This article summarizes the properties of the drugs frequently used for intravenous induction of anaesthesia. The mechanism of general anaesthesia is still largely unknown, and so the physicochemical properties, metabolism and side effects of these drugs are more relevant to their use than the way that they cause unconsciousness. This article also highlights new developments in drug administration and some newer agents. \u00a9 2010 Elsevier Ltd. All rights reserved.
\n \n\n \n \nWe recently reported that volatile anaesthetics directly depress the isolated glomus cell response to hypoxia, halothane more so than sevoflurane, in a manner mimicking the action of these agents on the human hypoxic ventilatory response. We wished to extend these investigations to action of another agent (isoflurane), and we planned to examine the effects of this agent and halothane on background K(+) channels. In an isolated rat pup glomus cell preparation intracellular calcium [Ca(2+)]i (measured using indo-1 dye), halothane and isoflurane (0.45-2.73 MAC) depressed the Ca(2+) transient response to hypoxia (p = 0.028), halothane more than isoflurane (p < 0.001). Evaluating the effects of halothane, isoflurane (both 2.5 MAC) and hypoxia on the open probability of background TASK-like K(+) channels in cell attached patch recordings, halothane in euoxia strongly increased channel activity (2 fold) but isoflurane only increased activity by 50% (p < 0.001). In the presence of hypoxia halothane also increased channel activity (3 fold) while isoflurane again only had weak effects (p = 0.004). Thus there were marked differences between these agents on K(+) channel activity, comparable to their effects on the hypoxia induced Ca(2+) transient. When glomus cells were exposed to a depolarising stimulus using 100 mM K(+), both halothane and isoflurane modestly reduced the magnitude of the resulting Ca(2+) transient (by 44% and 10% respectively, p < 0.001). We conclude that the effect of volatile anaesthetics on the glomus cell response to hypoxia is mediated at least in part by their effect on background K(+) channels, and that this plausibly explains their whole-body effect. An additional effect on voltage-gated Ca(2+) is also possible.
\n \n\n \n \nThe purpose of this study was to ascertain if effects of halothane and sevoflurane (0.18-1.45 MAC) on the magnitude of the rise in intracellular calcium ([Ca(2+)]i with approximately 90s hypoxia (measured using indo-1 dye) in rat pup carotid body type I glomus cells. paralleled their known effects on the human hypoxic ventilatory response, where halothane is more depressive. We also assessed these agents' effect on [Ca(2+)]i response to 100 mM K(+). Halothane depressed the [Ca(2+])i transient in hypoxia more than sevoflurane (p = 0.036). Both agents also depressed the [Ca(2+)]i response to K+ - halothane more than sevoflurane (p = 0.004). These actions reflect their known influence on human hypoxic ventilatory response, consistent with the notion that the cellular process underlies the whole-body effect. The responses to K(+), which depolarises the cell membrane, indicates that in addition to a putative effect on K(+) channels, voltage-activated Ca(2+) channels may also be involved in the anaesthetic effect.
\n \n\n \n \nIn humans the ventilatory response to sustained isocapnic hypoxia is biphasic: after an initial rapid rise there follows a steady decline of the next 20-30 min termed hypoxic ventilatory decline (HVD). It is not known whether this secondary phase resides in a reducing activity of the peripheral or the central chemoreflex. We wished to assess if the Ca(2+) transient that occurs in glomus cells in response to hypoxia exhibits a form of HVD with sustained hypoxia that parallels the human ventilatory response, or if it exhibits a different response. Glomus cells enzymatically isolated from rat pups were exposed to 10 min sustained hypoxia (5% CO(2) in N(2)), asphyxia (20% CO(2) in N(2)), hypercapnia (20% CO(2) in air), 100 mM K+ and 2 mM Ba(2+). Intracellular Ca(2+) transients [Ca(2+)]i were measured using indo-1 dye. Hypoxia elicited rapid increase in [Ca(2+)]i followed by a gradual persistent decline over 10 min to 50% of the peak value. Asphyxia also elicited a biphasic response, with the acute response twice as great as that for hypoxia and the subsequent decline also twice as large occurring over a similar time course. Hypercapnia- and hyperkalaemia-evoked [Ca(2+)]i responses displayed a more rapid initial decline (within 2- min) but then stabilised. Exposure to Ba(2+) evoked characteristic spiking activity in the [Ca(2+)]i signal. Although the glomus cell shows some adaptation of response to a variety of stimuli, its response to hypoxia is characterized by a biphasic response with continued secondary decline in [Ca(2+)]i in a manner akin to HVD.
