British journal of anaesthesia
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Published work on knowledge in regional anaesthesia has focused on competence, for instance by identifying numbers of procedures required to achieve competence, or by defining criteria for successful performance of blocks. We aimed to define expertise in regional anaesthesia and examine how it is acquired. ⋯ Expertise in regional anaesthesia extends beyond competence at technical performance; non-cognitive elements are also vital. Further work is needed to test our learning model, and the hypothesis that learning can be enhanced by deliberate promotion of the tacit elements of 'expertise' we have described.
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Neuraxial anaesthesia in adults decreases the dose of i.v. or inhalational anaesthetic needed to reach a desired level of sedation. Furthermore, spinal anaesthesia alone has a sedative effect. The mechanism behind this phenomenon is presumed to be decreased afferent stimulation of the reticular activating system after sympatholysis. We hypothesized that this mechanism is equally active in infants undergoing spinal anaesthesia. ⋯ These results suggest that sedation after spinal anaesthesia in infants is at least as pronounced as in adults. The sedative effect of spinal anaesthesia should be kept in mind when additional sedatives are administered, especially in former preterm infants.
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Sevoflurane protects the myocardium against ischaemic injury through protein kinase C (PKC) activation, mitochondrial K+ATP-channel (mitoK+ATP) opening and production of reactive oxygen species (ROS). However, it is unclear whether the type of ischaemia determines the involvement of these signalling molecules. We therefore investigated whether hypoxia (HYP) or metabolic inhibition (MI), which differentially inhibit the mitochondrial electron transport chain (ETC), are comparable concerning the relative contribution of PKC, mitoK+ATP and ROS in sevoflurane-induced cardioprotection. ⋯ PKC, mitoK+ATP and ROS are involved in sevoflurane-induced cardioprotection after HYP or MI, suggesting that the means of mitochondrial ETC inhibition does not determine the signal transduction pathway for cardioprotection by anaesthetics.