ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

This study was undertaken to determine if fentanyl and sufentanil could produce dose-related suppression of hemodynamic and hormonal responses to surgical stimulation. Eighty patients scheduled for elective CABG were studied in two consecutive protocols: protocol I was a randomized double-blind study of 40 patients who received a single dose of fentanyl (50 or 100 μg/kg) or sufentanil (10, 20, or 30 μg/kg). Hemodynamic measurements and hormonal concentrations (renin, aldosterone, cortisol, and catecholamines) were determined before and after induction and after intubation and sternotomy. Protocol II was an open randomized study of 40 patients who received sufentanil in one of four doses: 30 μg/kg as a single dose, 10 μg/kg plus infusion 0.05 μg·kg-1·min-1, 20 μg/kg plus infusion 0.1 μg·kg-1· min-1, or 40 μg/kg plus infusion 0.2 μg·kg-1· min-1. Hemodynamic measurements and plasma sufentanil and catecholamine concentrations were determined before and after induction and after intubation, sternotomy, and aortic cannulation. Both protocols defined a hemodynamic response as a 15% or more increase in systolic blood pressure (SBP) from control and a hormonal response 50% or more increase over control. During protocol I, 18 patients had a hemodynamic response (average increase in SBP 22.6±2%) and 35 patients had a total of 59 hormonal responses. During protocol II, 24 patients had a hemodynamic response (average increase in SBP - 31±3%) and there were 15 catecholamine responses. There were no differences between dose groups in either protocol. It was concluded that in these dose ranges, suppression of hemodynamic or hormonal stress responses is not related to opioid dose. Furthermore, the maintenance of high plasma opioid concentrations by opioid infusions does not decrease the incidence of these responses.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Changes in the electroencephalogram (EEG), mean arterial blood pressure (MABP), and hemoglobin saturation in brain vasculature of lightly anesthetized normothermic humans undergoing induced circulatory arrest for implantation of an automatic internal cardioverting defibrillator were studied. EEG was measured using a four-channel bipolar montage and hemoglobin saturation was measured transcranially using reflectance spectroscopy at 760 nm with an isosbestic reference at 800 nm. Hemoglobin saturation of blood in the quadriceps muscle was also measured. Thirty-two episodes of hypotension due to ventricular fibrillation were studied along with 31 episodes of hypotension related to ventricular tachycardia and rapid ventricular pacing. In a typical fibrillatory event there was a decrease in MABP followed almost immediately by changes in hemoglobin saturation of blood in the brain vasculature. The first changes in EEG were detected an average of 6.5s(P< 0.001, pairedttest) after the beginning of change of brain vascular hemoglobin. In some cases changes in hemoglobin saturation could be detected without changes in EEG. Desaturation curves from muscle and brain were significantly different, suggesting that the brain probe was measuring hemoglobin change in a rapidly metabolizing volume of tissue that was dissimilar to the skin, muscle, and bone monitored by the probe over the quadriceps muscle. Examination of the 32 episodes of circulatory arrest revealed a marked response that began immediately with recirculation characterized by an increase of the hemoglobin saturation signal from brain vasculature to above base-line as the duration of circulatory arrest exceeded 37 s, this response is termed reperfusion hyperoxia. When the duration of circulatory arrest was less than 37 s, hemoglobin saturation returned to baseline without a period of reperfusion hyperoxia. An early response to reperfusion after cardiac arrest characterized by a marked increase in brain vascular hemoglobin saturation was identified. This event may have significance in understanding the events leading to brain failure.