Anesthesia and analgesia
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Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialPostoperative analgesia with no motor block by continuous epidural infusion of ropivacaine 0.1% and sufentanil after total hip replacement.
We assessed the analgesic efficacy of postoperative epidural ropivacaine 0.1% with and without sufentanil 1 microgram/mL in this prospective, randomized, single-blinded study of 30 ASA physical status I-III patients undergoing elective total hip replacement. Lumbar epidural block using 0.75% ropivacaine was combined with either propofol sedation or general anesthesia for surgery. After surgery, the epidural infusion was commenced. Fifteen patients in each group received either an epidural infusion of 0.1% ropivacaine with 1 microgram/mL sufentanil (R + S) or 0.1% ropivacaine without sufentanil (R) at a rate of 5-9 mL/h. All patients had access to i.v. piritramide via a patient-controlled analgesia device. The R + S group consumed six times less piritramide over a 48-h infusion period than the R group (median 12.7 vs 73.0 mg; P < 0.001). Motor block was negligible for the study duration in both groups. Patient satisfaction was excellent. The incidence of adverse events, such as nausea, was similar. We conclude that a continuous epidural infusion of 0.1% ropivacaine with 1 microgram/mL sufentanil is more effective than ropivacaine alone in treating pain after elective hip replacement without motor block. ⋯ This is the first randomized study comparing the efficacy of the epidural combination of ropivacaine 0.1% and sufentanil 1 microgram/mL versus plain ropivacaine 0.1% in treating pain after hip replacement. We found that ropivacaine 0.1% and sufentanil 1 microgram/mL led to a sixfold reduction in opioid requirements after total hip replacement by producing a negligible motor block.
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Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialIntraoperative phenylephrine infusion decreases the magnitude of redistribution hypothermia.
Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 microgram.kg-1.min-1 phenylephrine i.v. or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol i.v. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients < 0 degree C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4 degrees C) than in those given phenylephrine (0.5 +/- 0.2 degree C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. ⋯ Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia.
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Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialPleural bupivacaine for pain treatment after nephrectomy.
The efficacy of pleural analgesia after nephrectomy is controversial. We therefore evaluated i.v. opioid requirements in patients with and without pleural bupivacaine. Patients undergoing elective nephrectomy were randomly assigned to receive postoperative i.v. piritramid alone (n = 18) or piritramid combined with pleural bupivacaine (n = 19). In the patients assigned to receive pleural analgesia, boluses of 20 mL of 0.25% bupivacaine were given at 6-h intervals via an pleural catheter that was inserted in the medial axillary line at the sixth intercostal space. Pain scores (10-cm visual analog scale) and opioid requirements were recorded over the first 2 postoperative days. One hour after pleural puncture, a chest radiograph was performed. The catheter was removed 48 h after insertion. Patient characteristics were similar in each group, as was the duration of surgery. Pain scores were similar in each group: 3.0 +/- 2.5 in those given pleural bupivacaine and 3.1 +/- 2.7 in those given piritramid alone. However, the piritramid requirement was significantly less in those given pleural bupivacaine (23 +/- 3 mg) than in those given piritramid alone (45 +/- 6 mg). Furthermore, the time from completion of surgery until the first opioid request was significantly longer in the patients who received bupivacaine (4.7 +/- 1.0 vs 2.8 +/- 1.0 h). One patient had a small pneumothorax that resolved without treatment. These data indicate that pleural analgesia is effective and provides a significant opioid-sparing effect. ⋯ We conclude that pleural analgesia significantly prolongs the time until postoperative opioid was first requested and halves the total required dose. These data indicate that pleural analgesia is effective and provides a significant opioid-sparing effect.
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Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialThe effect of hematocrit on cerebral blood flow velocity in neonates and infants undergoing deep hypothermic cardiopulmonary bypass.
Varying degrees of hemodilution are used during deep hypothermic cardiopulmonary bypass. However, the optimal hematocrit (Hct) level to ensure adequate oxygen delivery without impairing microcirculatory flow is not known. In this prospective, randomized study, cerebral blood flow velocity in the middle cerebral artery was measured using transcranial Doppler sonography in 35 neonates and infants undergoing surgery with deep hypothermic cardiopulmonary bypass. Patients were randomized to low Hct (aiming for 20%) or high Hct (aiming for 30%) during cooling on cardiopulmonary bypass (CPB). Systolic (V(s)), mean (Vm), and diastolic (Vd) cerebral blood flow velocity, as well as pulsatility index (PI = [V(s) - Vd]/Vm) and resistance index (RI = [V(s) - Vd]/V(s)) were recorded at six time points: postinduction, at cannulation, after 10 min cooling on CPB, rewarmed to 35 degrees C on CPB, immediately off CPB, and at skin closure. Vm was significantly lower in the high Hct group compared with that in the low Hct group during cooling (P < 0.01). Postinduction, the high Hct group demonstrated significantly lower Vd immediately off CPB (P < 0.01) and significantly lower Vm and V(s) at skin closure (P < 0.001). We conclude that there is an inverse relation between hematocrit and cerebral blood flow velocity during deep hypothermic cardiopulmonary bypass in neonates and infants. ⋯ There is an inverse relation between hematocrit and cerebral blood flow velocity during deep hypothermic cardiopulmonary bypass in neonates and infants. Further studies correlating Hct and cerebral blood flow velocity with cerebral metabolic rate and neurologic outcome are necessary to determine the optimal Hct during deep hypothermic cardiopulmonary bypass.
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Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Comparative Study Clinical TrialSevoflurane speeds recovery of baroreflex control of heart rate after minor surgical procedures compared with isoflurane.
Volatile anesthetics attenuate arterial baroreflex functions, whereas noxious stimuli may modify baroreflex-induced circulatory responses during anesthesia. We designed the present study to compare baroreflex control of heart rate during sevoflurane and isoflurane anesthesia in young healthy surgical patients. Baroreflex sensitivity was assessed in 24 patients randomized to receive either sevoflurane (n = 12) or isoflurane (n = 12) for general anesthesia. After an 8- to 10-h fast and no premedication, measurements of RR intervals obtained from electrocardiography and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline (Awake), during end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide before incision (Anesth), during surgery at end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide (Surg), and 20 min after tracheal extubation (Recov). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine (100-150 micrograms) and nitroprusside (100-150 micrograms) to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating RR intervals and SBP were determined to obtain baroreflex sensitivities. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during Anesth and Surg periods compared with Awake values in both anesthetic techniques. The pressor test sensitivity during the Recov period returned to the Awake value after sevoflurane (12.9 +/- 3.7 vs 11.0 +/- 8.7 ms/mm Hg [mean +/- SD]) but was still depressed after isoflurane anesthesia (13.9 +/- 8.0 vs 4.8 +/- 3.2 ms/mm Hg; P < 0.05). The depressor test sensitivities during the Recov period remained depressed after both anesthetic techniques. We conclude that both sevoflurane and isoflurane depress arterial baroreflex function during anesthesia and surgery, but the pressor test sensitivity was restored more quickly after sevoflurane than after isoflurane anesthesia. ⋯ Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. We found that baroreflex control of heart rate due to hypertensive perturbation returned to the preanesthetic level more quickly after sevoflurane than after isoflurane anesthesia.