Anesthesia and analgesia
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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
Glycine receptors mediate part of the immobility produced by inhaled anesthetics.
Many inhaled anesthetics potentiate the effect of glycine on inhibitory strychnine-sensitive glycine receptors in vitro, supporting the view that this receptor could mediate the immobility produced by inhaled anesthetics during noxious stimulation (i.e., would underlie minimum alveolar anesthetic concentration [MAC]). There are quantitative differences between anesthetics in their capacity to potentiate glycine's effect in receptor expression systems: halothane (most potentiation), isoflurane (intermediate), and cyclopropane (minimal). If glycine receptors mediate MAC, then their blockade in the spinal cord should increase the MAC of halothane more than that of isoflurane and isoflurane MAC more than cyclopropane MAC; the increases in MAC should be proportional to the receptor potentiation produced in vitro. Rats with chronically implanted intrathecal catheters were anesthetized with halothane, isoflurane, or cyclopropane. During intrathecal infusion of artificial cerebrospinal fluid, MAC was determined. Then MAC was re-determined during an infusion of 3, 12, 24, or 48 (isoflurane only) micro g/min of strychnine (strychnine blocks glycine receptors) in artificial cerebrospinal fluid. Strychnine infusion increased MAC in proportion to the enhancement of glycine receptors found in vitro. The maximum effect was with an infusion of 12 micro g/min. For the combined results at 12 and 24 micro g/min of strychnine, the increase in MAC correlated with the extent of in vitro potentiation (r(2) = 0.82). These results support the hypothesis that glycine receptors mediate part of the immobilization produced by inhaled anesthetics. ⋯ In vitro, halothane potentiates glycine's effect on strychnine-sensitive glycine receptors more than isoflurane and isoflurane more than cyclopropane. The present in vivo work indicates that antagonism of the glycine receptor with strychnine increases minimum alveolar anesthetic concentration for halothane more than isoflurane and isoflurane more than cyclopropane. Such results support the notion that glycine receptors may mediate part of the immobility produced by inhaled anesthetics.
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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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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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Anesthesia and analgesia · Jan 2003
Hemodilution does not alter arterial baroreflex control of heart rate in anesthetized dogs.
The cardiovascular effects of acute normovolemic hemodilution (ANH) are characterized by increased cardiac output and decreased systemic vascular resistance. However, whether arterial baroreflex function is altered by ANH remains undetermined. We assigned 23 anesthetized, mechanically ventilated dogs to mild ANH (hemoglobin, 7-8 g/dL; n = 11) or profound ANH (hemoglobin, 4-5 g/dL; n = 12) achieved by phlebotomy and simultaneous exchange with lactated Ringer's solution at 1:3 ratio to maintain constant central venous pressure and pulmonary artery occluded pressure. Baroreflex sensitivity was assessed by measurements of RR intervals of the electrocardiogram and mean arterial blood pressure (MAP) through a femoral artery catheter. Baroreflex responses were triggered by bolus IV injections of phenylephrine (25-75 micro g) and nitroprusside (50-100 micro g). The linear portion of the baroreflex curves relating RR intervals and MAP were used to determine baroreflex sensitivities. Compared with the predilution period, both ANH groups had significant increases in cardiac output and decreases in systemic vascular resistance (P < 0.01), whereas MAP and heart rate (HR) remained unchanged. However, no significant difference was detected between pre-ANH and post-ANH baroreflex sensitivities in either group. Our results indicate that arterial baroreflex control of HR is preserved during ANH to a hemoglobin concentration of 4-5 g/dL in anesthetized dogs. ⋯ Acute normovolemic hemodilution may be preoperatively used to minimize the requirement of allogeneic blood products during major surgery. We found that baroreflex function is preserved during mild (hemoglobin concentration, 7-8 g/dL) and profound hemodilution (hemoglobin concentration, 4-5 g/dL) in pentobarbital-anesthetized dogs.