A 69-yr-old, 51-kg woman was to undergo lung cancerresection. She had a history of partial pituitary macroad-enomectomy 30 mo earlier, acromegaly, hypertension, anddiabetes mellitus. She denied any history of coronary arterydisease. She developed dyspnea after climbing two flights ofstairs. Her medications were nifedipine, atenolol, perindo-pril, sandostatin, bromocriptine, and hydrocortisone. Preop-eratively, her blood pressure (BP) was 130/70 mm Hg andheart rate (HR) was 48 bpm. Electrocardiogram (ECG)showed left ventricular hypertrophy (LVH) and nonspecificT-wave changes in the lateral chest leads. The ECG revealedLVH and mild aortic regurgitation. Chamber sizes and leftventricular function were normal. Her hemoglobin was 125g/L. Mediastinoscopy performed 3 wk earlier was compli-cated by intraoperative (lead II) ST segment depression,which resolved with IV nitroglycerin without sequelae. Thepatient declined postoperative cardiac evaluation.For her thoracotomy, she had the standard monitors andan arterial catheter. Baseline BP was ~125/65 mm Hg, HRwas ~46 bpm, and the ST segment in lead II was normal.After the administration of fentanyl 100 g, propofol 80 mg,and rocuronium 40 mg, and 2 min of ventilation with oxy-gen and isoflurane (end-expiratory concentration, 0.7%), herleft main bronchus was intubated with a double-lumen tube.Postintubation BP was 160/85 mm Hg (HR, 47 bpm) and a3-mm ST segment depression was evident on lead II. Threeminutes later, her BP was 124/65 mm Hg, HR was 44 bpm,and the ST segment depression persisted (Fig. 1). In view ofher disease and refusal of cardiac investigation, we pro-ceeded with surgery. The right thoracotomy was along theT4 dermatome. Soon after, the lead II signal quality deteri-orated, and lead III was used subsequently. Her BP waslabile, but her ST segment did not change by 1 mm with BPfluctuations. Her maximum HR was 59 bpm. Nitroglycerin82–117 g/min maintained the BP at 126–150/60–80 mmHg and improved the ST segment to 2.9 mm. However,because of a decrease in Spo