Anesthesia and analgesia
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Anesthesia and analgesia · Jul 2002
Comparative StudyE-cylinder-powered mechanical ventilation may adversely impact anesthetic management and efficiency.
Anesthesiologists often administer care outside the operating room. These locations may depend on gas cylinders for their oxygen source more than the operating suites supplied by dedicated central pipelines. Using full E-cylinders, we determined the oxygen consumption of two often used, pneumatically driven anesthesia ventilators to answer three questions: How much time is available when mechanically ventilating patients in the setting of absent or malfunctioning central oxygen pipeline? How much oxygen is used by the ventilator to drive the bellows? How does changing the inspiratory to expiratory ratio and the inspiratory flow (Narkomed ventilator only) influence oxygen use? At a ventilation of 5 L/min, we found that mechanical ventilation consumes between 59% and 85% of the available oxygen in an E-cylinder to drive the ventilator at fresh gas flows ranging from 1 to 10 L/min. The time span until the low oxygen alarm sounded ranged from 38 to 99 min. Alteration of the inspiratory flow but not the inspiratory to expiratory ratio had a significant impact. Clinicians must recognize that mechanical ventilation using E-cylinders rapidly depletes this sole oxygen source and could jeopardize patient safety. Conversely, manual or spontaneous ventilation with low fresh gas flows minimizes oxygen depletion. ⋯ The time available to ventilate patients with an E-cylinder tank as the sole oxygen source was found to be as short as 38 min. Clinicians must recognize that mechanical ventilation using oxygen cylinders rapidly depletes oxygen and could jeopardize patient safety.
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Anesthesia and analgesia · Jul 2002
An investigation of monoamine receptors involved in antinociceptive effects of antidepressants.
We attempted to determine which monoamine receptor subtypes are predominantly involved in antidepressant-induced antinociception. Antinociceptive effects were evaluated by using formalin tests with rats. Antidepressants acting as potent inhibitors of norepinephrine reuptake (nisoxetine, nortriptyline, and maprotiline) or inhibiting reuptake of both norepinephrine and serotonin (5-HT) (imipramine and milnacipran) induced dose-dependent antinociception. Simultaneous intraperitoneal administration of antidepressants and either prazosin (alpha(1) antagonist) or ketanserin (5-HT(2) antagonist) significantly antagonized antinociceptive effects. Fluvoxamine (selective serotonin reuptake inhibitor) induced antinociception less potently than other antidepressants and was significantly antagonized by ketanserin, but not prazosin. Ondansetron (5-HT(3) antagonist) significantly antagonized antinociception by 10 mg/kg of imipramine. In contrast, SDZ-205,557 (5-HT(4) antagonist) markedly enhanced antinociception by small-dose (2.5 mg/kg) imipramine. Imipramine-induced antinociception was significantly antagonized by intracerebroventricular administration of prazosin or ketanserin, but not by yohimbine (alpha(2) antagonist) or ondansetron, and was significantly enhanced by intracerebroventricularly administered SDZ-205,557. These findings suggest that alpha(1) adrenoceptors and 5-HT(2) receptors in the brain are involved in antidepressant-induced antinociception. In addition, the results suggested functional interactions between noradrenergic and serotonergic neurons as mechanisms for antidepressant-induced antinociception. ⋯ Formalin tests of rats treated with antidepressants and antagonists of monoamine receptors indicate that alpha(1) adrenoceptors, serotonin (5-HT)(2) receptors, and 5-HT(3) receptors are involved in antidepressant-induced antinociception, suggesting functional interactions between noradrenergic and serotonergic neurons as mechanisms of antidepressant-induced antinociception.
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Anesthesia and analgesia · Jul 2002
Letter Case ReportsKnotting of an epidural catheter like a tie.