ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe development of metabolic acidosis during cardiopulmonary bypass (CPB) is well recognized but poorly understood. The authors hypothesized that the delivery of pump prime fluids is primarily responsible for its development. Accordingly, acid–base changes induced by the establishment of CPB were studied using two types of priming fluid (Haemaccel, a polygeline solution, and Ringer’s Injectionvs.Plasmalyte 148) using quantitative biophysical methods.MethodsA prospective, double-blind, randomized trial was conducted at a tertiary institution with 22 patients undergoing CPB for coronary artery bypass surgery. Sampling of arterial blood was performed at three time intervals: before CPB (t1), 2 min after initiation of CPB at full flows (t2), and at the end of the case (t3). Measurements of Na+, K+, Mg2+, Cl−, HCO3−, phosphate, Ca2+, albumin, lactate, and arterial blood gases at each collection point were performed. Results were analyzed in a quantitative manner.ResultsImmediately on delivery of pump prime fluids, all patients developed a metabolic acidosis (base excess: 0.95 mEq/l (t1) to −3.65 mEq/l (t2) (P< 0.001) for Haemaccel–Ringer’s and 1.17 mEq/l (t1) to −3.20 mEq/l (t2). The decrease in base excess was the same for both primes (−4.60vs.−4.37; not significant). However, the mechanism of metabolic acidosis was different. With the Haemaccel–Ringer’s prime, the metabolic acidosis was hyperchloremic (&Dgr; Cl−, +9.50 mEq/l; confidence interval, 7.00–11.50). With Plasmalyte 148, the acidosis was induced by an increase in unmeasured anions, most probably acetate and gluconate. The resolution of these two processes was different because the excretion of chloride was slower than that of the unmeasured anions (&Dgr; base excess from t1to t3= −1.60 for Haemaccel–Ringer’svs.+1.15 for Plasmalyte 148;P= 0.0062).ConclusionsCardiopulmonary bypass–induced metabolic acidosis appears to be iatrogenic in nature and derived from the effect of pump prime fluid on acid–base balance. The extent of such acidosis and its duration varies according to the type of pump prime.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundPreoperative acute normovolemic hemodilution (ANH) is an excellent model for evaluating the effects of different colloid solutions that are free of bicarbonate but have large chloride concentrations on acid–base equilibrium.MethodsIn 20 patients undergoing gynecologic surgery, ANH to a hematocrit of 22% was performed. Two groups of 10 patients each were randomly assigned to receive either 5% albumin or 6% hydroxyethyl starch solutions containing chloride concentrations of 150 and 154 mm, respectively, during ANH. Blood volume (double label measurement of plasma and red cell volumes), pH, Paco2, and serum concentrations of sodium, potassium, chloride, lactate, ionized calcium, phosphate, albumin, and total protein were measured before and 20 min after completion of ANH. Strong ion difference was calculated as serum sodium plus serum potassium minus serum chloride minus serum lactate. The amount of weak plasma acid was calculated using a computer program.ResultsAfter ANH, blood volume was well maintained in both groups. ANH caused slight metabolic acidosis with hyperchloremia and a concomitant decrease in strong ion difference. Plasma albumin concentration decreased after hemodilution with 6% hydroxyethyl starch solution and increased after hemodilution with 5% albumin solution. Despite a three-times larger decrease in strong ion difference after ANH with 6% hydroxyethyl starch solution, the decrease in pH was nearly the same in both groups.ConclusionsANH with 5% albumin or 6% hydroxyethyl starch solutions led to metabolic acidosis. A dilution of extracellular bicarbonate or changes in strong ion difference and albumin concentration offer explanations for this type of acidosis.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe intent of this study was to evaluate the impact of the commonly used colloids—hetastarch and albumin—on in vivo acid–base balance. From this evaluation, a better understanding of the mechanism of dilutional acidosis was expected.MethodsIn a prospective, randomized fashion, 11 healthy volunteers were administered 15 ml/kg hetastarch solution, 6%, or 15 ml/kg albumin, 5%, intravenously over 30 min. Four weeks later, the study subjects were administered the other colloid. Arterial blood gas and electrolyte parameters were measured at baseline and at 30, 60, 90, 120, 210, and 300 min after colloid administration. Pre- and postlaboratory values were compared within groups using a pairedttest and a Wilcoxon signed rank test and between groups using repeated-measures analysis of variance and a Wilcoxon rank sum test.ResultsThirty min after infusion, subjects who were administered hetastarch showed statistically significant changes (P< 0.05) in base excess (from 2.5 ± 0.9 mEq/l to 0.7 ± 1.1 mEq/l), HCO3−concentration (from 27 ± 1.0 mEq/l to 25 ± 1.3 mEq/l), Cl−concentration (from 108 ± 2 mEq/l to 112 ± 2 mEq/l), albumin concentration (from 4.4 ± 0.2 g/dl to 3.5 ± 0.5 g/dl), and arterial carbon dioxide tension (Paco2; from 40.8 ± 2.3 mmHg to 39.2 ± 3.2 mmHg), whereas only the albumin concentration (from 4.4 ± 0.2 g/dl to 4.8 ± 0.6 g/dl) changed significantly in the albumin-treated group.ConclusionsDecreases in base excess were observed for 210 min after hetastarch administration but not after albumin. The mechanism for this difference is discussed.