronine (FT3) and free
levothyroxine (FT4)), with a marked elevation of reverse T3, recognized as the
euthyroid sick syndrome (ESS) or low-T3 syndrome. The ESS is also often associated with depressed myocardial function, sometimes referred to as the '
stunned myocardium'. Its clinical effects may vary from minimal hemodynamic impairment to
cardiogenic shock. Medical management may range from
aspirin alone to placement of a left
ventricular assist device. With adequate supportive
therapy, recovery usually occurs within days or weeks. The effect of T3/T4
therapy has been studied in three conditions in which the ESS and myocardial functional depression have been documented - i) transient regional
myocardial ischemia and reperfusion, ii) transient global
myocardial ischemia in patients undergoing cardiac surgery on
cardiopulmonary bypass, and iii) transient inadequate global myocardial perfusion in
brain-dead potential organ donors. Under all three conditions,
myocardial ischemia leads to rapid loss of high-energy
phosphates, accumulation of myocardial tissue
lactate, and probably loss of homeostasis of cytosolic
calcium, which may further increase cell injury. There is an inability to generate
ATP through the Krebs cycle, which reduces the high-energy
phosphate pool essential for all cell
ATPases. Under all three conditions, following administration of T3/T4, the myocardial dysfunction was rapidly reversed. We, therefore, cautiously advocate the use of thyroid hormonal
therapy to any patient with the ESS and/or a
stunned myocardium.