Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe central nervous system and cardiovascular effects of levobupivacaine and ropivacaine in healthy volunteers.
We compared the central nervous system (CNS) and cardiovascular effects of levobupivacaine and ropivacaine when given IV to healthy male volunteers (n = 14) in a double-blinded, randomized, crossover trial. Subjects received levobupivacaine 0.5% or ropivacaine 0.5% after a test infusion with lidocaine to become familiar with the early signs of CNS effects (e.g., tinnitus, circumoral paresthesia, hypesthesia). The development of CNS symptoms was assessed at 1-min intervals and study drug administration was terminated when the first CNS symptoms were recognized. Thereafter, symptoms were recorded at 1-min intervals until symptom resolution. Hemodynamic variables were assessed by transthoracic electrical bioimpedance. Continuous 12-lead electrocardiogram monitoring was also performed. There was no significant difference between levobupivacaine and ropivacaine for: the mean time to the first onset of CNS symptoms (P = 0.870), mean total volume of study drug administered at the onset of the first CNS symptom (P = 0.595), stroke index (P = 0.678), cardiac index (P = 0.488), acceleration index (P = 0.697), PR interval (P = 0.213), QRS duration (P = 0.637), QT interval (P = 0.724), QTc interval (P = 0.737), and heart rate (P = 0.267). Overall, fewer CNS symptoms were reported for levobupivacaine than ropivacaine (218 versus 277). This study found that levobupivacaine and ropivacaine produce similar CNS and cardiovascular effects when infused IV at equal concentrations, milligram doses, and infusion rates. ⋯ This study compared directly, for the first time, the toxicity of levobupivacaine and ropivacaine in healthy volunteers. Levobupivacaine and ropivacaine produced similar central nervous system and cardiovascular effects when infused IV at equal concentrations, milligram doses, and infusion rates.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Comparative Study Clinical TrialA comparison of two regional anesthetic techniques for outpatient knee arthroscopy.
Small dose lidocaine spinal anesthesia and 3% 2-chloroprocaine epidural anesthesia provided comparable discharge times for outpatient knee arthroscopy. The incidence of transient neurologic symptoms with small-dose lidocaine spinal anesthesia was 12%.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialChoice of electrocardiography lead does not affect the usefulness of the T-wave criterion for detecting intravascular injection of an epinephrine test dose in anesthetized children.
Accidental intravascular injection of an epinephrine-containing test dose increases T-wave amplitude of lead II electrocardiogram (EKG) in anesthetized children. We designed this study to test whether the choice of EKG lead would affect the usefulness of simulated intravascular test dose. We studied 32 ASA physical status I infants and children (aged 6-49 mo) undergoing elective surgeries during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen. When hemodynamic stability was obtained, all subjects received IV saline 0.1 mL/kg, followed 4 min later by an IV test dose (0.1 mL/kg) consisting of 1% lidocaine with 1:200,000 epinephrine (epinephrine 0.5 microg/kg) via a peripheral vein to simulate the intravascular injection of the test dose. Heart rate and systolic blood pressure were recorded every 20 and 60 s, respectively, and leads II (n = 32), V(5) (n = 32) and either lead I (n = 15) or III (n = 17), choosing the one with greater preinjection T-wave amplitude, were continuously recorded for 4 min after the saline and the test dose injections. An IV test dose produced significant increases in heart rate, systolic blood pressure, and T-wave amplitude of all EKG leads studied in all subjects, whereas IV saline elicited no changes in these variables. Maximal increases in T-wave amplitude of leads II, I, III, and V(5) were 158% +/- 69%, 175% +/- 78%, 147% +/- 89%, and 170% +/- 72%, respectively (mean +/- SD, P > 0.05). There was no significant difference in temporal changes in T-wave amplitude among the 4 leads, and sensitivity and specificity were 100% on the basis of the T-wave criterion irrespective of the lead examined. Our results indicate that leads II, I, III, and V(5) of EKG are equally effective for detecting intravascular injection of the epinephrine-containing test dose in sevoflurane-anesthetized children. ⋯ To determine whether an epidurally administered local anesthetic has been accidentally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that increases in T-wave amplitude in leads I, II, III, and V(5) of the electrocardiogram are equally sensitive and specific for detecting intravascular injection of the epinephrine-containing test dose in sevoflurane-anesthetized infants and children.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialIntravenous alprostadil, an analog of prostaglandin E1, prevents thiamylal-fentanyl-induced bronchoconstriction in humans.
