A 60-year-old 120-kg woman with severe aortic stenosis presented for aortic valve replacement. She presented with progressive exertional dyspnea, paroxysmal nocturnal dyspnea, and two-pillow orthopnea. Other pertinent conditions included hypertension, morbid obesity, and chronic phlebitis. Peak systolic pressure gradient was 75 mmHg, and the calculated aortic valve area was less than 1 cm 2. Cardiac catheterization also showed mild coronary atherosclerosis and normal left ventricular function. Preoperative medications included methyldopa, hsinopril, and warfarin. Warfarin was discontinued 6 days before surgery. Physical examination showed a grade I I I /VI systolic ejection murmur at the right upper sternal border that radiated to the carond arteries. Her chest x-ray showed mild interstitial fibrosis but was otherwise normal. Electrocardiogram (ECG) showed sinus rhythm, left ventrlcular hypertrophy, an old inferior myocardial infarction, and mtraventricular conduction delay. Laboratory results included a white blood cell count of 6,200/ixL, Hgb 13.5 g/dL, hematocrit 40.3%, and prothrombin time 13.4 seconds (normal range 11.0 to 12.0 seconds). After premedicatlon with morphine, 6 nag intramuscularly, the patient was brought to the operating room and placed supine on the operating room table. Routine monitors (ECG, nonmvaswe blood pressure (BP); pulse oxlmeter) were applied, and a pulmonary artery catheter was placed without difficulty via the right internal jugular vein. After several unsuccessful attempts at placing a 20-G right femoral arterial catheter, a 20-G 15-cm left femoral arterial catheter was placed with some difficulty. The right femoral artery had been successfully punctured with a Seldinger needle, but difficulties in advancing a guideline precluded successful cannulahon. General anesthesia was induced using etomidate, 0.1 mg/kg, fentanyl, 8 Ixg/kg, midazolam, 30 ixg/kg, and succinylcholine, 1.2 mg/kg. General anesthesia was maintained using fentanyl, 30 txg/kg, and isoflurane, up to 0.8 minimum alveolar concentration for BP control. Hemoglobin concentration after anesthetic reduction was 12.3 g/dL. The prebypass period was uneventful with mlmmal blood loss, and 1,500 mL of lactated Ringer's solution was administered intravenously before cardiopulmonary bypass (CPB). Anticoagulataon was achieved with 300 U/kg of heparin, and the activated clotting time was maintained at greater than 400 seconds throughout CPB for a total heparln dose of 40,000 units. Representatwe hemodynamics before CPB were BP 95/55, pulmonary artery (PA) pressure 26/16, right atrial pressure (CVP) 11, and cardiac index (CI) 1.8 L/min/m 2. The extracorporeal circuit was primed with 1,500 mL of balanced salt solution, 500 mL of 5% mannmtol solution, and 5,000 units of heparin. The initial hemoglobin concentration during CPB was 7.3 g/dL, which was increased to 8.8 g/dL by the end of CPB with 2 units of packed red blood cells (RBCs). An additional 1,200 mL of Plasmalyte was administered during bypass. Blood loss during CPB was conserved by a Haemonetics Cell Saver (Haemonetics, Inc, Bramtree, MA) device and did not appear excessive. The patient separated easily from bypass with a central venous pressure (CVP) of 3 mmHg and PA pressures of 28/13 mmHg. CI was 2.5 L/min/m 2, and protamine, 350 mg, was administered over 15 minutes. Soon after the protamine infusion was completed, the patient's systolic blood pressure (SBP) decreased to 64 mmHg. Intravenous hetastarch 6% was administered to maintain adequate CVP and PA diastolic pressures. However, even after 1,000 mL of hetastarch, hypotensmon continued. PAL pressure remained around 28/15 mmHg, while CVP remained less than 5 mmHg. CI was 4 to 4.5 L/min/m 2, whereas systemic vascular resistance (SVR) was 500 to 600 dyne/s/cm -5. With SBP m the 60s (mmHg) and mean arterial pressure (MAP) m the high 40s (mmHg), an anaphylactic or anaphylactoid reaction to protamine was presumed to be causing the hypotension. Diphenhydramine, 50 mg, and hydrocortisone, 120 rag, were administered intravenously, an epinephrine bolus (100 Ixg) was administered, and an epinephrine infusion was begun at 8 ixg/min. This therapy increased SBP into the 80s (mmHg), which was maintained by repeated 100-1xg boluses of epinephrine and by increasing the epinephrine infusion rate to 10 to 20 ~g/min. ABG