Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1998
Randomized Controlled Trial Comparative Study Clinical TrialRocuronium versus succinylcholine: are they equally effective during rapid-sequence induction of anesthesia?
The purpose of our study was to assess the onset and quality of muscle paralysis and intubation conditions with succinylcholine (Sch) or rocuronium (Roc) during rapid-sequence induction. Patients were randomly assigned to receive thiopental (5 mg/kg) and Sch (1.5 mg/kg) or thiopental (5 mg/kg) and Roc (1.2 mg/kg). The anesthesiologists performing the endotracheal intubation were blinded by standing with their back to the patient. Thirty seconds after drug administration, laryngoscopy was performed. Intubating conditions were scored, the clinical onset of apnea was noted, and a train-of-four monitor recorded data. All patients were ASA physical status I-III and scheduled for emergency procedures; both groups were demographically similar. Thirteen patients received Roc and 13 received Sch. There was no significant difference between the two groups in the number of patients receiving excellent intubating scores (P = 0.41) or in the combined number of patients receiving good and excellent scores (P = 1.0). There was no significant difference in time of onset of apnea for Sch (22+/-13 s) versus Roc (16+/-8s). The return of the first twitch response was significantly faster with Sch (5.05+/-2.5 min) compared with Roc (17.3+/-21.7 min) (P = 0.0001). ⋯ In pediatric patients scheduled for emergency surgery, thiopental 5 mg/kg and rocuronium 1.2 mg/kg provided conditions for the completion of intubation in <60 s comparable to those provided by thiopental 5 mg/kg and succinylcholine 1.5 mg/kg. We conclude that rocuronium is a reasonable substitute for succinylcholine in children for rapid-sequence intubation when a rapid return to spontaneous respiration is not desired.
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Anesthesia and analgesia · Dec 1998
Randomized Controlled Trial Clinical TrialThe use of metoprolol and glycopyrrolate to prevent hypotensive/bradycardic events during shoulder arthroscopy in the sitting position under interscalene block.
Sudden profound hypotensive and/or bradycardic events (HBE) have been reported in >20% of patients undergoing shoulder arthroscopy in the sitting position under interscalene block anesthesia. Retrospective studies suggest that the administration of beta-blockers is safe and may decrease the incidence of these episodes. We performed a randomized, prospective study to evaluate prophylaxis of these events. One hundred fifty patients were randomized to one of three groups (placebo; prophylactic metoprolol to achieve a heart rate <60 bpm or a maximal dose of 10 mg; or prophylactic glycopyrrolate to achieve a heart rate >100 bpm or a maximal dose of 6 microg/kg) immediately after the administration of the interscalene block. Blood pressure control was achieved with IV enalaprilat as needed. The incidence of HBE was 28% in the placebo group versus 5% in the metoprolol group (P = 0.004). The rate of 22% in the glycopyrrolate group was not significantly different from placebo. Preoperative heart rate and arterial blood pressure, intraoperative sedation score, IV fluids, and enalaprilat use were similar in those patients who had a HBE compared with those who did not. Many aspects of this clinical setting are similar to tilttable testing for patients with recurrent vasovagal syncope, in which beta-adrenergic blockade with metoprolol has also been shown to be effective. We conclude that the Bezold-Jarisch reflex is the most likely mechanism for these events. ⋯ Episodes of acute hypotension and bradycardia occur during shoulder arthroscopy in the sitting position under interscalene block. In this study, we demonstrate that metoprolol, but not glycopyrrolate, markedly decreases the incidence of these episodes when given prophylactically immediately after the administration of the block.
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Anesthesia and analgesia · Dec 1998
Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane.
Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. ⋯ Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.
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Anesthesia and analgesia · Dec 1998
The role of the N-methyl-D-aspartic acid receptor in the relaxant effect of ketamine on tracheal smooth muscle.
Ketamine and magnesium (Mg2+), well known bronchodilators, have been used to treat patients with status asthmaticus. Both can block the N-methyl-D-aspartic acid (NMDA) receptor. NMDA receptors exist in the airway, and their activation seems to be linked to the release actions of sensory neuropeptides resulting in increased airway tone. We sought to determine whether ketamine relaxes the guinea pig trachea contracted by histamine by blocking the NMDA receptor. Female guinea pigs (250-400 g) were killed with an overdose of pentobarbital. The trachea was removed and cut spirally into strips 3 mm wide and 15 mm long. The strips were mounted in a 10-mL organ bath filled with Tyrode's solution bubbled through with 95% O2/5% CO2 at 37 degrees C. Strip contractions were measured isometrically with a force displacement transducer. We then studied the effect of NMDA receptor antagonists on histamine-induced tracheal contraction. In this protocol, we examined the effect of ketamine, Mg2+, zinc (Zn2+), or MK-801 (a noncompetitive NMDA receptor blocker) on strips contracted by 10(-5) M histamine. After full contraction was attained, ketamine (0.5-1.5 mM), MgSO4 (2-8 mM), ZnCl2(0.2-0.8 mM), or MK-801 (1.5-6 x 10(-5) M) was added, and the strip tension was measured again. We also studied the effect of NMDA on the relaxation by ketamine. After full contraction by 10(-5) M histamine, 0.5-1.5 mM KET was added alone or in combination with 0.1 mM NMDA, and the strip tension was measured again. Finally, we measured the effect of MK-801 on the relaxant effect of ketamine. After full contraction by 10(-5) M histamine, 0.5-2 mM ketamine was added alone or in combination with 0.75 or 1.5 x 10(-5) M MK-801, and the strip tension was measured again. All NMDA receptor antagonists tested reversed the tracheal contraction induced by histamine in a dose-dependent manner. However, neither the agonist NMDA nor the noncompetitive receptor blocker MK-801 affected tracheal relaxation induced by ketamine. We conclude that ketamine relaxes the tracheal smooth muscle contracted by histamine through a mechanism independent of NMDA receptors. The decreased bronchomotor tone induced by ketamine is probably due to interference with a Ca2+-requiring step necessary to maintain the contraction caused by histamine. ⋯ Stimulation of the N-methyl-D-aspartic acid (NMDA) receptor in the airway results in airway constriction. The bronchodilator ketamine blocks the NMDA receptor. However, ketamine relaxes the guinea pig trachea contracted by histamine through a mechanism independent of the NMDA receptor.