Alterations in Sympathetic Nervous System Activity with Intraoperative Hypothermia during Coronary Artery Bypass Surgery: ConclusionIt is conceivable that the tachyarrhythmias encountered during CABS and rewarming may be responsive to short-acting beta adrenergic blockade in light of the elevated levels of free T3 and T4. add comment
Serum ACE activity, when corrected for hemodilution, was unchanged during CABS and hypothermia. However, the mean postoperative ACE activity in our patients was lower than the stated normal value- and also below preoperative values in any age- and disease-matched group. We have described lowered ACE activity in critically ill patients, including a group of postoperative CABS patients who had intraoperative hypothermia. Kuroda et al studied 14 pediatric patients who underwent surface cooling to 24°C and heart surgery. They described an increased angiotensin I/angiotensin II ratio during these surgeries and implied that ACE activity was decreased; however, they did not show a statistical difference between values measured before and after cooling. Also, Favre et al investigated 13 adult patients undergoing extra-corporeal circulation with pulmonary bypass and found a rise in the angiotensin I/angiotensin II ratio, again implying a decreased activity of ACE. We conclude that the lowering of the postoperative serum ACE activity likely occurred after the induction of bypass and systemic hypothermia, but before the rewarming process was started.
A transient elevation in plasma catecholamine concentrations during rapid systemic cooling as the core temperature is lowered to 28°C, a subsequent suppression of NE below a temperature of 28°C, and a rebound phenomenon during rewarming have been examined. These results suggest an activation of the SNS between 37° and 28°C and suppression of SNS activity below 28°C. Simultaneously we have observed a rise in serum FT3, FT, and T4 concentrations occurring abruptly after the onset of bypass and hypothermia. By understanding the hypothermia-related changes in circulating catecholamine and thyroid hormone concentrations, clinicians may better understand mechanisms underlying the responsivity of certain patients to adrenergic receptor agonists and antagonists.