Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2003
Minimum alveolar anesthetic concentration of isoflurane with different xenon concentrations in Swine.
For patients requiring a fraction of inspired oxygen more than 0.3, the use of xenon (Xe) as the sole anesthetic is limited because of its large minimum alveolar anesthetic concentration (MAC) of 71%. This warrants investigating the combination of Xe with other inhaled anesthetics. We therefore investigated the influence of Xe on the MAC of isoflurane. The study was performed in 10 swine (weight, 28-35 kg) ventilated with Xe 0%, 15%, 30%, 40%, 50%, and 65% in oxygen. For each Xe concentration, various concentrations of isoflurane were administered in a step-wise design. For each combination, a supramaximal pain stimulus (claw-clamp) was applied, and the appearance of a withdrawal reaction was recorded. The isoflurane MAC was defined as the end-tidal concentration required to produce a 50% response rate. At each Xe concentration, the responses to the pain stimulus were categorized, and a logistic regression model was fitted to the results to determine isoflurane MAC. Isoflurane MAC was decreased by inhalation of Xe in a nonlinear manner from 1.92% (95% confidence interval, 1.70%-2.15%) with 0% Xe to 1.17% (95% confidence interval, 0.75%-1.59%) with 65% Xe. Although this indicates partial antagonism of the two anesthetics, a combination of Xe with isoflurane may prove valuable for patients requiring a fraction of inspired oxygen more than 0.3. ⋯ We investigated the influence of the anesthetic gas xenon on the minimum alveolar anesthetic concentration (MAC) for isoflurane (another anesthetic gas). The study was performed in 10 swine ventilated with fixed xenon and various concentrations of isoflurane. The isoflurane MAC is decreased by inhalation of xenon in a nonlinear relationship.
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Anesthesia and analgesia · Jan 2003
Modulation of GABA(A) receptor function by nonhalogenated alkane anesthetics: the effects on agonist enhancement, direct activation, and inhibition.
At clinically relevant concentrations, ethers, alcohols, and halogenated alkanes enhance agonist action on the gamma-aminobutyric acid(A) (GABA(A)) receptor, whereas nonhalogenated alkanes do not. Many anesthetics also directly activate and/or inhibit GABA(A) receptors, actions that may produce important behavioral effects; although, the effects of nonhalogenated alkane anesthetics on GABA(A) receptor direct activation and inhibition have not been studied. In this study, we assessed the abilities of two representative nonhalogenated alkanes, cyclopropane and butane, to enhance agonist action, directly activate, and inhibit currents mediated by expressed alpha(1)beta(2)gamma(2L) GABA(A) receptors using electrophysiological techniques. Our studies reveal that cyclopro- pane and butane enhance agonist action on the GABA(A) receptor at concentrations that exceed those required to produce anesthesia. Neither nonhalogenated alkane directly activated nor inhibited GABA(A) receptors, even at concentrations that approach their aqueous saturated solubilities. These results strongly suggest that the behavioral actions of nonhalogenated alkane anesthetics do not result from their abilities to enhance agonist actions, directly activate, or inhibit alpha(1)beta(2)gamma(2L) GABA(A) receptors and are consistent with the hypothesis that electrostatic interactions between anesthetics and their protein binding sites modulate GABA(A) receptor potency. ⋯ When normalized to either their in vivo anesthetic potencies or hydrophobicities, cyclopropane and butane are 1-1.5 orders of magnitude less potent enhancers of agonist action on alpha(1beta2gamma2L) GABA(A) receptors than isoflurane. Additionally, cyclopropane and butane fail to directly activate or inhibit receptors, even at near aqueous saturating concentrations. Thus, it is unlikely that either enhancement or inhibition of the most common GABA(A) receptor subtype in the brain accounts for the behavioral activities of cyclopropane and butane.