\n \n\n \n \nPURPOSE: Anecdotally, many hospitals experience shortfalls in anaesthetic consultant staffing. This paper aims to investigate whether these subjective experiences are confirmed objectively. DESIGN/METHODOLOGY/APPROACH: The paper hypothesises that a simple model that estimated service delivery capability using consultant entitlements to annual and other types of leave would not (null hypothesis) accurately predict the magnitude of any shortfall that existed. It also hypothesises that excessive leave-taking was an important cause of any shortfall. A comparison is made between the model predictions for total leave taken and service delivery with results from a real data set from a large university teaching hospital's department of anaesthetics. FINDINGS: The model prediction for leave (median total 45 days absence in a year per consultant, range (30-59)) closely matched the reality (median 41 days (tenth-ninetieth deciles 30-69)). Consequently, both model predictions and the real data for annual elective service delivery agreed: median 228 sessions (193-266) vs 232 (183-266) per consultant respectively. Taking into account likely service delivery by trainees (2,304-4,140 elective sessions in total annually) the predicted shortfall of 2,220 sessions was very close to the true elective service shortfall of 2,148 sessions for the department as a whole over the year. PRACTICAL IMPLICATIONS: Rejecting the null hypothesis, it is concluded that a simple model that estimates elective service delivery using leave entitlements as the main factor can accurately predict actual service capability for a department. There is no evidence that excessive leave-taking occurs. ORIGINALITY/VALUE: The paper computes an estimate that 2.2-2.6 consultants per functional operating theatre are necessary to ensure that staffing matches the elective workload.
\n \n\n \n \nPURPOSE: This paper sets out to investigate whether demand for gynaecological theatre time could be described in terms of the time required to undertake elective operations booked for surgery, and so help match the capacity to this. DESIGN/METHODOLOGY/APPROACH: A questionnaire assessed the estimates for total operation time for seven common operations, sent to surgeons, anaesthetists and nursing staff in one tertiary referral and one district general hospital (total 49 staff; response rate 58 per cent), and estimates were obtained from theatre computer logs. Average timings for each operation were then applied to cases added from clinics to the waiting list at the district general, to yield the mean demand for elective surgery, and were also applied to emergencies to estimate emergency workload. Finally these demand estimates were compared with the theatre capacity available. FINDINGS: The paper found no difference between the estimates of the three staff groups or between these and the theatre logs (p = 0.669), nor did it find that estimates differed between the two centers (p = 0.628). Including emergencies, the mean (95 per cent confidence intervals) demand at the district general was 2438 (1952-2924) min/week. RESEARCH LIMITATIONS/IMPLICATIONS: Although the paper modelled the variation in demand using the relevant variation in operation times, any additional variation caused by differences in booking rates from clinics over time was not nodelled. The minimum period over which data should be collected was not established. PRACTICAL IMPLICATIONS: The paper finds that the existing capacity of 1680 min/week did not match these needs and, unless it was increased, a rise in waiting lists was predictable. ORIGINALITY/VALUE: The paper concludes that time estimates for scheduled operations can be better used to assess the need for surgical operating capacity than current measures of demand or capacity.
\n \n\n \n \nThe ventilatory response to carbon dioxide (CO2) measured by modified rebreathing (SrVE) is closer to that measured by the steady-state method (SsVE) than is the response measured by Read's rebreathing method. Furthermore, the value estimated by the steady-state method depends upon the number of data points used to measure it. We planned to assess if these observations were also true for cerebral blood flow (CBF), as measured by steady-state (SsCBF) and modified rebreathing (SrCBF) tests. Six subjects undertook two protocols, one in the steady-state and one with modified rebreathing. SsVE depended upon the number of data points used to calculate it, and SsVE and SrVE were similar. However, this was not the case with SsCBF, and SsCBF was much higher than SrCBF. These findings are consistent with the notions that the specific CO2 stimulus differs for CBF control as compared with ventilation (VE) control, and that prior hypocapnia has an effect on CBF and VE for longer than the duration of the hypocapnia.
\n \n\n \n \nThis study was a systematic review of the anesthetic effect on carotid body response to hypoxia. We undertook a systematic literature search (electronic plus manual) for full-paper articles in English that used methodologies enabling any anesthetic effect to be located to the carotid body. We found just 7 articles that met our inclusion criteria, incorporating 16 separate studies. Anesthetic (mean dose +/- SD 0.70 +/- 0.33 MAC) significantly depressed carotid body response by 24% (p = 0.041). There were no differences between individual agents (halothane, enflurane, isoflurane) and no influence of the use of neuromuscular blockade or of species (although the data were sufficiently sparse to interpret such sub-group analysis with caution).
\n \n\n \n \nThis article summarizes the properties of the drugs frequently used for intravenous induction of anaesthesia. The mechanism of general anaesthesia is still largely unknown, and so the physicochemical properties, metabolism and side effects of these drugs are more relevant to their use than the way that they cause unconsciousness. This article also highlights some historical aspects of anaesthesia and new developments in drug administration. \u00a9 2007 Elsevier Ltd. All rights reserved.
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