Anesthesia and analgesia
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Anesthesia and analgesia · Dec 2001
Randomized Controlled Trial Clinical TrialEsmolol promotes electroencephalographic burst suppression during propofol/alfentanil anesthesia.
This study examined the effects of an esmolol infusion on the electroencephalogram during propofol/alfentanil IV anesthesia. After informed consent, 20 patients were randomly assigned into four groups on the basis of two target alfentanil concentrations (alfentanil 50 or 150 ng/mL) and of a saline or esmolol infusion. Bispectral index (BIS), burst suppression ratio (SR), and physiologic variables were continuously monitored. A 30-min blinded infusion of saline or esmolol was started after establishing a stable baseline and followed by a washout period. The electroencephalogram was significantly suppressed by esmolol (BIS, 37 +/- 6 to 22 +/- 6, 40% decrease [mean +/- SD]; SR, 5 +/- 7 to 67 +/- 23, 13.4-fold increase) compared with baseline in the small-dose alfentanil groups. Discontinuation of esmolol reversed the response. BIS and SR were unaffected by placebo infusion. Twelve-minute to 16-min hysteresis between esmolol administration and the onset of half-maximal cortical suppression was observed. Physiologic variables and serum propofol and alfentanil concentrations were not significantly altered by esmolol. Although the mechanism remains unclear, significant cortical depression and the onset of burst suppression during a stable, computer-controlled propofol/alfentanil anesthetic was associated with esmolol infusion. ⋯ This study demonstrated the suppression of cerebral cortical electrical activity after blinded esmolol infusion during propofol/alfentanil anesthesia. A significant lag was noted between infusion and half-maximal effect (12-16 min). Whether esmolol, a metabolite, or a secondary process was responsible for this cortical suppression remains unknown and requires further study.
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Anesthesia and analgesia · Dec 2001
Randomized Controlled Trial Comparative Study Clinical TrialThe continuous recording of blood pressure in patients undergoing carotid surgery under remifentanil versus sufentanil analgesia.
We compared the hemodynamic stability during carotid endarterectomy of remifentanil with that of sufentanil anesthesia. Fifty-six patients were randomly assigned into Remifentanil (n = 27) or Sufentanil (n = 29) groups. In the Remifentanil group, IV propacetamol (2 g) and morphine (0.1 mg/kg) were infused 30 min before skin closure. In the Sufentanil group, patients received 2 g propacetamol. Beat-to-beat recordings of systolic arterial blood pressure (SBP) and heart rate (HR) were stored on a computer. The maximum and minimum values of BP and HR after induction, at intubation, during the surgical procedure, and after the operation and the coefficients of variation of SBP and HR were used as indices of hemodynamic stability. The coefficients of variation of SBP and HR were similar in both groups during and after surgery. However, at intubation, maximal SBP was higher in the Sufentanil group (P < 0.05). Decreased propofol doses and isoflurane end-tidal concentrations were used in the Remifentanil group. At recovery, a similar profile of SBP and HR was found in both groups. We conclude that intra- and posthemodynamic stability was similar with remifentanil or sufentanil in patients undergoing carotid endarterectomy. However, remifentanil was more effective for blunting the increase in SBP at intubation without increasing the blood pressure-decreasing effect of induction. Intraoperative remifentanil use was associated with a decreased amount of hypnotic drug administered. ⋯ Beat-to-beat recordings of heart rate and blood pressure in patients undergoing carotid surgery revealed that hemodynamic stability was similar with remifentanil or sufentanil anesthesia both during and after surgery. Remifentanil was more effective in limiting the increase in blood pressure associated with intubation without increasing the blood pressure-lowering effect of induction or the blood pressure response to recovery.
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Anesthesia and analgesia · Dec 2001
Randomized Controlled Trial Clinical TrialNeostigmine combined with bupivacaine, clonidine, and sufentanil for spinal labor analgesia.