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Reports of anesthesia personnel shortages in 2001 led to the first comprehensive analysis of labor supply and demand for anesthesiologists since 1993. We now update this analysis and forecast, incorporating newly available data about residency composition, American Board of Anesthesiology and Certified Registered Nurse Anesthetist certification, the 2002 residency match, surgical facilities, and the US physician workforce. In addition, US residency programs were surveyed; national health care utilization and economic data were reviewed. Adjusted for the new information, our model still shows an anesthesiologist shortfall in 2002, projected to continue through 2005. We now estimate a current shortage of 1100-3800 anesthesiologists in 2002, on the basis of past service demand growth assumptions of 2%-3%, respectively. By 2005 this number is expected to be 500-3900, depending on a future service demand growth of 1.5%-2%, respectively. To avoid a surplus of anesthesiologists in 2006-2010, our model suggests that the number of graduates should level out at 1600 yearly, with a 1.5% service demand growth. To forecast the anesthesia personnel market more accurately, thereby helping supply match demand, substantially better quantification of future demand for anesthesia services is needed. If sustained growth in service demand >1.5% is likely, entry into the specialty should be encouraged beyond the current level. ⋯ With updates from training programs, surgical activity, and other sources, our previously described model estimates a continuing shortfall of 1000-3800 anesthesiologists in 2002 and 500-3900 in 2005, assuming that service demand growth is 1.5% or 2% annually. If service growth >1.5% is likely, entry into the specialty should be encouraged beyond current levels.
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Anesthesia and analgesia · Jan 2003
One-lung ventilation with high tidal volumes and zero positive end-expiratory pressure is injurious in the isolated rabbit lung model.
We tested the hypothesis that one-lung ventilation (OLV) with high tidal volumes (VT) and zero positive end-expiratory pressure (PEEP) may lead to ventilator-induced lung injury. In an isolated, perfused rabbit lung model, VT and PEEP were set to avoid lung collapse and overdistension in both lungs, resulting in a straight pressure-time (P-vs-t) curve during constant flow. Animals were randomized to (a) nonprotective OLV (left lung) (n = 6), with VT values as high as before randomization and zero PEEP; (b) protective OLV (left lung) (n = 6), with 50% reduction of VT and maintenance of PEEP as before randomization; and (c) control group (n = 6), with ventilation of two lungs as before randomization. The nonprotective OLV was associated with significantly smaller degrees of collapse and overdistension in the ventilated lung (P < 0.001). Peak inspiratory pressure values were higher in the nonprotective OLV group (P < 0.001) and increased progressively throughout the observation period (P < 0.01). The mean pulmonary artery pressure and lung weight gain values, as well as the concentration of thromboxane B(2), were comparatively higher in the nonprotective OLV group (P < 0.05). A ventilatory strategy with VT values as high as those used in the clinical setting and zero PEEP leads to ventilator-induced lung injury in this model of OLV, but this can be minimized with VT and PEEP values set to avoid lung overdistension and collapse. ⋯ One-lung ventilation with high tidal volumes and zero positive end-expiratory pressure (PEEP) is injurious in the isolated rabbit lung model. A ventilatory strategy with tidal volumes and PEEP set to avoid lung overdistension and collapse minimizes lung injury during one-lung ventilation in this model.
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Although both alpha2-adrenergic agonists and cyclooxygenase inhibitors produce analgesia, their exact sites of action and interaction remain unclear. A previous report demonstrated a surprising inhibition of antinociception in rats from intrathecal clonidine by co-administered ketorolac. There are no other reports of interaction between these two classes of analgesics. We therefore reexamined this interaction, determining the effect of intrathecal clonidine and ketorolac alone and in combination in normal rats. Clonidine, but not ketorolac, produced antinociception to noxious hind paw thermal stimulation. The addition of ketorolac significantly enhanced the effect of clonidine, indicating a synergistic interaction for analgesia. Although the reasons for the discrepancy between this and the previous report are unclear, these results are consistent with previous studies that indicate an antinociceptive action of intrathecal alpha2-adrenergic agonists in the normal condition, a lack of such effect for cyclooxygenase inhibitors, and positive reinforcing effects of these two systems when co-stimulated. ⋯ Spinal injection of the alpha2-adrenergic agonist clonidine and the cyclooxygenase inhibitor ketorolac results in a synergistic interaction for antinociception in normal animals, suggesting that the combination of these drugs will enhance rather than detract from the analgesia of either alone.