Anesthesia and analgesia
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Anesthesia and analgesia · Aug 1999
Epidural anesthesia and analgesia are not impaired after dural puncture with or without epidural blood patch.
Previous reports have noted a decrease in the success of subsequent epidural anesthesia and analgesia in patients who have undergone prior dural puncture with or without an epidural blood patch. Our retrospective study evaluated the success of epidural anesthesia and analgesia in all patients at the Mayo Clinic who had received a prior epidural blood patch over a 12-yr period. Each epidural blood patch patient was matched to two patients undergoing epidural anesthesia after previous dural puncture (without epidural blood patch) and to two patients undergoing epidural anesthesia after previous epidural anesthetic (without dural puncture/blood patch). These patients were matched for the duration of time between the initial procedure and subsequent epidural anesthetic and the indication (surgery, labor analgesia, postoperative analgesia) for which the subsequent epidural was performed. Subsequent epidural anesthesia was successful in 28 of 29 (96.6%, exact 95% CI 82.2%-99.9%) patients who had undergone prior blood patch, 55 of 58 (94.8%, 85.6%-98.9%) patients with a history of dural puncture, and 55 of 58 (94.8%, 85.6%-98.9%) patients who had had previous epidural anesthesia. There was no significant difference in the success rate of subsequent epidural anesthesia among groups. We conclude that prior dural puncture, with or without epidural blood patch, does not affect the success rate of subsequent epidural anesthesia. ⋯ Patients with postdural puncture headache should not be denied the benefits of an epidural blood patch because of concerns about the impairment of subsequent epidural anesthetics. The success rate of subsequent epidural anesthesia and analgesia in patients who have undergone dural puncture with or without epidural blood patch is similar to that of patients who have undergone two prior epidural anesthetics.
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Anesthesia and analgesia · Aug 1999
Ventilatory response to CO2 in children with obstructive sleep apnea from adenotonsillar hypertrophy.
We measured the ventilatory response to CO2 as an indicator of respiratory control dysfunction in children with obstructive sleep apnea (OSA) scheduled for adenotonsillectomy. Measurements were performed in unpremedicated children via an endotracheal tube under 0.4%-0.5% end-tidal halothane anesthesia. Mean ventilatory CO2 response slopes for 11 children with OSA requiring adenotonsillectomy (Group I) were compared with those for 14 children without OSA requiring adenotonsillectomy (Group II) and 15 children without OSA requiring nonairway surgery (Group III). The mean ventilatory slope corrected for body surface area for Groups I, II, and III were 539 +/- 338, 828 +/- 234, and 850 +/- 380 mL.min-1.mm Hg ETCO2(-1).m-2, respectively (P < 0.05, Group I versus Groups II and III). Historical data--including snoring, apneic episodes > 10 s, daytime hypersomnolence, and nocturnal enuresis--defined those with OSA. Obesity occurred more frequently in patients with OSA and with depressed ventilatory responses (P < 0.001). Children with OSA from adenotonsillar hypertrophy have a diminished ventilatory response to CO2 stimulation, compared with those without OSA symptoms. The depressed response may account, in part, for the reported increased risk of perioperative respiratory complications in this population. ⋯ Children with obstructive sleep apnea undergoing adenotonsillar surgery are at risk of postoperative respiratory compromise. We found that patients with a clinical history suggesting obstructive sleep apnea have a diminished ventilatory response to CO2 rebreathing, compared with controls.
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Anesthesia and analgesia · Aug 1999
Assessing the relative quality of anesthesiology and critical care medicine Internet mailing lists.
We studied the relative quality of a subset of anesthesiology and critical care medicine Internet mailing lists regarding the publishing capacity of their members to compare them with the major journals and conferences regarding these specialties. Using systematic searches on MEDLINE and according to the Science Citation Index 1995, we investigated the impact factor of mailing list subscribers, of the first authors of the selected articles, and of the first authors of published abstracts from conferences. We studied six mailing lists, seven journals, and four conferences. Journals and conferences showed a higher percentage of published authors and higher average impact factor among their first authors than the mailing lists did per subscriber. However, when only the subset of publishing authors from the three media was considered, no significant differences were found. We conclude that qualified authors may be found among the subscribers of Internet medical mailing lists on anesthesiology and critical care medicine. These professional discussion groups could complement peer-reviewed publications and conferences in professional information exchange and continuing medical education. ⋯ Internet publishing is not governed by rules that assure certain basic quality standards. Methods for assessing these standards are needed. We compared discussion groups with medical journals and conferences on anesthesiology and critical care medicine by calculating the impact factor of their members and first authors, respectively. Our study shows that qualified authors may be found in all three media.
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Anesthesia and analgesia · Aug 1999
The combined effects of sevoflurane and remifentanil on central respiratory activity and nociceptive cardiovascular responses in anesthetized rabbits.
We studied the effects of sevoflurane and remifentanil, alone and in combination, on phrenic nerve activity (PNA), resting heart rate (HR), arterial pressure (MAP), and changes in HR (delta HR) and MAP (delta MAP) evoked by electrical stimulation of tibial nerves in anesthetized rabbits. The 50% effective dose (95% confidence intervals) for the depressant effects of sevoflurane on delta HR, delta MAP, and PNA were 2.3 (1.8%-2.6%), 2.7 (2.3%-2.9%), and 3.4 (3.1%-3.7%), respectively, and for remifentanil were 0.100 (0.050-0.132), 0.850 (0.720-1.450), and 0.090 (0.080-0.145) microgram.kg-1.min-1, which were reduced to 0.046 (0.021-0.065), 0.110 (0.080-0.200), and 0.030 (0.020-0.040) microgram.kg-1.min-1, respectively, by 1% sevoflurane. Depression of evoked cardiovascular responses relative to PNA was greater for sevoflurane and less for remifentanil both alone and in combination with sevoflurane. Sevoflurane acted synergistically with remifentanil on PNA and delta MAP, but not delta HR, for which their combined effect was additive. Coadministration of 1% sevoflurane with the highest infusion rate of remifentanil (1.6 micrograms.kg-1.min-1) used during combined administration reduced resting HR and MAP by 25% (P < 0.05) and 41% (P < 0.05), respectively, which was greater than the predicted reductions of only 14% and 15% if their combined effects had been additive. We conclude that sevoflurane caused a relatively greater depression of nociceptive cardioaccelerator and pressor responses compared with PNA and vice versa for remifentanil. When coadministered, their combined effects on PNA, resting HR, MAP, and delta MAP were synergistic, whereas they were merely additive for delta HR. ⋯ Although sevoflurane caused relatively greater depression of nociceptive cardiovascular responses compared with phrenic nerve activity, remifentanil either alone or combined with sevoflurane caused a much greater depression of phrenic nerve activity than cardio-accelerator and pressor responses. This could imply that, during major surgery using anesthesia combining sevoflurane and remifentanil, spontaneous ventilation is not acceptable, and depression of the resting circulation may be much greater than anticipated.