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of propofol, nitrous oxide, and/or isoflurane on efferent activity of sympathetic muscle nerve fibers (MSA) were studied using percutaneous microneurographic recordings from the peroneal nerve. Eight ASA Physical Status I patients (30–70 yr of age) scheduled for otorhinolaryngeal surgery entered the study. The effects of propofol (2–2.5 mg·kg-1· min-1) induction, tracheal intubation, and maintenance of anesthesia with isoflurane (0.3%, 0.6%, and 1.2% end-tidal concentrations) and/or 70% nitrous oxide were studied with respect to MSA, arterial blood pressure, heart rate, and indices of skin blood flow (laser doppler photometry and finger pulse plethysmography). Induction of anesthesia with propofol decreased MSA to 34 ± 2% (mean ± SEM) (P< 0.05), and subsequent tracheal intubation increased MSA rapidly to 151 ± 23% (P< 0.05) of the control level. Isoflurane administration both with and without nitrous oxide led to a decrease of MSA (P< 0.05). However, during nitrous oxide/isoflurane anesthesia (1.0 MAC) MSA was 76 ± 38% higher than when isoflurane was used alone, although this implied a decrease in anesthetic depth to 0.5 MAC. This indicates that nitrous oxide and isoflurane have opposite effects on sympathetic outflow. During undisturbed propofol, nitrous oxide, and/or isoflurane administration (up to 1.0 MAC), MSA retained its normal pulse synchronous pattern, indicating that modulation of sympathetic outflow from arterial baroreceptors was still present. Skin blood flow increased sevenfold to tenfold in association with propofol induction (P< 0.05) and was maintained at an 11− to 19-fold increase during nitrous oxide and/or isoflurane anesthesia, without any difference between the two anesthetics. The changes of skin blood flow were unrelated to MSA, indicating that sympathetic activity to the skin is functionally dissociated from that to muscle.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Eleven myasthenia gravis and seven control patients were studied during N2O/O2-fentanyl anesthesia to determine the ED50, ED95, and maintenance requirement of vecuronium using both mechanomyography and electromyography. The ED95of vecuronium was 17 (range 8–34) μg/kg in patients with myasthenia gravis, and this was significantly related to patient's acetylcholine receptor antibody titer (r= −0.75,P< 0.01). The average ED95value was 250% greater in control than in myasthenic patients (P< 0.01). The hourly requirement of vecuronium to maintain an 80–90% neuromuscular blockade was 38 ± 10 μg/kg in myasthenic and 120 ± 27 μg/kg in control patients (P< 0.001). When these requirements were related to individual ED95doses, they were comparable indicating similar time durations of effect of vecuronium following an equipotent dose in myasthenic and in control patients.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

To determine whether maturational changes in body composition and organ function affect distribution and elimination of and sensitivity to atracurium, the authors determined the pharmacokinetics and pharmacodynamics of atracurium in six infants and five children and compared these results with those obtained in five adults. Atracurium, 15.8 ± 1.7 μg · kg-1· min-1, was infused iv for 6–11 min to subjects anesthetized with nitrous oxide (60%) and halothane (0.9 MAC, age-adjusted) and twitch tension of the adductor pollicis muscle was measured. Plasma samples were obtained for 120 min; concentrations of atracurium were determined using a liquid chromatographic assay. A two-compartment pharmacokinetic model, adapted to account for elimination of atracurium from both central and peripheral compartments, was fit to the plasma concentration data; an effect-compartment model was fit to the twitch tension data. Volume of distribution at steady state (210 ± 118, 129 ± 44, and 100 ± 22 ml/kg for infants, children, and adults, respectively) and total clearance (7.9 ± 2.0, 6.8 ± 1.6, and 5.3 ± 0.9 ml · kg-1· min-1for the three groups) decreased with increasing age, Neither elimination half-life (20.0 ± 5.1, 17.2 ± 5.1, and 15.7 ± 2.5 min for the three groups) nor the steady state plasma concentration that resulted in 50% neuromuscular blockade (363 ± 118, 444 ± 121, and 436 ± 122 ng/ml for the three groups) varied with age. The authors conclude that these results are consistent with and explain the previously reported findings that recovery from the neuromuscular effects of atracurium is minimally affected by age. In addition, age-related changes in atracurium's volume of distribution at steady state are similar to those for vecuronium andd-tubocurarine; these changes presumably result from these muscle relaxants distributing into the extracellular fluid space the volume of which decreases during the first year of life.