We previously found that spinal clonidine prolongs labor analgesia when combined with spinal bupivacaine and sufentanil. We sought to determine whether the addition of spinal neostigmine to these drugs would further enhance labor analgesia. By use of a combined spinal/epidural technique, 36 patients were randomized to receive a hyperbaric spinal injection of bupivacaine 2.5 mg plus clonidine 50 microg and sufentanil 10 microg with or without neostigmine 10 microg. Pain, maternal hemodynamics, fetal heart rate, nausea, pruritus, sedation, motor block, sensory levels to pinprick, and maternal oxygen saturation were assessed at regularly specified intervals after spinal injection until additional analgesia was requested. The duration of spinal analgesia was similar between groups (215 +/- 60 min in the Control group versus 205 +/- 62 min in the Neostigmine group). Likewise, pain scores, the duration of labor, Apgar scores, and side effects were similar between groups except that patients administered neostigmine experienced significantly more nausea and vomiting (53% vs 7%, P = 0.01). We conclude that spinal neostigmine 10 microg produces severe nausea and does not potentiate the duration of spinal analgesia in laboring women from spinal bupivacaine, clonidine, and sufentanil. ⋯ Spinal neostigmine 10 microg as an adjunct to spinal bupivacaine, clonidine, and sufentanil produces severe nausea and fails to potentiate analgesia in laboring women.
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Anesthesia and analgesia · Dec 2001
Case ReportsThe use of a "reverse" axis (axillary-interscalene) block in a patient presenting with fractures of the left shoulder and elbow.
A patient presented for surgery to repair a fractured left shoulder and elbow and requested regional anesthesia. Most upper extremity operations require a single brachial plexus nerve block. The position of the two fractures however required the use of two separate approaches, an interscalene and an axillary approach.
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Anesthesia and analgesia · Dec 2001
Comparative StudyThe comparative electrophysiologic and hemodynamic effects of a large dose of ropivacaine and bupivacaine in anesthetized and ventilated piglets.
Ropivacaine is less potent and less toxic than bupivacaine. We administered these two local anesthetics in a cardiac electrophysiologic model of sodium thiopental-anesthetized and ventilated piglets. After assessing the stability of the model, bupivacaine (4 mg/kg) and ropivacaine (6 mg/kg) were given IV in two groups (n = 7) of piglets. No alteration in biological variables was reported throughout the study. Bupivacaine and ropivacaine similarly decreased mean aortic pressure from 99 +/- 22 to 49 +/- 31 mm Hg and from 87 +/- 17 to 58 +/- 28 mm Hg, respectively, and decreased the peak of the first derivative of left ventricular pressure from 1979 +/- 95 to 689 +/- 482 mm Hg/s and from 1963 +/- 92 to 744 +/- 403 mm Hg/s, respectively. Left ventricular end-diastolic pressure was similarly increased from 6 +/- 5 to 9 +/- 5 mm Hg and from 6 +/- 4 to 12 +/- 4 mm Hg, respectively. Bupivacaine and ropivacaine similarly lengthened the cardiac cycle length (R-R; from 479 +/- 139 to 706 +/- 228 ms and from 451 +/- 87 to 666 +/- 194 ms, respectively), atria His (from 71 +/- 15 to 113 +/- 53 ms and from 64 +/- 6 to 86 +/- 10 ms, respectively), and QTc (QTc = QT x R-R(-0.5), Bazett formula; from 380 +/- 71 to 502 +/- 86 ms and from 361 +/- 33 to 440 +/- 56 ms, respectively) intervals. Bupivacaine altered to a greater extent the PQ (the onset of the P wave to the Q wave of the QRS complex) (from 97 +/- 20 to 211 +/- 60 ms versus from 91 +/- 8 to 145 +/- 38 ms, P < 0.05), QRS (from 58 +/- 3 to 149 +/- 34 ms versus from 60 +/- 5 to 101 +/- 17 ms, P < 0.05), and His ventricle interval (from 25 +/- 4 to 105 +/- 30 ms vs from 25 +/- 4 to 60 +/- 30 ms, P < 0.05) than ropivacaine. A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent. ⋯ A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent.