The purpose of this prospective study was to define the effect of cardiopulmonary bypass (CPBP) on thyroid function. Blood samples were obtained from 14 patients the day of admission, postanesthetic induction, post-heparination, following institution of CPBP, the nadir of hypothermia, before termination of CPBP, and 2, 8, and 24 hrs postoperatively. TSH, TBG, Total T-4, Total T-3 and reverse T-3 (rT-3), an inactive metabolite of T-4, heretofore never reported with CPBP, were assayed by radioimmunoassay. Free T-3 (ft-3) was assayed by equilibrium dialysis. Data were compared by paired T-tests for all time intervals against preoperative values. Total T-3 (T-3), the most active thyroid hormone, and fT-3 values were significantly depressed (75 and 50% respectively) following CPBP for 24 hrs (p<0.05). Reverse T-3 demonstrated a four-fold rise at 8 and 24 hrs postoperatively (p<0.05), but no change at 2 hrs postoperatively. TBG was decreased at all sampling time (p<0.)5). TSH, T-4 and fT-4 remained within normal ranges at all sampling times. These results indicate that CPBP simulates the """"""""Euthyroid Sick Syndrome"""""""" as seen in severe burn and critically ill patients. There was marked postoperative depression of T-3 and fT-3 with increased rT-3, while TSH, T-4 and fT-4 remained within normal ranges. These data indicate utilization of fT-3 with concomitant abnormal deiodination of T-4 to rT-3 or abnormal deiodination of rR-3 to T2 (the breakdown product of rT-3). It is concluded that CPBP produces a blunted response of TSH to low T-3 and T-4. The deleterious hemodynamic effects of hypothyroidism are well established. These data provide a basis for intravenous administration of T-3 in the treatment of low cardiac output syndrome following cardiopulmonary bypass.
