Anesthesiology
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Anesthesiologists routinely increase the delivered anesthetic concentration before surgical stimulation in anticipation of increased anesthetic requirement to achieve certain goals (e.g., amnesia, unconsciousness, and immobility). Electroencephalographic monitoring is one method of determining indirectly anesthetic effect on the brain. The present study investigated the effect of surgical stimuli on the concentration-response relation of desflurane-induced electroencephalographic changes. ⋯ During surgery, higher concentrations of the volatile anesthetic are required to achieve a desired level of cortical electrical activity and, presumably, anesthesia.
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Carbon monoxide (CO) is produced by reaction of isoflurane, enflurane, and desflurane in desiccated carbon dioxide absorbents. The inspiratory CO concentration depends on the dryness and identity of the absorbent and anesthetic. The adaptation of existing mathematical models to a rebreathing circuit allows identification of patient factors that predispose to more severe exposures, as identified by carboxyhemoglobin concentration. ⋯ This model predicts that patients with low hemoglobin quantities will have more severe CO exposures based on the attainment of a higher carboxyhemoglobin concentration. This includes patients of small size (pediatric population) and patients with anemia.
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Recent reports suggest that one type of learning, fear conditioning to context, requires more neural processing than a related type, fear conditioning to tone. To determine whether these types of learning were differentially affected by anesthesia, the authors applied isoflurane during the training phases of fear conditioning paradigms for freezing to context and freezing to tone. ⋯ Suppression of fear conditioning to tone required approximately twice the isoflurane concentration that suppressed fear conditioning to context. Thus, the concentration of anesthetic required to suppress learning may depend on the neural substrates of learning. Our results suggest that isoflurane concentrations greater than 0.5 MAC may be needed to suppress both forms of fear conditioning.
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Efficacy of acute normovolemic hemodilution assessed as a function of fraction of blood volume lost.
It has been recommended that intraoperative acute normovolemic hemodilution (ANH) be considered for patients expected to experience surgical blood loss of 20% or more of their blood volume. Previous mathematical analyses have not evaluated the potential efficacy of ANH in terms of fraction of blood volume lost. Since decrease of oxygen-carrying capacity is a function of erythrocyte loss relative to blood volume, the purpose of this analysis was to provide an assessment of ANH applicable to all blood volumes and to determine whether this recommendation is appropriate. ⋯ This analysis suggests that surgical blood loss should be 0.50 or more for ANH to begin to "save" erythrocytes and 0.70 or more of the patient's blood volume for ANH to save 1 unit erythrocytes, for the usual surgical patient with an initial hematocrit of 0.32-0.36 and a transfusion "trigger" hematocrit (the value at which transfusion is initiated) of 0.18-0.21.
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Randomized Controlled Trial Comparative Study Clinical Trial
Airway anesthesia alone does not explain attenuation of histamine-induced bronchospasm by local anesthetics: a comparison of lidocaine, ropivacaine, and dyclonine.
Lidocaine inhalation attenuates histamine-induced bronchospasm while evoking airway anesthesia. Because this occurs at plasma concentrations much lower than those required for intravenous lidocaine to attenuate bronchial reactivity, this effect is likely related to topical airway anesthesia and presumably independent of the specific local anesthetic used. Therefore, the authors tested the effect of dyclonine, lidocaine, and ropivacaine inhalation on histamine-induced bronchospasm in 15 volunteers with bronchial hyperreactivity. ⋯ Both lidocaine and the new amide local anesthetic ropivacaine significantly attenuate histamine-induced bronchospasm. In contrast, dyclonine, despite its longer lasting and more intense local anesthesia, does not alter histamine-evoked bronchoconstriction and irritates the airways. Thus, airway anesthesia alone does not necessarily attenuate bronchial hyperreactivity. Other properties of inhaled local anesthetics may be responsible for attenuation of bronchial hyperreactivity.