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe minimum alveolar concentration (MAC)-awake is a traditional index of hypnotic potency of an inhalational anesthetic. The MAC-awake of xenon, an inert gas with anesthetic properties (MAC = 71%), has not been determined. It is also unknown how xenon interacts with isoflurane or sevoflurane on the MAC-awake.MethodsIn the first part of the study, 90 female patients received xenon, nitrous oxide (N2O), isoflurane, or sevoflurane supplemented with epidural anesthesia (n = 36 for xenon and n = 18 per group for other anesthetics). In the second part, 72 additional patients received either xenon or N2O combined with the 0.5 times MAC-awake concentration of isoflurane or sevoflurane (0.2% and 0.3%, respectively, based on the results of the first part; n = 18 per group). During emergence, the concentration of an assigned anesthetic (xenon or N2O only in the second part) was decreased in 0.1 MAC decrements every 15 min from 0.8 MAC or from 70% in the case of N2O until the patient followed the command to either open her eyes or to squeeze and release the investigator’s hand. The concentration midway between the value permitting the first response to command and that just preventing it was defined as the MAC-awake.ResultsThe MAC-awake were as follows: xenon, 32.6 ± 6.1% (mean ± SD) or 0.46 ± 0.09 MAC; N2O, 63.3 ± 7.1% (0.61 ± 0.07 MAC); isoflurane, 0.40 ± 0.07% (0.35 ± 0.06 MAC); and sevoflurane, 0.59 ± 0.10% (0.35 ± 0.06 MAC). Addition of the 0.5 MAC-awake concentrations of isoflurane and sevoflurane reduced the MAC-awake of xenon to 0.50 ± 0.15 and 0.51 ± 0.16 times its MAC-awake as a sole agent, but that of N2O to the values significantly greater than 0.5 times its MAC-awake as a sole agent (0.68 ± 0.12 and 0.66 ± 0.14 times MAC-awake;P< 0.01, analysis of variance and Dunnett’s test).ConclusionsThe MAC-awake of xenon is 33% or 0.46 times its MAC. In terms of the MAC-fraction, this is smaller than that for N2O but greater than those for isoflurane and sevoflurane. Unlike N2O, xenon interacts additively with isoflurane and sevoflurane on MAC-awake.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundIn most publications about myasthenia, monitoring neuromuscular blockade during anesthesia is recommended. In healthy patients, the relation of blockade between muscles has been established, but there is little information about the relation in myasthenic patients. Our objective was to investigate whether the relation between the orbicularis oculi and adductor pollicis muscles is the same in healthy patients and myasthenic patients.MethodsAfter anesthesia was induced with 4–6 mg/kg thiopental and 2 &mgr;g/kg fentanyl, followed by 2% sevoflurane and 60% nitrous oxide in oxygen, 10 healthy patients and 10 myasthenic patients received 0.025 and 0.01 mg/kg vecuronium, respectively. Neuromuscular monitoring was performed with use of accelerometry at the orbicularis oculi and the adductor pollicis muscles by stimulating the temporal branch of the facial nerve and the ulnar nerve.ResultsThe relation of blockade between these two muscles was not the same in healthy patients and myasthenic patients: in healthy patients, the maximum neuromuscular blockade with 0.025 mg/kg vecuronium was less in the orbicularis oculi than in the adductor pollicis (median 72%vs.91%;P< 0.05); in contrast, in myasthenic patients, the blockade with 0.01 mg/kg vecuronium was greater in the orbicularis oculi than in the adductor pollicis (median 96%vs.62%;P< 0.05).ConclusionNeuromuscular monitoring at the orbicularis oculi may overestimate blockade in myasthenic patients. Extubation must be performed when the muscle most sensitive to neuromuscular blocking agents is recovered. Therefore, neuromuscular monitoring at the orbicularis oculi is recommended to avoid persistent neuromuscular blockade in patients with myasthenia gravis.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe ability of intravenous lidocaine to prevent intubation-induced bronchospasm is unclear. The authors performed a prospective, randomized, double-blind, placebo-controlled trial to test the ability of intravenous lidocaine and inhaled albuterol to attenuate airway reactivity after tracheal intubation in asthmatic patients undergoing general anesthesia.MethodsSixty patients were randomized to receive either 1.5 mg/kg intravenous lidocaine or saline, 3 min before tracheal intubation. An additional 50 patients were randomized to receive 4 puffs of inhaled albuterol or placebo 15–20 min before tracheal intubation. Anesthesia was induced with propofol. Immediately after intubation and at 5-min intervals, transpulmonary pressure and airflow were recorded, and lower pulmonary resistance (RL) was calculated. Isoflurane was administered after the initial two measurements to assess reversibility of bronchoconstriction. A bronchoconstrictor response to intubation was defined as RLgreater than or equal to 5 cm H2O · l−1· s−1in the first two measurements after intubation and RLsubsequently decreasing by 50% or more after isoflurane.ResultsThe lidocaine and placebo groups were not different in the peak RLbefore administration of isoflurane (8.2 cm H2O · l−1· s−1vs.7.6 cm H2O · l−1· s−1) or frequency of airway response to intubation (lidocaine 6 of 30vs.placebo 5 of 27). In contrast, the albuterol group had lower peak RL(5.3 cm H2O · l−1· s−1vs.8.9 cm H2O · l−1· s−1;P< 0.05) and a lower frequency of airway response (1 of 25vs.8 of 23;P< 0.05) than the placebo group.ConclusionsInhaled albuterol blunted airway response to tracheal intubation in asthmatic patients, whereas intravenous lidocaine did not.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundHypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia.MethodsEight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 &mgr;g · kg−1· min−1) and sevoflurane (1.0–1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation.ResultsThe threshold Paco2to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 ± 4 mmHg (mean ± SD) during sevoflurane anesthesia and 61 ± 4 mmHg during propofol anesthesia (P= 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg.ConclusionsEven mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID