Anesthesiology
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Cricoid cartilage pressure induced to prevent pulmonary aspiration from regurgitation of gastric contents has been recommended, and its efficacy requires a force greater than 40 Newtons. For regurgitation to occur, both an increase in gastric pressure and relaxation of the lower esophageal sphincter (LES) are necessary. However, the effect of cricoid cartilage pressure on the LES is unknown. This study evaluated the effects of cricoid cartilage pressure on LES in human volunteers. ⋯ These findings may explain the occurrence of pulmonary aspiration before tracheal intubation despite application of cricoid cartilage pressure.
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The pharmacokinetics and pharmacodynamics of remifentanil were studied in 65 healthy volunteers using the electroencephalogram (EEG) to measure the opioid effect. In a companion article, the authors developed complex population pharmacokinetic and pharmacodynamic models that incorporated age and lean body mass (LBM) as significant covariates and characterized intersubject pharmacokinetic and pharmacodynamic variability. In the present article, the authors determined whether remifentanil dosing should be adjusted according to age and LBM, or whether these covariate effects were overshadowed by the interindividual variability present in the pharmacokinetics and pharmacodynamics. ⋯ Based on the EEG model, age and LBM are significant demographic factors that must be considered when determining a dosage regimen for remifentanil. This remains true even when interindividual pharmacokinetic and pharmacodynamic variability are incorporated in the analysis.
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Brief ischemic periods render the myocardium resistant to infarction from subsequent ischemic insults by a process called ischemic preconditioning. Volatile anesthetics have also been shown to be cardioprotective if administered before ischemia. The effect of preconditioning alone and combined with halothane or isoflurane on hemodynamic recovery and preservation of adenosine triphosphate content in isolated rat hearts was evaluated. ⋯ The results indicate that preconditioning, halothane, and isoflurane provide significant protection against ischemia. The combination of preconditioning and halothane or isoflurane did not improve hemodynamic recovery but did increase preservation of adenosine triphosphate.
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Randomized Controlled Trial Clinical Trial
Local anesthetic administration for awake direct laryngoscopy. Are glossopharyngeal nerve blocks superior?
Glossopharyngeal nerve (GPN) blocks may provide reliable analgesia for awake direct laryngoscopy, although this has not been evaluated prospectively. This study was designed to determine if GPN blocks provide a superior route of local anesthetic administration for awake direct laryngoscopy as measured by hemodynamic, gag, and subjective pain responses. ⋯ Glossopharyngeal nerve blocks do not provide a superior route of local anesthetic administration for awake direct laryngoscopy. Two minutes of 2% viscous lidocaine S&G followed by 10% lidocaine spray was the anesthetic route preferred by participants and laryngoscopists.
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Anesthetic induction and maintenance with propofol are associated with decreased blood pressure that is, in part, due to decreased peripheral resistance. Several possible mechanisms whereby propofol could reduce peripheral resistance include a direct action of propofol on vascular smooth muscle, an inhibition of sympathetic activity to the vasculature, or both. This study examined these two possibilities in humans by measuring the forearm vascular responses to infusions of propofol into the brachial artery (study 1) and by determining the forearm arterial and venous responses to systemic (intravenous) infusions of propofol after sympathetic denervation of the forearm by stellate blockade (study 2). ⋯ In contrast to SNP infusions, propofol infusions into the brachial artery of conscious persons caused no significant vascular responses, despite the presence of therapeutic plasma concentrations of propofol within the forearm. The effects of propofol anesthesia on FVR and FVC are similar to the effects of sympathetic denervation by stellate ganglion blockade. Thus the peripheral vascular actions of propofol appear to be due primarily to an inhibition of sympathetic vasoconstrictor nerve activity.