Prostaglandin (PG) E(1) relaxes airway smooth muscle in animals. However, no clinical data have been published on the bronchorelaxant effects of IV alprostadil, an analog of PGE(1). We have described experimental thiamylal-fentanyl-induced bronchoconstriction in humans; we now report the effect of IV alprostadil on thiamylal-fentanyl-induced bronchoconstriction. Thirty-two patients were allocated randomly to a control group (n = 16) and alprostadil group (n = 16). Anesthesia was induced with thiamylal 5 mg/kg and vecuronium 0.3 mg/kg and maintained with a continuous infusion of thiamylal 15 mg. kg(-1). h(-1). The lungs of the patients were ventilated with 50% nitrous oxide in oxygen. Twenty minutes after the induction of anesthesia, patients in the control group were given a continuous infusion of normal saline 20 mL/h, and those in the alprostadil group received a continuous infusion of alprostadil 0.2 micro g. kg(-1). min(-1) (20 mL/h), both for 60 min. Both groups were then given fentanyl 5 micro g/kg. Systolic and diastolic arterial blood pressure, heart rate, mean airway resistance (Rawm), expiratory airway resistance (Rawe), and dynamic lung compliance (Cdyn) were measured at the baseline, just before the fentanyl injection (T30), at three consecutive 6-min intervals after fentanyl injection (T36, T42, and T48), and 30 min after fentanyl injection (T60). Baseline Rawm, Rawe, and Cdyn values were comparable between groups. In the control group, both Rawm and Rawe were significantly increased at T36-60, and Cdyn was significantly decreased at T36-60 compared with the baseline. Patients given alprostadil showed no change in Rawm, Rawe, or Cdyn at T36-60. Thus, IV alprostadil seems to have a bronchodilator effect in humans. ⋯ IV alprostadil, an analog of prostaglandin E(1), prevents thiamylal-fentanyl-induced bronchoconstriction in humans. This finding suggests that IV alprostadil has a bronchodilator effect.
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Anesthesia and analgesia · Aug 2003
Clinical Trial Controlled Clinical TrialThe relationship between expired concentration of sevoflurane and sympathovagal tone in children.
In children, sevoflurane depresses parasympathetic tone during induction more than halothane. The effects of sevoflurane on parasympathetic activity could explain the difference in heart rate (HR) changes described between infants and children. In this study, we sought to determine the relationship between the end-tidal concentration of sevoflurane and sympathetic and parasympathetic tone in children by spectral analysis of RR intervals. Thirty-three children, ASA physical status I, who required elective surgery were studied. In 10 children (Group A), recordings were performed while gradually decreasing the inspired sevoflurane concentration from 8% to the beginning of clinical awakening. In 23 other children (Group B), recordings were performed while children were awake and at a steady-state of 1 and 2 minimum alveolar anesthetic concentration of sevoflurane. A time-varying autoregressive modeling of the interpolated RR sequences was performed, and spectral density in low-frequency (LF; 0.04-0.15 Hz) and high-frequency (HF; 0.15-0.55 Hz) bands was calculated. In Group A, HR slowing paralleled the decrease in expired sevoflurane concentration. Conversely, the decrease in expired concentration of sevoflurane led to an increase in systolic blood pressure (SBP), HF, LF, and LF/HF. The increase in LF/HF preceded the increase in HF. In Group B, the baseline HF power spectrum and normalized values HFnu (HFnu = HF/LF + HF) were significantly increased in children older than 3 yr. Changes in HR induced by sevoflurane were negatively correlated with baseline HF and HFnu (R(2) = 0.6; P < 0.001). These results demonstrate that withdrawal of parasympathetic tone is the main determinant for the change in HR induced by sevoflurane. ⋯ The effects of sevoflurane on parasympathetic activity could explain the difference in heart-rate changes described between infants and children during induction. This study describes the changes in heart rate and its variability induced by sevoflurane in children and shows that these changes are related to parasympathetic tone before the induction of anesthesia.