Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2002
Randomized Controlled Trial Comparative Study Clinical TrialPulmonary-to-systemic blood flow ratio effects of sevoflurane, isoflurane, halothane, and fentanyl/midazolam with 100% oxygen in children with congenital heart disease.
The cardiovascular effects of volatile anesthetics in children with congenital heart disease have been studied, but there are limited data on the effects of anesthetics on pulmonary-to-systemic blood flow ratio (Qp:Qs) in patients with intracardiac shunting. In this study, we compared the effects of halothane, isoflurane, sevoflurane, and fentanyl/midazolam on Qp:Qs and myocardial contractility in patients with atrial (ASD) or ventricular (VSD) septal defects. Forty patients younger than 14 yr old scheduled to undergo repair of ASD or VSD were randomized to receive halothane, sevoflurane, isoflurane, or fentanyl/midazolam. Cardiovascular and echocardiographic data were recorded at baseline, randomly ordered 1 and 1.5 mean alveolar anesthetic concentration (MAC) levels, or predicted equivalent fentanyl/midazolam plasma levels. Ejection fraction (using the modified Simpson's rule) was calculated. Systemic (Qs) and pulmonary (Qp) blood flow was echocardiographically assessed by the velocity-time integral method. Qp:Qs was not significantly affected by any of the four regimens at either anesthetic level. Left ventricular systolic function was mildly depressed by isoflurane and sevoflurane at 1.5 MAC and depressed by halothane at 1 and 1.5 MAC. Sevoflurane, halothane, isoflurane, or fentanyl/midazolam in 1 or 1.5 MAC concentrations or their equivalent do not change Qp:Qs in patients with isolated ASD or VSD. ⋯ Sevoflurane, halothane, isoflurane, and fentanyl/midazolam do not change pulmonary-to-systemic blood flow ratio in children with atrial and ventricular septal defects when administered at standard anesthetic doses with 100% oxygen.
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Anesthesia and analgesia · Nov 2002
Randomized Controlled Trial Comparative Study Clinical TrialA comparison of metoclopramide and lidocaine for preventing pain on injection of diazepam.
We compared the ability of metoclopramide with IV lidocaine pretreatment to abolish pain from a diazepam injection. In a randomized, prospective, double-blinded, placebo-controlled clinical trial, 159 patients (ASA physical status I and II), aged 20-70 yr old, were allocated to one of three groups. Placebo and study drugs were injected IV immediately before 0.1 mg/kg of diazepam into a dorsal hand vein. Patients in Groups 1, 2, and 3 received 2 mL of placebo, 2 mL of lidocaine 1%, and 2 mL of metoclopramide (10 mg), respectively. The patient's response was graded using a 4-point scale. Any score other than 0 represented pain on injection. We observed that the incidence of pain on diazepam injection was 83% in the placebo group, which was decreased to 70% and 39% in patients pretreated with metoclopramide and lidocaine, respectively. Although there was no significant difference in the incidence of pain in Groups 1 and 3 (P > 0.05), Group 3 showed significantly less patients with severe pain scores than Group 1 as diazepam was injected (P < 0.000). Group 2 showed a significantly less frequent incidence of pain than the saline (P < 0.000) and the metoclopramide (P < 0.002) groups as diazepam was injected. The intensity of pain in Group 2 was significantly less than Group 3 (P = 0.012). The intensity of diazepam injection pain was intense with placebo as compared with other groups (P < 0.000). Metoclopramide, rather than lidocaine pretreatment, may be a reasonable analgesic alternative for painful injections. ⋯ Metoclopramide, rather than lidocaine pretreatment, may be a reasonable analgesic alternative to decrease pain from a diazepam injection, especially when there is a medical condition in which lidocaine should be used very cautiously.
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Anesthesia and analgesia · Nov 2002
Randomized Controlled Trial Comparative Study Clinical TrialAttenuation of pain in a randomized trial by suppression of peripheral nociceptive activity in the immediate postoperative period.
Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The beta-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain. ⋯ Suppression of postoperative pain immediately after surgery attenuates the pain experienced 1 to 2 days after surgery. These findings suggest that pain after minor surgery can be prevented by blocking the development of pain processes that amplify pain for days after surgery.
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Anesthesia and analgesia · Nov 2002
Randomized Controlled Trial Clinical TrialHalothane, isoflurane, and fentanyl increase the minimally effective defibrillation threshold of an implantable cardioverter defibrillator: first report in humans.
Placing an implantable cardioverter defibrillator (ICD) involves the induction of ventricular fibrillation, whereupon the minimally effective defibrillation energy threshold (DFT) is determined. We evaluated the effects of 0.7% halothane, 1% isoflurane, or 1.5 micro g/kg of IV fentanyl during N(2)O/oxygen-based general anesthesia (GA) or those of subcutaneous 1.5% lidocaine plus IV 0.35 mg/kg of propofol on the DFT during ICD implantation in humans (n = 20 per group). Thirty minutes after the first set of DFT measurements under such conditions, the inhaled anesthetics were withdrawn, and all three GA groups received fentanyl 1 microg/kg IV (second set). A third set was taken 30 min later, before the GA patients awakened and when only N(2)O/oxygen was delivered for GA. The lidocaine plus propofol patients were given the same IV propofol bolus 1 min before each fibrillation/defibrillation trial and at the same time points as the three GA groups. The first DFTs were 16.1 +/- 2.2 J (halothane), 17.7 +/- 2.7 J (isoflurane), 16.4 +/- 2.9 J (fentanyl), and 12.9 +/- 3.8 J (lidocaine plus propofol) (P = 0.01). The second set of DFTs were significantly lower than the first sets for the halothane (P = 0.01) and isoflurane (P = 0.02), but not the fentanyl or lidocaine plus propofol, regimens. The third DFTs were significantly (P < 0.01) lower than the first ones for the three GA groups, but not for the lidocaine plus propofol patients. Thus, halothane, isoflurane, and fentanyl increased DFT values during ICD implantation in humans, whereas lidocaine plus intermittent small-dose IV propofol minimized these thresholds. ⋯ Halothane, isoflurane, and IV fentanyl added to N(2)O/oxygen-based general anesthesia similarly increase minimal defibrillation threshold energy requirements (DFT) during cardioverter defibrillator implantation in humans. Subcutaneous lidocaine plus intermittent small-dose IV propofol minimizes DFT compared with these general anesthetics while providing equal patient satisfaction.
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Anesthesia and analgesia · Nov 2002
Randomized Controlled Trial Clinical TrialPrevention of nausea and vomiting with tandospirone in adults after tympanoplasty.
We have hypothesized that the 5-hydroxytrypta-mine-1A receptor agonist tandospirone reduces postoperative nausea and vomiting (PONV). In a double-blinded, randomized design, 3 groups of 30 patients each received 1 of the following oral medications 90 min before arrival in the operating room, together with famotidine 20 mg: 1) placebo (P group), 2) tandospirone 10 mg (T10 group), or 3) tandospirone 30 mg (T30 group). Standard anesthetic regimens and techniques were applied for all patients. All episodes of PONV were recorded during the following time intervals: 0-3 h and 3-24 h after the end of general anesthesia. The incidence of a complete response, defined as no PONV and no need for other rescue antiemetics, was significantly more frequent in the T30 group than in the P group during 0-24 h (P = 0.019), especially during 3-24 h (P = 0.007) after general anesthesia. In conclusion, premedication with oral tandospirone is effective against PONV in patients undergoing tympanoplasty under general anesthesia. ⋯ Oral tandospirone reduced the incidence of postoperative nausea and vomiting without significant adverse effects in adults undergoing tympanoplasty under general anesthesia.