Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialOral clonidine premedication reduces the awakening concentration of isoflurane.
Because clonidine has analgesic and sedative properties, it may influence the awakening concentration or dose of an anesthetic. To investigate the effects of oral clonidine premedication on emergence from isoflurane anesthesia, we studied 61 ASA physical status I or II patients undergoing superficial operations. They were randomly allocated to one of three groups according to the dose of clonidine they received: the clonidine-2.5 group (n = 21), clonidine-5 group (n = 20), and control group (n = 20) received approximately 2.5, 5, or 0 microg/kg oral clonidine, respectively, in addition to 20 mg of famotidine 90 min before general anesthesia induction. Anesthesia was induced by thiamylal 5 mg/kg, and tracheal intubation was facilitated with succinylcholine 1.5 mg/kg I.V. Anesthesia was maintained with a 1.1% end-tidal isoflurane concentration and 67% N2O in oxygen, while ventilation was controlled to maintain end-tidal CO2 tension between 33 and 38 mm Hg. After surgery, N2O was discontinued while the end-tidal isoflurane concentration was maintained at 1.1%. After confirming the end-tidal N2O concentration of 0%, isoflurane was discontinued. The end-tidal isoflurane concentration at the time when patients responded to a standardized verbal command to open their eyes was recorded as MAC-Awake. The MAC-Awake values in the clonidine-5 group (0.22% +/- 0.09% [mean +/- SD]) was significantly less than those in the clonidine-2.5 and control groups (0.28% +/- 0.07% and 0.30% +/- 0.07%, respectively, P < 0.05). The wake-up time, from discontinuance of isoflurane until arousal, was longer in the clonidine-2.5 and clonidine-5 groups than in the control group (17.3 +/- 8.0, 16.9 +/- 7.0, and 10.6 +/- 5.3 min, respectively; P < 0.05). In conclusion, oral clonidine premedication 5 microg/kg decreases the awakening concentration of isoflurane, and arousal from isoflurane anesthesia is prolonged with oral clonidine in a dose of 2.5-5 microg/kg. ⋯ Preanesthetic medication with oral clonidine, 2.5-5 microg/kg, is associated with prolonged recovery from isoflurane anesthesia in adults.
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialThe effect of needle gauge and lidocaine pH on pain during intradermal injection.
Local anesthetics can produce pain during skin infiltration. We designed a randomized, prospective trial to determine whether needle gauge and/or solution pH affect pain during the intradermal infiltration of lidocaine. After approval by our institution's human studies review board, 40 healthy adult volunteers gave their consent to participate in this study. All of the volunteers randomly received four intradermal injections. Each volunteer was blinded as to the content of the intradermal injections and to which needle size was used for each injection. Each volunteer randomly received a 0.25-mL intradermal injection of the following four solutions: 1) lidocaine 2% administered through a 25-gauge needle (lido-25); 2) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate, pH 7.26) administered through a 25-gauge needle (lido-bicarb-25); 3) lidocaine 2% administered through a 30-gauge needle (lido-30); and 4) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate) administered through a 30-gauge needle (lido-bicarb-30). In each patient, the injection site was in the same region for each of the four injections. The skin wheal was tested for appropriate anesthesia using a 19-gauge needle on the skin wheal. A visual analog pain score was recorded after each intradermal injection. The pain scores were significantly higher in the lido-25 (3.2 +/- 0.2) group than in the lido-30 (2.5 +/- 0.3), lido-bicarb-25 (1.9 +/- 0.2), and lido-bicarb-30 (1.3 +/- 0.2) groups. The lido-bicarb-30 injection was also rated as less painful than the lido-30 injection. We found no differences between the lidobicarb-25 and the lido-bicarb-30 injections. Complete analgesia for the 19-gauge needle pain stimulus was achieved in all patients for each injection. We conclude that, overall, the pain intensity of an intradermal injection of 2% lidocaine is low. The addition of sodium bicarbonate to 2% lidocaine decreases the pain associated with an intradermal skin wheal, and although the use of a 30-gauge needle decreases the pain of injection, the addition of sodium bicarbonate seems to have a greater overall effect than needle size. ⋯ Forty volunteers randomly received four intradermal injections consisting of 2% lidocaine with or without sodium bicarbonate via a 25- or 30-gauge needle. The addition of bicarbonate had a greater overall effect than needle size in decreasing the pain associated with the intradermal injection of lidocaine.
