Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe effect of mixing lidocaine with propofol on the dose of propofol required for induction of anesthesia.
Lidocaine is used to reduce pain associated with propofol injection, either mixed with propofol or preceding it as a separate injection. The addition of lidocaine to propofol causes destabilization of the emulsion and reduces anesthetic potency in rats and humans. We conducted a randomized double-blinded study on 67 patients to assess the effect of mixing lidocaine with propofol on the dose of propofol required for the induction of anesthesia. Patients in Group S (n = 32) received IV lidocaine 0.2 mg/kg followed by an infusion of propofol whereas those in Group M (n = 35) received IV normal saline (placebo) followed by an infusion of a freshly prepared mixture of propofol 1%/lidocaine 1% in 10:1 volume ratio. The infusion was stopped when the subjects lost consciousness, as detected by the syringe-drop method. There was no statistically significant difference between the two groups in the mean (95% confidence interval) doses of propofol required for loss of consciousness: 2.0 (1.8-2.2) mg/kg for Group S versus 1.9 (1.7-2.0) mg/kg for Group M (P = 0.206). Mixing 20 mg of lidocaine with 200 mg of propofol is unlikely to affect the dose of propofol required for the induction of anesthesia. ⋯ Adding lidocaine to propofol destabilizes the propofol emulsion. A randomized double-blinded trial found no statistically significant difference in the doses of propofol required for the induction of anesthesia whether administered as a freshly prepared propofol 1%/lidocaine 1% 10:1 mixture or as a separate injection after a dose of lidocaine.
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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 TrialThe effect of small dose fentanyl on the emergence characteristics of pediatric patients after sevoflurane anesthesia without surgery.
We designed this study to measure the effect of a small dose of IV fentanyl on the emergence characteristics of pediatric patients undergoing sevoflurane anesthesia without any surgical intervention. Thirty-two ASA physical status I or II pediatric outpatients receiving sevoflurane anesthesia for magnetic resonance imaging scans were enrolled and assigned in a random and double-blinded manner to receive either placebo (saline) or 1 micro g/kg IV fentanyl 10 min before discontinuation of their anesthetic. The primary outcome measure was the percentage of patients with emergence agitation. We also evaluated the duration of agitation and time to meet hospital discharge criteria. Patients who received fentanyl had a decreased incidence of agitation (12% versus 56%) when compared with placebo. There was no significant difference in time to meet hospital discharge criteria. We conclude that the addition of a small dose of fentanyl to inhaled sevoflurane anesthesia decreases the incidence of emergence agitation independent of pain control effects. ⋯ The addition of a small dose of fentanyl given to patients undergoing nonsurgical sevoflurane anesthesia resulted in a significant decrease in emergence agitation in a prospective, randomized, and controlled trial involving pediatric patients.
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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.