We reported anesthetic management of a parturient of Jehova’s Witness with severe anemia(Hb: 5.8g/dl), undergoing emergent hysterectomy. Her massive bleeding continued following dilatation and curettage for missed abortion. Anesthesia was induced with propofol, fentanyl and rocuronium and maintained with sevoflurane and remifentanil. Hypotension after induction of anesthesia was treated with volume loading with 5% albumin and repeated bolus injection of phenylephrine. Although continuous infusion of dopamine was given to maintain blood pressure after start of the operation, ST segment depression was noted in II, III and aVF. Then, dopamine was replaced by noradrenaline and thereafter, ST depression was alleviated. Considering the episode of ST depression and the value of Hb of 2.8g/dl at end of the operation, the patient was transported to ICU without extubation and under sedation with propofol to suppress the oxygen consumption. The patient was extubated on 10th postoperative day without any respiratory or neurological complications. The present case suggests that perioperative management to suppress the oxygen consumption may be a useful for a patient of Jehova’s Witness with severe anemia.

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The aim of this study was to assess the usefulness of an arterial pressure-based cardiac output(APCO) monitoring system in the postperative management of patients undergoing esophagectomy. The FloTrac monitor(Edwards Lifescience) was used in three extubated patients who underwent radical operation for transthoracic esophagectomy with three field lympho node resection. Stroke volume variation, calculated for each respiratory cycle and displayed on the Vigileo monitor, could predict intravascular hypovolemia. It is suggested that the Vigileo monitor with FloTrac is an accurate predictor of intravascular hypovolemia and is a useful indicator for assessing the appropriateness and timing of applying fluid for improving circulatory stability during the postperative period of esophagectomy under spontaneous respiration.

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Since clonidine has a negative chronotropic effect and inhibits catecholamine release, it may blunt sympathetic-mediated heart rate acceleration secondary to vasodilation, thereby enhancing the hypotensive effect of vasodilators. In this study we examined whether preanesthetic clonidine medication would alter the hypotensive effect of nicardipine in surgical patients during general anesthesia.
After approval by the local ethical committee and informed consent, 60 surgical patients, ASA I, 24-67 yr, were selected for this study. The patients received oral clonidine approximately 5 μg/kg(clonidine-5 group, n＝20) or 2.5 μg/kg(clonidine-2.5 group, n＝19) 90 min before anesthesia, while the remaining 21 patients received no clonidine(control group). General anesthesia was induced with thiopental approximately 5 mg/kg, and maintained with an end-tidal concentration of isoflurane 0.3-0.9% and nitrous oxide 67% in oxygen after tracheal intubation. After obtaining hemodynamic stability, nicardipine 10 μg/kg was injected IV in 5 seconds. Blood pressure and heart rate were measured at 1-min intervals for 10 min following nicardipine. Data(mean±SD) were analyzed using ANOVA and Bonferroni’s multiple-comparison test, with P<0.05 being significant.
There were no significant differences with respect to demographic and pre-nicardipine hemodynamic data. The maximum decreases in mean blood pressure following nicardipine did not differ among the three groups(−15±5, −13±5, −13±6 mmHg in the clonidine-5, clonidine-2.5, and control groups, respectively).
These results suggest that oral clonidine 2.5 or 5 μg/kg medication did not enhance the hypotensive effect of nicardipine in normotensive patients during isoflurane anesthesia.

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