British journal of anaesthesia
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Randomized Controlled Trial Clinical Trial
Management of opioid-induced pruritus: a role for 5-HT3 antagonists?
We have evaluated the efficacy of ondansetron in the prevention of opioid-induced pruritus in a prospective, randomized, double-blind, placebo-controlled study. Using a 'human model' of opioid-induced pruritus, 80 ASA I-II patients about to undergo routine surgery were given either ondansetron 4 mg i.v. or 0.9% saline i.v. (40 in each group), 30 min before alfentanil 10 mg kg-1 i.v. During the following 5 min, patients were observed for signs of perinasal scratching and at 5 min were asked about symptoms of pruritus. ⋯ There was a significant reduction in the incidence of scratching in patients receiving ondansetron compared with placebo (42.5% vs 70%, respectively, P = 0.013). The incidence of itching in the ondansetron group was less than that in the placebo group but this was not statistically significant (30% vs 42.5%, respectively, P = 0.245). We conclude that the 5-HT3 antagonist ondansetron may have a role in the management of opioid-induced pruritus.
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Randomized Controlled Trial Clinical Trial
Effect of nitrous oxide on myogenic motor potentials evoked by a six pulse train of transcranial electrical stimuli: a possible monitor for aortic surgery.
Intraoperative recording of myogenic motor potentials evoked by transcranial electrical stimulation (tcMEP) is a method of monitoring the integrity of the vulnerable motor pathways during thoracoabdominal aortic aneurysm (TAAA) surgery. Deflation of the left lung during TAAA surgery may result in impairment of arterial oxygenation. Ventilation with nitrous oxide may cause further desaturation. ⋯ There was no significant difference in the coefficients of variation for tcMEP between the three nitrous oxide anaesthetic regimens. Our results suggest that increasing doses of nitrous oxide reduce the MEP waveform to six pulse transcranial electrical stimulation, but even with 60% nitrous oxide in oxygen, the tcMEP were recordable and as reproducible as with 20% and 40% nitrous oxide regimens. The method is sufficiently robust for use in aortic surgery.
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Propofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). ⋯ Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex.
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Bupivacaine induces fatal arrhythmia when accidentally injected i.v. or overdosed, whereas lidocaine is used as an anti-arrhythmic agent. We have suggested recently that the anti-arrhythmic effect of lidocaine may be explained by suppression of ATP-sensitive potassium (KATP) channels. Therefore, it could be argued that different sensitivities of KATP channels to both drugs could be a reason for their different arrhythmic and anti-arrhythmic properties. ⋯ Binding of bupivacaine influenced the gating of this channel, but did not reduce the conductance of the open channel. Bupivacaine and lidocaine were equipotent in blocking KATP channels. However, because of its excessive block of the sodium channel in the inactivated state, block of KATP channels by bupivacaine will only enhance its cardiotoxicity.