Hemodynamic compensation during acute normovolemic hemodilution.

To the Editor:— Acute normovolemic hemodilution (ANH) causes a reduction in arterial oxygen content because of reduced hemoglobin concentration. The primary compensatory mechanism during ANH is an increase in cardiac output to maintain systemic oxygen delivery. 1,2 Therefore, the lower limit of an acceptable hemoglobin concentration is related to how low hemoglobin can be reduced without jeopardizing the ability of the heart to sustain an augmented pumping requirement. Previous studies have shown that the tolerance to ANH was diminished when the heart had a perfusion deficit, e.g. , critical coronary stenosis, or when it was pharmacologically depressed with either disopyramide or isoflurane. 3–5 Not surprisingly, Van der Linden et al. 6 demonstrated similar findings during pharmacologic depression by the anesthetics halothane and ketamine. The authors found that the critical hemoglobin concentration at low anesthetic doses was approximately 3 g/dl (a value consistent with that found by us in dogs anesthetized with “low doses” of either isoflurane or fentanyl–midazolam 2,3 ), whereas this value was increased to approximately 5 g/dl at high anesthetic doses. They explained their findings on a complete blunting of the compensatory increases in cardiac output during ANH and attribute this effect to an enhanced cardiodepressive action of the anesthetics at the high doses. dual-chamber pacemaker radiofrequency Frequency of the possible imped-ance, of 4.2–7.0 intravenous general anesthesia, four 12-min radiofrequency ablations were performed, two in the and two in the superior portions of the At the start of radiofrequency ablation, the pacemaker rate from 63 to 96 beats/min (fig. an irregular pacing rhythm with intermittent runaway pacing during application of the radiofrequency current (fig. of complete atrioventricular identified. To the Editor:— The anesthesiology literature describing coronary spasm after intravascular injection of an ergot alkaloid used for the treatment of uterine atony is limited to one case report. 1 I herein report a similar case in association with intramyometrial injection of the drug. An otherwise healthy (there were, specifically, no coronary risk factors) 36-year-old white woman (height, 165 cm; weight, 71 kg; gravida 2, para 1) at 39 weeks’ gestation required an elective repeat cesarean delivery for fetal macrosomia, which was conducted under spinal anesthesia. After the uneventful delivery of the fetus and despite uterine massage and a continuous intravenous oxytocin infusion, the uterus remained atonic. A single intramyometrial injection of 0.2 mg methylergonovine maleate was administered by the obstetrician. The patient reported the almost immediate onset of a severe left-sided substernal chest pain, radiating to her left arm, and shortness of breath. Blood pressure was 110/61 mmHg, heart rate was 86 beats/min, respi- ratory rate was 18 breaths/min, and oxygen saturation was 100%. The electrocardiogram revealed normal sinus rhythm with nonspecific T- wave abnormalities and transient ST-segment elevation. The rapid onset of chest pain after administration of Methergine (Novartis Phar- maceuticals, East Hanover, NJ) and the patient’s report of chest tight-ness after a drug given to help the uterus contract at the time of her first cesarean delivery (which had not been conveyed to the anesthesiologist and the obstetrician before the current event) led, in this case, to the prompt diagnosis and immediate treatment of myocardial ischemia. The clinical symptoms (chest pain) and the electrocardiographic changes were reversed with intravenous injection of 3.5 (cid:3) g/kg nitroglycerin,