Pathophysiology and treatment of venous air embolism--a review.
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Biomedical subjects
Publications and source records attributed to E S Munson.
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Cyclopropane requirement (MAC) in rats was determined before, during, and after repeated exposure to anaesthetic concentrations of cyclopropane and halothane for one hour every day for 20 and 30 days, respectively. MAC values during and after exposure ranged from 93 to 103 per cent (mean = 99 per cent) of control values, which indicates a lack of significant tolerance to cyclopropane or a cross-tolerance between cyclopropane and halothane.
The minimum alveolar concentration (MAC) of cyclopropane was determined in young (mean age, 32 yr; n = 16) and older (mean age, 81 yr; n = 12) surgical patients. Cyclopropane requirement was 23% lower in the elderly (P less than 0.01). This reduction in anesthetic requirement with age is similar to that reported previously for halothane and isoflurane and supports the thesis of a general effect of age on anesthetic requirement.
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Adverse effects may occur when patients with air in the pleural space or in the cerebral ventricles breathe nitrous oxide. We developed an animal model to learn whether similar adverse effects are associated with the inhalation of nitrous oxide when air is present in the subcutaneous space. We induced extensive subcutaneous emphysema in swine and measured oxygen and carbon dioxide tensions in systemic arterial and mixed venous blood; cardiac output; intravascular, airway, and pre-sternal subcutaneous pressures; total pulmonary-thoracic static compliance; and thoracic girth before and after a 45 minute period of breathing 75 per cent nitrous oxide in oxygen. Cardiac output decreased from 3.13 +/- 0.51 l/min to 2.40 +/- 0.62 l/min (p less than 0.05); no other values changed significantly. No significant adverse cardiorespiratory effects resulted from the transfer of inhaled nitrous oxide to the subcutaneous space in this animal model.
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Arrhythmogenic doses of epinephrine were determined in six mongrel dogs anesthetized at 1.4 MAC halothane initially in the absence of local anesthetics and then at increasing arterial plasma levels of lidocaine, bupivacaine, and etidocaine. The authors gave epinephrine intravenously at 5 microgram/kg/min and calculated the arrhythmogenic dose as a function of time until two or more premature ventricular contractions occurred within a 10-sec period. The control arrythmogenic dose of epinephrine was 4.66 +/- 0.46 microgram/kg (mean +/- SEM). Arrythmogenic doses of epinephrine were increased significantly after each dose of lidocaine, bupivacaine, and etidocaine. With the largest doses studied, local anesthetic plasma levels were frequently in the toxic range. The data show that lidocaine, bupivacaine, and etidocaine equally protect against epinephrine-induced arrhythmias in dogs anesthetized with halothane.
The authors studied the effects of pancuronium, 14--200 micrograms/kg, on epinephrine-induced arrhythmias (premature ventricular contractions) in dogs anesthetized with halothane, 1.4 MAC. Neither muscle relaxant significantly affected the arrhythmogenic dose of epinephrine. This finding indicates that the usual guidelines for the administration of epinephrine during halothane anesthesia are not affected by concomitant administration of the two nondepolarizing muscle relaxants studied.
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