Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1998
Randomized Controlled Trial Comparative Study Clinical TrialA comparison of the reliability of two techniques of left double-lumen tube bronchial cuff inflation in producing water-tight seal of the left mainstem bronchus.
A double-lumen endobronchial tube (DLT) bronchial cuff inflation technique that reliably ensures effective water-tight isolation of the two lungs has not been determined. In this study, 20 patients undergoing thoracic surgery requiring a left DLT had the bronchial cuff of the DLT inflated by one of two techniques. In Group 1, the cuff was inflated to produce an air-tight seal of the left bronchus using the underwater seal technique. In Group 2, the cuff was inflated to a pressure of 25 cm H2O. After bronchial cuff inflation in both groups, water-tight bronchial seal was tested by instilling 2 mL of 0.01% methylene blue (MB) above the bronchial cuff of the DLT. Fifteen minutes later, fiberoptic bronchoscopy was performed via the bronchial lumen of the DLT to determine whether MB had seeped past the bronchial cuff. Cuff volume was 0.75+/-0.64 and 0.76+/-0.46 mL, cuff pressure was 30.1+/-27.0 and 25.0+/-0.0 cm H2O (mean+/-SD), and MB was positively identified in two and five patients in Groups 1 and 2, respectively. The difference in cuff volume and pressure and the higher MB seepage in Group 2 compared with Group 1 was not statistically significant. In both groups, MB seepage occurred only when the bronchial cuff volume was <1 mL and when the patients were positioned in the left lateral decubitus position. These findings suggest that the risk of aspiration is greatest when the DLT is positioned in the dependent lung and when the bronchial cuff volume is <1 mL. ⋯ Water-tight sealing of the left bronchus by DLT bronchial cuff was tested after cuff inflation using two different techniques. Neither air-tight bronchial seal nor cuff pressure of 25 cm H2O guaranteed protection against aspiration. The risk of aspiration was greatest when the DLT was positioned in the dependent lung and when the bronchial cuff volume was < 1 mL.
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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 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.
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Anesthesia and analgesia · Nov 1998
The effect of fibrin glue patch in an in vitro model of postdural puncture leakage.
We studied the possibility of stopping a continuing transdural leakage with fibrin glue, a biologic adhesive, in an in vitro model. The model was made by sealing the bottom of a tube filled with saline to a height of 50 cm with a human lyophilized dural specimen. Dural punctures were performed with a 17-gauge Tuohy needle. The needle was then withdrawn, and 0.8 mL of fibrin glue was injected through the same needle to seal the defect. The column was refilled 3 min after sealing. The pressure in the intrathecal chamber was measured during the procedure. Macroscopic and microscopic histological studies of the dura and the fibrin plug were performed. In the five cases studied, the leak was sealed by the fibrin plug at closing pressures of 25-35 cm H2O, and no further leakage was detected after refilling. The dural specimens showed a fibrin glue plug stuck at the edges of the hole. We conclude that fibrin glue stops leakage of fluid from dural holes created by a 17-gauge Tuohy needle in an in vitro pressurized model. ⋯ We explored the possibility of repairing a cerebrospinal fluid leak produced by an accidental dural puncture during epidural anesthesia by percutaneously injecting tissue adhesive in vitro. This technique seems promising for the prophylaxis and treatment of the headache associated with this leakage but requires further study in vivo.