Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2002
A new teaching model for resident training in regional anesthesia.
The adequacy of resident education in regional anesthesia is of national concern. A teaching model to improve resident training in regional anesthesia was instituted in the Anesthesiology Residency in 1996 at Duke University Health System. The key feature of the model was the use of a CA-3 resident in the preoperative area to perform regional anesthesia techniques. We assessed the success of the new model by comparing the data supplied by the Anesthesiology Residency to the Residency Review Committee for Anesthesiology for the training period July 1992-June 1995 (pre-model) and the training period July 1998-June 2001 (post-model). During the 3-yr training period, the pre-model CA-3 residents (n = 12) performed a cumulative total of 80 (58-105) peripheral nerve blocks (PNBs), 66 (59-74) spinal anesthetics, and 133 (127-142) epidural anesthetics. The CA-3 post-model residents (n = 10) performed 350 (237-408) PNBs, 107 (92-123) spinal anesthetics, and 233 (221-241) epidural anesthetics (P < 0.0001). All results are reported as median (interquartile range). We conclude that our new teaching model using our CA-3 residents as block residents in the preoperative area has increased their clinical exposure to PNBs. ⋯ Inadequate exposure to peripheral nerve blocks has been a national problem. A teaching model instituted at Duke University Health System has resulted in a fourfold increase in exposure to peripheral nerve blocks compared with the national averages.
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Anesthesia and analgesia · Nov 2002
Case ReportsArterial catheter pressure cable corrosion leading to artifactual diagnosis of hypotension.
Arterial pressure cable corrosion leads to artifactual hypotension despite a normally appearing waveform.
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Anesthesia and analgesia · Nov 2002
Comparative StudyThe analgesic effect of xenon on the formalin test in rats: a comparison with nitrous oxide.
To investigate the analgesic effects of xenon, we performed formalin tests in rats under 0.5 minimum alveolar anesthetic concentration xenon or nitrous oxide and stained the lumbar spinal cord for c-fos (n = 18) and the phosphorylated N-methyl-D-aspartate (NMDA) receptor (n = 24) by using the avidin-biotin-peroxidase method. After 20 min of 79% xenon, 68% nitrous oxide, or 100% inhaled oxygen, 10% formalin (100 microL) was injected into the left rear paw of the animals except for a control group. Nociceptive behavior was observed for 1 h. The rats were killed 2 h after the formalin injection, and the lumbar spinal cord was stained for c-fos or the phosphorylated NMDA receptor immunohistochemically. Animals in the xenon and nitrous oxide groups showed less nociceptive behavior than did the oxygen group. Although the number of c-fos-positive cells in the lumbar spinal cord in the nitrous oxide group was not decreased, that in the xenon group decreased. The number of phosphorylated NMDA receptor-positive cells in the xenon group was significantly less than in the nitrous oxide and oxygen groups. Inhaled xenon suppressed nociceptive behaviors, c-fos expression, and activation of the NMDA receptor during the formalin test in rats. These results confirm that xenon's analgesic effects result from inhibition of the NMDA receptor. ⋯ Inhaled xenon suppressed nociceptive behaviors, c-fos expression, and activation of the N-methyl-D-aspartate receptor during the formalin test in rats. Xenon's analgesic effect was speculated to result from the inhibition of the N-methyl-D-aspartate receptor in vivo.
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Anesthesia and analgesia · Nov 2002
Isoflurane does not produce a second window of preconditioning against myocardial infarction in vivo.
The administration of a volatile anesthetic shortly before a prolonged ischemic episode exerts protective effects against myocardial infarction similar to those of ischemic preconditioning. A second window of preconditioning (SWOP) against myocardial infarction can also be elicited by brief episodes of ischemia when this occurs 24 h before prolonged coronary artery occlusion. Whether remote exposure to a volatile anesthetic also causes delayed myocardial protection is unknown. We tested the hypothesis that the administration of isoflurane 24 h before ischemia produces a SWOP against infarction. Barbiturate-anesthetized dogs (n = 25) were instrumented for measurement of hemodynamics, including aortic and left ventricular (LV) pressures and LV +dP/dt(max), and subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size and coronary collateral blood flow were assessed with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. Two groups of dogs received 1.0 minimum alveolar anesthetic concentration isoflurane for 30 min or 6 h that was discontinued 30 min (acute) or 24 h (delayed) before ischemia and reperfusion, respectively. A control group of dogs did not receive isoflurane. Infarct size was 27% +/- 3% of the LV area at risk in the absence of pretreatment with isoflurane. Acute, but not remote, administration of isoflurane reduced infarct size (12% +/- 1% and 31% +/- 3%, respectively). No differences in hemodynamics or transmural myocardial perfusion during or after occlusion were observed between groups. The results indicate that isoflurane does not produce a SWOP when administered 24 h before prolonged myocardial ischemia in vivo. ⋯ Isoflurane mimics the beneficial effects of ischemic preconditioning by protecting myocardium against infarction when it is administered shortly before a prolonged ischemic episode. However, unlike ischemic preconditioning, isoflurane does not produce a second window of protection 24 h after administration in dogs.