Anesthesia and analgesia
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Anesthesia and analgesia · Mar 1996
The response to varying concentrations of inhaled nitric oxide in patients with acute respiratory distress syndrome.
We investigated the response to varying concentrations of inhaled nitric oxide (NO) in 18 patients with acute respiratory distress syndrome (ARDS). The study was divided into two parts. In Part 1, 5-40 ppm of inhaled NO was evaluated in 10 patients with ARDS. ⋯ While the maximum hemodynamic and oxygenation responses to inhaled NO are achieved at approximately 1 ppm, it appears that the maximum hemodynamic response is observed at lower concentrations (0.1 ppm) of inhaled NO than the improvement in oxygenation (1-10 ppm). Higher concentrations of NO do not produce any further change in these variables. It appears that the baseline PVRI may be the best marker predicting a beneficial response to NO.
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Anesthesia and analgesia · Mar 1996
Comparative StudyComparative electrophysiologic and hemodynamic effects of several amide local anesthetic drugs in anesthetized dogs.
Large and equipotent doses of several local anesthetics were administered in a cardiac electrophysiologic model on closed-chest dogs. Five groups of pentobarbital-anesthetized dogs were each given intravenously 16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocaine, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of atrioventricular node conduction (AH), and marked hemodynamic depression, represented by a decrease in mean aortic pressure (MAoP), in the peak of first derivative of left ventricular pressure (LVdP/dt(max)) and by an increase in left ventricular end-diastolic pressure (LVEDP). ⋯ We conclude that mepivacaine induced moderate cardiotoxicity. In contrast, lidocaine induced dramatic hemodynamic depression while etidocaine and bupivacaine markedly impaired both electrophysiologic and hemodynamic variables. This double impairment could explain the great difficulty in resuscitating patients who have had cardiotoxic accidents induced by etidocaine or bupivacaine.
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The anesthetist exerts axial force on the laryngoscope handle to expose the glottis. The anesthetist must also apply a perpendicular force to balance the torque on the laryngoscope. Several studies have measured axial force during direct laryngoscopy, but none has measured torque. ⋯ Peak force and torque demonstrated stress relaxation, a viscous property of biologic tissues. Force and torque decreased monoexponentially to approximately 70% of peak values with a half-time of 4 +/- 0.3 s. The phenomenon occurred in spite of administration of muscle relaxants, and was probably due to stress relaxation of pharyngeal tissues that are passively stretched during laryngoscopy.