Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2005
The impact of acoustic stimulation on the AEP monitor/2 derived composite auditory evoked potential index under awake and anesthetized conditions.
The AEP Monitor/2 features an auditory evoked potential (AEP) and electroencephalogram (EEG)-derived hybrid index of the patient's hypnotic state. The composite AEP index (AAI) is preferably calculated from the AEP, but in case of low signal quality it is based entirely on the spontaneous EEG. We investigated the impact of auditory input on the AAI in 16 patients with correctly positioned headphones for acoustic stimulation and headphones disconnected from the patient's ears under awake and anesthetized conditions. The AAI and the Narcotrend Index (NI), another EEG-based measure of hypnotic depth, were recorded simultaneously. AAI values under awake and anesthetized conditions were higher with correctly positioned headphones than with headphones disconnected from the patient's ears (P < 0.05) but remained within the range indicating the patient's actual hypnotic state as given by the manufacturer of the monitor. Under awake conditions with correctly positioned headphones we observed frequent fluctuations between AEP-derived and EEG-derived AAI, whereas with headphones disconnected from the patient's ears the AAI calculation was completely EEG based. Acoustic stimulation had no impact on the Narcotrend Index. Although relevant misinterpretations of the patient's hypnotic state as a consequence of a turnover from AEP-derived to EEG-derived AAI values should not occur, an improved harmonization of the two methods of indexing would be desirable. ⋯ The AEP Monitor/2 generates an Index (AAITM) indicating the patient's hypnotic state by analyzing either auditory evoked potentials (AEP) or spontaneous electroencephalographic (EEG) activity. We demonstrate that, though significantly different under AEP-derived or EEG-derived conditions, AAI values remain within the range indicating the patient's actual hypnotic state as given by the manufacturer of the device.
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Epidural catheters (EC) are often used in pediatric patients for intraoperative and postoperative pain relief. The small anatomical structures and catheter insertion under general anesthesia make it more difficult to perform EC and to prevent damage. In this study we investigated the use of ultrasound (US) in detecting neuraxial structures during insertion and placement of EC in children. ASA I-II children scheduled for elective surgery under combined general and epidural anesthesia were studied. Patients received balanced anesthesia using sevoflurane, opioids and rocuronium. Before EC insertion US examination in a lateral position was done to visualize and identify neuraxial structures. Quality of visualization and site and depth of structures were recorded. Using a sterile kit to hold the US probe in position and enable the visualization of the neuraxial structures, an epidural cannula was inserted, using the loss of resistance technique, as the EC passed under US control to the desired level. Of 25 children, 23 were evaluated. Epidural space, ligamentum flavum, and dural structures were clearly identified and the depth to skin level estimated in all patients. Loss of resistance was visualized in all patients with a lumbar epidural approach. Correlation of US measured depth and depth of loss of resistance was 0.88. In eight of 23 patients EC could be visualized during insertion and in 11 others it could be visualized with additional US planes. US is an excellent tool to identify neuraxial structures in both infants and children. The size and the incomplete ossification of the vertebra allow exact visualization and localization of the depth of the epidural space, the loss of resistance, and all relevant neuraxial structures. ⋯ Epidural catheters in children are mostly inserted under sedation or general anesthesia. This study showed that the use of ultrasound could help visualize all relevant neuraxial structures and their site and depth from the skin.
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Several anesthetic drugs are nicotinic antagonists at or below levels used for anesthesia, including ketamine and volatile anesthetics. In contrast, propofol does not inhibit nicotinic receptors. To determine the potential behavioral ramifications of nicotinic inhibition by ketamine, we determined the doses of ketamine required to induce immobility, impair the righting reflex, and cause analgesia in the absence and presence of several nicotinic ligands. Propofol was used as a control in similar experiments. When used as a sole anesthetic drug, 383 +/- 22 mg/kg ketamine intraperitoneally (IP) was required for immobility and 180 +/- 17 mg/kg IP impaired righting reflex. Propofol, 371 +/- 34 mg/kg IP, induced immobility whereas 199 mg/kg IP inhibited the righting reflex. Nicotinic antagonists had no effect on the dose of propofol or ketamine required for either end-point. When nociceptive responses were tested at subhypnotic doses, no pronociceptive or antinociceptive phase was identified for propofol, whereas analgesia was induced at ketamine doses larger than 60 mg/kg IP. The broad-spectrum nicotinic antagonist mecamylamine enhanced the analgesic action of ketamine. These findings are different than those seen with volatile anesthetics, where nicotinic inhibition is thought to be responsible for a pronociceptive action. Such a phase is possibly obscured by analgesia induced as a result of N-methyl-d-aspartic acid antagonism by ketamine. ⋯ Ketamine and volatile anesthetics, but not propofol, inhibit neuronal nicotinic acetylcholine receptors in clinically relevant concentration ranges. Nicotinic inhibition by ketamine is not related to its immobilizing or sedating effects but may play a role in ketamine's analgesic action.