Anesthesiology
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Cutaneous infiltration of dilute solutions of epinephrine for hemostasis during halothane anesthesia can result in ventricular dysrhythmias. Our clinical experience, published reports, and a study comparing piglets with adult swine suggest that children may be less susceptible than adults to dysrhythmias under these conditions. We therefore undertook a prospective survey of heart rate and rhythm in halothane-anesthesized children who received subcutaneous epinephrine for hemostasis. ⋯ The authors conclude that children tolerate higher doses of subcutaneous epinephrine than adults during halothane anesthesia. The arrhythmogenic dose of epinephrine in children receiving halothane has yet to be determined, but at least 10 micrograms/kg of epinephrine infiltration may be used safely in normocarbic and hypocarbic pediatric patients without congenital heart disease. The presence of PAC and tachycardia emphasize the need for continuous ECG monitoring and caution during halothane anesthesia with epinephrine injection.
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The authors investigated whether the increases in venous admixture and intrapulmonary shunt which occur with increases in cardiac output (Qt) results from an effect mediated by mixed venous PO2 (PVO2) or an effect mediated by the increase in pulmonary blood flow. Using a veno-venous bypass system thay were able to alter PVO2 independent of variations in Qt and vice versa. During room air ventilation of dogs with normal lungs at constant Qt, an increase in PVO2 from 33 +/- 7 (mean +/- SD) to 54 +/- 9 mmHg (P less than 0.05) resulted in a decrease in venous admixture from 22 +/- 11 to 13 +/- 4% (P less than 0.05). ⋯ The authors conclude that during oxygen ventilation, normal dogs have shunts which are unaffected by changes in blood flow or PVO2. Increases in pulmonary blood flow increase venous admixture during room air ventilation, while increases in PVO2 decrease venous admixture during air ventilation. In edematous lungs, increases in either PVO2 or pulmonary blood flow increase shunt.
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Exposure of triiodothyronine (T3)-pretreated rats to 1.3% isoflurane, 1.8% enflurane, or 1% halothane in 21% oxygen (air) for two hours resulted in hepatic centrilobular necrosis. The incidence of the liver lesion was 28, 24, and 92% after exposure to isoflurane, enflurane, and halothane, respectively. Histopathologic grading indicated that the necrosis was more severe after halothane than after isoflurane or enflurane anesthesia. ⋯ Liver necrosis did not occur in pentobarbital anesthetized (40 mg/kg, intraperitoneally) T3-pretreated rats. These results indicate that isoflurane and enflurane, like halothane, can induce hepatic centrilobular necrosis in T3-pretreated rats. The mechanism for liver toxicity of these volatile anesthetic agents in this model remains to be determined.
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Comparative Study
Anesthetic potencies of isoflurane, halothane, and diethyl ether for various end points of anesthesia.
In experiments with rats, the authors compared potency ratios and slopes of dose-effect curves of isoflurane, halothane, and diethyl ether for three end points of anesthesia: loss of righting reflex (RR), abolition of purposeful movement (PM) response to painful stimuli, and abolition of heart rate (HR) response to painful stimuli. Determinations of potency were based on the direct measurement of brain concentrations of anesthetics with the use of gas chromatography. It was found that the ratio of the PM ED50 to RR ED50 was 2.41 for isoflurane, 1.74 for halothane, and 1.25 for diethyl ester. ⋯ The ratios of HR ED50 to PM ED50 were not significantly different for the studied agents and there were no differences found between the slopes of the dose-effect curves for PM and HR. The results suggest that heart rate response to a noxious stimuli in contrast to the righting reflex is depressed by inhalation anesthetics through a mechanism similar to that underlying the depression of purposeful movement response to a noxious stimuli. Heart rate response to a noxious stimuli might be used as an alternative index for the measurement of anesthetic potency.