Anesthesia and analgesia
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Anesthesia and analgesia · Aug 1998
Randomized Controlled Trial Clinical TrialIncidence and time course of cardiovascular side effects during spinal anesthesia after prophylactic administration of intravenous fluids or vasoconstrictors.
We studied the time course of arterial hypotension and/or bradycardia requiring treatment during spinal anesthesia and compared the efficacy of i.v. fluid or vasoconstrictor administration for the prevention of these side effects. Patients (n = 1066) were randomly allocated to either a volume group (lactated Ringer's solution 15 mL/kg within 15 min before spinal anesthesia), a dihydroergotamine group (10 microg/kg i.m. 15 min before anesthesia), or a placebo group. All patients breathed O2-enriched air during spinal anesthesia (4 mL of plain 0.5% bupivacaine). With the placebo, there were side effects (mean incidence 22.9%) for up to 45 min after the start of anesthesia. Dihydroergotamine reduced the incidence of side effects, preferentially the late ones, more (mean incidence 11.8%) than fluid administration (mean incidence 16.9%), which was effective only during the first 15 min of anesthesia. Both heart rate and arterial pressure decreased within 15 min before the manifestation of symptoms. In a subgroup of patients, the incidence of side effects (8%) was greatly reduced by the intraoperative application of both sedatives and opioids. We conclude that cardiovascular side effects may occur at any time during spinal anesthesia. Fluid administration reduced the incidence of early events, but dihydroergotamine the late events. ⋯ Cardiovascular side effects requiring treatment occurred at any time during spinal anesthesia in our placebo-controlled study, regardless of the prophylactic regimen (fluid infusions versus dihydroergotamine).
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Anesthesia and analgesia · Aug 1998
Randomized Controlled Trial Clinical TrialThe efficacy of intrathecal neostigmine, intrathecal morphine, and their combination for post-cesarean section analgesia.
We designed this study to evaluate the postoperative analgesic efficacy and safety of intrathecal (i.t.) neostigmine, i.t. morphine, and their combination in patients undergoing cesarean section under spinal anesthesia. Seventy-nine term parturients were randomly divided into four groups to receive isotonic sodium chloride solution 0.2 mL, neostigmine 25 microg, morphine 100 microg, or the combination of i.t. neostigmine 12.5 microg and morphine 50 microg with i.t. 0.5% hyperbaric bupivacaine 12 mg. There were no significant differences among the four groups with regard to spinal anesthesia, maternal blood pressure and heart rate, or fetal status. Postoperative analgesia was provided by i.v. patient-controlled analgesia (PCA) using fentanyl and ketorolac. Compared with the saline group, the time to first PCA use was significantly longer in the neostigmine group (P < 0.001), with lower 24-h analgesic consumption (P < 0.001). Nausea and vomiting were the most common side effects of i.t. neostigmine (73.7%). Analgesic effectiveness was similar between the neostigmine and morphine groups. Compared with the neostigmine group, the combination group had significantly prolonged analgesic effect and reduced 24-h PCA consumption (P < 0.05) with less severity of nausea and vomiting (P = 0.058). Compared with the morphine group, the combination group tended to have prolonged times to first PCA use (P = 0.054) with a lower incidence of pruritus (P < 0.03). ⋯ Intrathecal (i.t.) neostigmine 25 microg produced postoperative analgesia for cesarean section similar to that of i.t. morphine 100 microg, but with a high incidence of nausea and vomiting. The combination of i.t. neostigmine 12.5 microg and i.t. morphine 50 microg may produce better postoperative analgesia with fewer side effects than i.t. neostigmine 25 microg or i.t. morphine 100 microg alone.
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Anesthesia and analgesia · Aug 1998
A molecular description of how noble gases and nitrogen bind to a model site of anesthetic action.
