Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1998
Clinical TrialRespiratory effects of desflurane anesthesia on spontaneous ventilation in infants and children.
Volatile anesthetics depress spontaneous ventilation in a dose-dependent manner with variations in effects among different drugs. The goal of this prospective study was to assess respiratory changes during spontaneous ventilation using desflurane/O2/N2O anesthesia in two groups of children. Both groups were undergoing minor surgery and consisted of children < 2 yr old (Group I) and children > 2 yr old (Group II). They were examined at 0.5, 1, and 1.5 minimum alveolar anesthetic concentration desflurane anesthesia. Induction of anesthesia was performed via a face mask and a mixture of O2/N2O (40:60) with halothane. At lease 20 min after stopping halothane, the respiratory variables were recorded on desflurane anesthesia. Tidal volume and minute ventilation decreased significantly (P <0.05) as desflurane increased from 0.5 to 1.5 MAC in both groups. At 1.5 MAC, the respiratory rate was greater in Group II than in Group I (P <0.05). In both groups, the increase in end-tidal CO2 was significant at 1.5 MAC versus 1 and 0.5 MAC (P <0.05). Apnea, i.e., no respiratory movement for 20 s, occurred at 1.5 MAC in one patient in each group. The respiratory duty cycle did not change in any of the groups. Both indices of paradoxical respiration--amplitude index and delay index--did not change. ⋯ Desflurane induces respiratory depression at concentrations higher than 1 minimum alveolar anesthetic concentration mainly due to a decrease in tidal volume. Therefore, desflurane at high concentrations should be used cautiously in infants and children with spontaneous ventilation.
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Anesthesia and analgesia · Nov 1998
Clinical TrialPharmacokinetics and pharmacodynamics of cisatracurium after a short infusion in patients under propofol anesthesia.
Fourteen patients, ASA physical status I or II, were recruited to assess the pharmacokinetic-pharmacodynamic relationship of cisatracurium under nitrous oxide/sufentanil/propofol anesthesia. The electromyographic response of the abductor digiti minimi muscle was recorded on train-of-four stimulation of the ulnar nerve. A 0.1-mg/kg dose of cisatracurium was given as an infusion over 5 min. Arterial plasma concentrations of cisatracurium and its major metabolites were measured by using high-performance liquid chromatography. A nontraditional two-compartment pharmacokinetic model with elimination from central and peripheral compartments was used. The elimination rate constant from the peripheral compartment was fixed to the in vitro rate of degradation of cisatracurium in human plasma (0.0237 min(-1)). The mean terminal half-life of cisatracurium was 23.9+/-3.3 min, and its total clearance averaged 3.7+/-0.8 mL x min(-1) x kg(-1). Using this model, the volume of distribution at steady state was significantly increased compared with that obtained when central elimination only was assumed (0.118+/-0.027 vs 0.089+/-0.017 L/kg). The effect-plasma equilibration rate constant was 0.054+/-0.013 min(-1). The 50% effective concentration (153+/-33 ng/mL) was 56% higher than that reported in patients anesthetized with volatile anesthetics, which suggests that, compared with inhaled anesthetics, a cisatracurium neuromuscular block is less enhanced by propofol. ⋯ The drug concentration-effect relationship of the muscle relaxant cisatracurium has been characterized under balanced and isoflurane anesthesia. Because propofol is now widely used as an IV anesthetic, it is important to characterize the biological fate and the concentration-effect relationship of cisatracurium under propofol anesthesia as well.
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Anesthesia and analgesia · Nov 1998
Clinical TrialThe effect of the prone position on pulmonary mechanics is frame-dependent.
By compressing the abdomen and restricting chest wall movement, the prone position compromises pulmonary compliance. For spine surgery, placing the anesthetized patient into the prone position increases the risk of improper ventilation. In this study, we tested the hypothesis that the compromise in pulmonary compliance is related to the patient's body habitus and the surgical frame used to support the patient while in the prone position. Seventy-seven adult patients were divided into three groups according to body mass index: normal (n = 36) < or = 27 kg/m2, heavy (n = 21) 28-31 kg/m2, and obese (n = 20) > or = 32 kg/m2. Patients were placed in the prone position supported by chest rolls, a Wilson frame, or the Jackson spinal surgery table (Jackson table) according to the surgeon's preferences. Peak airway pressure (at the proximal endotracheal tube), pleural pressure (esophageal balloon), and mean arterial pressure were recorded in the supine position and prone position within 15 min of the turn. Dynamic mean (+/- SD) pulmonary compliance (mL/cm H2O) decreased when turning from the supine to the prone position in all three body mass groups when using chest rolls (normal 37+/-5 to 29+/-6; heavy 43+/-2 to 34+/-4; obese 42+/-8 to 32+/-6) or the Wilson frame (normal 39+/-6 to 32+/-7; heavy 43+/-16 to 34+/-10; obese 36+/-11 to 28+/-9). The dynamic pulmonary compliance was not altered in patients positioned on the Jackson table. Regardless of body habitus, using the Jackson table for prone positioning was not associated with a significant alteration in pulmonary or hemodynamic variables. We conclude that moving patients from the supine to the prone position during anesthesia results in a decrease in pulmonary compliance that is frame-dependent but that is not affected by body habitus. ⋯ We hypothesized that compromise in pulmonary compliance in the prone position is related to the patient's body mass index and the surgical frame used. In this study, we demonstrated that prone positioning during anesthesia results in a decrease in pulmonary compliance that is frame-dependent but that is not affected by body mass index.
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Anesthesia and analgesia · Nov 1998
The effects of milrinone and its mechanism in the fatigued diaphragm in dogs.
We studied the effects of milrinone and its mechanism in nonfatigued and fatigued diaphragms in dogs. In Group Ia (n = 5), animals without fatigue, defined as the inability to sustain muscle force, received only maintenance fluids. In Group Ib (n = 5), dogs without fatigue were given a bolus injection (50 microg/kg) followed by continuous infusion (0.5 microg x kg(-1) x min(-1)) of milrinone. In Groups IIa, IIb, and IIc (n = 8 in each), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. After producing fatigue, only maintenance fluids were administered (Group IIa); milrinone (50 microg/kg loading dose plus 0.5 microg x kg(-1) x min(-1) maintenance dose) was administered (Group IIb); or nicardipine 5 microg x kg(-1) x min(-1) was infused simultaneously with milrinone (Group IIc). Diaphragmatic contractility was assessed with transdiaphragmatic pressure (Pdi). No differences in Pdi were observed in Groups Ia and Ib. After the fatigue-producing period, Pdi at low-frequency (20-Hz) stimulation decreased from the prefatigued values in Groups IIa, IIb, and IIc (P < 0.05), whereas the decrease was minimal at high-frequency (100-Hz) stimulation. Compared with Group IIa, Pdi to each stimulus increased during milrinone infusion in Group IIb (P < 0.05). In Group IIc, the augmentation of Pdi in the fatigued diaphragm by milrinone was not abolished with an administration of nicardipine. In conclusion, milrinone improves contractility in the fatigued canine diaphragm but not via its effect on transmembrane calcium movement. ⋯ Diaphragmatic fatigue may contribute to the development of respiratory failure. Milrinone increases contractility in the fatigued diaphragm and thereby may have an inotropic action on the improvement of diaphragmatic fatigue.