The use of etomidate for induction of anesthesia in patients requiring urgent coronary artery surgery provides good cardiovascular stability. However, long-term etomidate infusions may cause transient signs of adrenocortical suppression. The purpose of this study was to determine whether an induction bolus dose of etomidate would cause clinically relevant endocrine dysfunction in urgent coronary artery bypass patients. With institutional review board approval, 11 patients were prospectively randomized to a diazepam (control) or etomidate rapid sequence induction. The diazepam group (n = 6; mean, 69 years) received 0.4 mg/kg of diazepam. The etomidate group (n = 5; mean, 54 years) received 0.3 mg/kg of etomidate. Maintenance anesthesia included nitrous oxide, oxygen, pancuronium, and fentanyl in increments up to 32 μg/kg. Hemodynamics, cortisol, epinephrine, and norepinephrine were measured both intraoperatively and postoperatively. The only significant differencebetween the two groups in hemodynamic parameters was a higher heart rate in the etomidate group. Both agents adequately controlled the stress response to intubation as judged from the levels of epinephrine, norepinephrine, and cortisol. However, in both groups epinephrine and norepinephrine increased between intubation and removal of the aortic cross-clamp. Cortisol also increased from the time of cross-clamp removal to 12 and 24 hours post-bypass. During anesthesia and surgery in the pre-bypass period, there was a decrease in cortisol over time in the etomidate group, and there was an increase with diazepam. Thus, etomidate provided stable hemodynamics, possible mild intraoperative adrenocortical suppression, a depressed hormonal stress response to intubation, and a normal hormonal reaction to the later part of surgery and the postoperative period. © 1988.