How some noble and diatomic gases produce anesthesia remains unknown. Although these gases have apparently minimal capacities to interact with a putative anesthetic site, xenon is a clinical anesthetic, and argon, krypton, and nitrogen produce anesthesia at hyperbaric pressures. In contrast, neon, helium, and hydrogen do not cause anesthesia at partial pressures up to their convulsant thresholds. We propose that anesthetic sites influenced by noble or diatomic gases produce binding energies composed of London dispersion and charge-induced dipole energies that are sufficient to overcome the concurrent unfavorable decrease in entropy that occurs when a gas molecule occupies the site. To test this hypothesis, we used the x-ray diffraction model of the binding site for Xe in metmyoglobin. This site offers a positively charged moiety of histidine 93 that is 3.8 A from Xe. We simulated placement of He, Ne, Ar, Kr, Xe, H2, and N2 sequentially at this binding site and calculated the binding energies, as well as the repulsive entropy contribution. We used free energies obtained from tonometry experiments to validate the calculated binding energies. We used partial pressures of gases that prevent response to a noxious stimulus (minimum alveolar anesthetic concentration [MAC]) as the anesthetic endpoint. The calculated binding energies correlated with binding energies derived from the in vivo (ln) data (RTln[MAC], where R is the gas constant and T is absolute temperature) with a slope near 1.0, indicating a parallel between the Xe binding site in metmyoglobin and the anesthetic site of action of noble and diatomic gases. Nonimmobilizing gases (Ne, He, and H2) could be distinguished by an unfavorable balance between binding energies and the repulsive entropy contribution. These gases also differed in their inability to displace water from the cavity. ⋯ The Xe binding site in metmyoglobin is a good model for the anesthetic sites of action of noble and diatomic gases. The additional binding energy provided by induction of a dipole in the gas by a charge at the binding site enhanced binding.
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Anesthesia and analgesia · Aug 1998
Valuing the work performed by anesthesiology residents and the financial impact on teaching hospitals in the United States of a reduced anesthesia residency program size.
We performed a financial analysis at a large university tertiary care hospital to determine the incremental cost of replacing its anesthesiology residents with alternative dependent providers (i.e., certified registered nurse anesthetists in the operating room, advanced practice nurses and physician assistants outside the operating room). The annual average net cost of an anesthesiology resident during a 3-yr residency is approximately $38,000, and residents performed an average of $89,000 of essential clinical work annually based on replacement costs. The incremental cost (replacement labor cost minus net resident cost) to replace all essential clinical duties performed by an anesthesiology resident at Duke University Medical Center and affiliated hospitals is approximately $153,000 throughout 3 yr of clinical anesthesiology training. If this approach were applied nationwide, incremental costs of substitution would range from $36,000,000 to $93,000,000 per year. We conclude that maintaining clinical service in the face of anesthesiology residency reductions can have a marked impact on the overall cost of providing anesthesiology services in teaching hospitals. Simply replacing residents with alternate nonphysician providers is a very expensive option. ⋯ We sought to calculate the financial burden resulting from a decreased number of anesthesiology residents. Replacing each resident's essential clinical work with similarly skilled healthcare providers would cost hospitals approximately $153,000 over the course of a 3-yr residency. Varying projections yield future nationwide costs of $36,000,000 to $93,000,000 per year. Simply replacing residents with alternate nonphysician providers is a very expensive option.
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Anesthesia and analgesia · Aug 1998
Modifications of the inotropic responses to alpha- and beta-adrenoceptor stimulation by propofol in rat myocardium.
Propofol induces cardiovascular depression but without significant effect on intrinsic myocardial contractility in many species. However, its interactions with adrenoceptor stimulation are unknown. We studied the effects of propofol (1 and 10 microg/mL) and its solvent on the inotropic response induced by phenylephrine (10(-8)-10(-4) M) or isoproterenol (10(-8)-10(-4) M) in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, calcium 0.5 mM, stimulation frequency 12 pulses/min). We also studied the lusitropic effects in isotonic and isometric conditions. In control groups, phenylephrine (127% +/- 3% of baseline; P < 0.05) and isoproterenol (169% +/- 11% of baseline; P < 0.05) induced a positive inotropic effect. Propofol (10 microg/mL) completely abolished the positive inotropic effect of phenylephrine (100% +/- 3% of baseline; P = not significant). In contrast, at the lowest concentration (1 microg/mL), propofol did not modify the positive inotropic effect of phenylephrine. Propofol did not modify the inotropic effect of isoproterenol. Propofol (10 microg/mL) enhanced the positive lusitropic effect of isoproterenol under low-load (P < 0.05) but not under high-load conditions. ⋯ A high concentration of propofol abolished the positive inotropic effect of alpha- but not beta-adrenoceptor stimulation and enhanced the positive lusitropic effect of beta-adrenoceptor stimulation.