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Anesthesia and analgesia · Feb 1998
Catecholamine activation in the vasomotor center on emergence from anesthesia: the effects of alpha2 agonists.
The rostral ventrolateral medulla (RVLM) controls the vascular system and may contribute to postoperative hypertension. It comprises adrenergic cardiovascular neurons, a site for action of alpha2-adrenergic agonists. Because alpha2 agonists minimize perioperative circulatory activation, we asked the following question: do alpha2 agonists, such as clonidine and mivazerol, blunt the catecholamine activation observed in the RVLM on emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetics. With in vivo electrochemistry, a catechol signal was recorded in the RVLM during 150 min of stable halothane anesthesia (saline-halothane group); for 120 min after halothane discontinuation (saline-emergence group); after emergence and administration of the reference alpha2 agonist, clonidine 7 microg/kg or 21 microg/kg I.V. (50% or 90% effective dose [ED50 or ED90], respectively); and after emergence and administration of a new alpha2 agonist, mivazerol 20 microg/kg or 150 microg/kg I.V. (ED50 or ED90). Under halothane, dose-response curves for the RVLM catecholamine signal were constructed for mivazerol and an alpha2 antagonist, idazoxan (ED50 2.3 mg/kg I.V.). Stable halothane anesthesia (n = 5) led to no change in mean arterial pressure (MAP), heart rate (HR), or catechol signal (CAOC). During emergence from anesthesia, the MAP, HR, and CAOC increased (n = 5). Clonidine led to a near total suppression of the RVLM catecholamine activation noticed on emergence from anesthesia (n = 5). Hypertension was partially blunted with clonidine 7 microg/kg (n = 5). Tachycardia was partially blunted with mivazerol 20 microg/kg (n = 5). Pretreatment with idazoxan suppressed all the effects of mivazerol (n = 5). ⋯ On emergence from anesthesia, alpha2 agonists modify the activity of adrenergic cardiovascular neurons located within the vasomotor center, as assessed by in vivo electrochemistry. We provide a rationale for the use of alpha2 agonists on emergence from anesthesia in coronary/hypertensive patients.
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Anesthesia and analgesia · Feb 1998
The effect of halothane and sevoflurane on fatigue-induced changes in hamster diaphragmatic contractility.
The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. ⋯ This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility.
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Anesthesia and analgesia · Feb 1998
Pharmacokinetics of the enantiomers of bupivacaine and mepivacaine after epidural administration of the racemates.
We investigated the pharmacokinetics of the enantiomers of bupivacaine and mepivacaine after epidural injection of the racemate of each drug into six surgical patients. After epidural administration of either bupivacaine/HCl (115 mg) or mepivacaine/HCl (460 mg), blood samples were collected for 24 h. Unbound fractions were determined by using ultrafiltration for bupivacaine and equilibrium dialysis for mepivacaine. Concentrations in plasma, ultrafiltrate, and dialysate were determined by using stereoselective high-performance liquid chromatography. Peak plasma concentrations of R(+)-bupivacaine (389 +/- 93 ng/mL) and R(-)-mepivacaine (1350 +/- 430 ng/mL) were smaller than those of S(-)-bupivacaine (449 +/- 109 ng/mL, P < 0.0001) and S(+)-mepivacaine (1740 +/- 490 ng/mL, P < 0.002), respectively. However, the unbound peak concentrations of R(+)-bupivacaine (20 +/- 11 ng/mL) were larger than those of S(-)-bupivacaine (15 +/- 9 ng/mL, P < 0.005); unbound peak concentrations of R(-)-mepivacaine (485 +/- 158 ng/mL) and S(+)-mepivacaine (460 +/- 139 ng/mL) did not differ. These observations reflect differences in the systemic disposition (distribution and elimination) of the enantiomers, because the systemic absorption was not enantioselective with either drug. This study supports the opinion that the use of single enantiomers, rather than racemates, is preferable, particularly for bupivacaine. ⋯ Measurements of the plasma concentrations of the enantiomers of bupivacaine and mepivacaine after epidural administration of the racemates demonstrated that the systemic disposition, but not the systemic absorption, of these drugs is enantioselective and supports the opinion that the use of single enantiomers, rather than racemates, is preferable.