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The pressure in either the radial (n = 88) or proximal brachial artery (n = 82) was compared with aortic pressure before and after cardiopulmonary bypass (CPB) in patients receiving coronary artery bypass grafts. Radial artery pressures were measuredvia20-G 5-cm long catheters, brachial artery pressuresvia20-G 12.7-cm catheters, and aortic pressures were measuredviaa luer port in the aortic perfusion cannula. Transducers were connectedvia122-cm long tubing. For the various systems, mean natural frequencies were 16.1 to 17.7 Hz and damping coefficients were 0.16 to 0.27. Before CPB the brachial systolic, diastolic, and mean pressures were 108.2 ± 5.2%, 100.9 ± 2.8%, and 99.6 ± 2.3% of aortic; respective radial pressures were 113.9 ± 9.6%, 99.5 ± 2.8%, and 98.4 ± 2.8% of aortic. Immediately after CPB the brachial pressures were 99.5 ± 7.5%, 98.9 ± 3.5%, and 97.4 ± 2.9% of aortic, whereas respective radial pressures were 92.1 ± 14.6%, 94.7 ± 5.6%, and 90.8 ± 7.4%. All brachial and radial as a per cent of aortic pressure medians were significantly different, and except for prebypass diastolic and mean, the variance for brachial pressures was significantly less than that for pressures in the radial artery. The prebypass brachial correlation (r) with aortic for systolic, diastolic, and mean were 0.90, 0.98, and 0.98; respective radial correlations with aortic were 0.78, 0.97, and 0.95. Postbypass brachial systolic, diastolic, and mean correlations were 0.91, 0.97, and 0.98; radial were 0.50, 0.93, and 0.83. Brachial artery pressures were more accurate and reliable than radial artery pressures.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effect of three different depths of enflurane anesthesia (1.0, 1.4, and 1.8 MAC) upon laryngeal and respiratory responses to tracheal instillation of distilled water in nine female patients in whom a double-cuffed endotracheal tube had been inserted was investigated. The laryngeal responses were monitored by measuring the pressure in the saline-filled cuff positioned within the larynx, and the respiratory responses were monitored by measuring ventilatory flow and tracheal airway pressure. Increases in laryngeal cuff pressure in response to tracheal irritation were 19.7 ± 4.5 cmH2O (mean ± SD) at 1.0 MAC, 13.9 ± 3.6 cmH2O at 1.4 MAC, and 7.6 ± 1.8 cmH2O at 1.8 MAC, respectively (P< 0.01 for anesthetic dose). At 1.0 MAC of enflurane anesthesia, tracheal instillation of saline caused immediate laryngeal constriction and all components of the tracheal response, such as apnea, expiration reflex, cough reflex, and spasmodic panting. At 1.4 and 1.8 MAC, the same stimulation caused only apnea and constriction of the larynx in the majority of patients. These results indicate that changes in depth of anesthesia can modify the laryngeal and respiratory responses to tracheal irritation. The close association of laryngeal and respiratory responses may be an integral part of the defensive reflex synergism.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Characteristics of nocturnal sleep were investigated in six patients after anesthesia and cholecystectomy and in another six after anesthesia and gastroplasty. All night polysomnographic recordings were obtained while each patient slept in a private surgical ward room through two nights before and five or six nights after operation. Anesthesia included thiopental, N2O, isoflurane, and fentanyl. Postoperative analgesia was provided with parenteral morphine. Other aspects of care were routine. Nocturnal sleep was markedly disturbed after both surgical procedures. Throughout the operative night and subsequent one or two nights, sleep was highly fragmented with the usual recurring cycles of sleep stages completely disrupted. Slow wave sleep was suppressed and rapid eye movement (REM) sleep virtually eliminated. During the following 2–4 nights, as other aspects of sleep recovered, REM sleep reappeared and then increased to greater than the preoperative amount. This increased REM sleep was marked by a heavy density of eye movement activity along with frequent patient reports of unusually distressing dreams or vivid nightmares. It is concluded that anesthesia with upper abdominal surgery leads to a severe disruption of nocturnal sleep followed by the release of highly intense REM sleep about the middle of the first postoperative week.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Serial serum ionized calcium concentrations were measured before and after administration of either calcium chloride or calcium gluconate during the anhepatic stage of liver transplantation in 15 patients to determine the release of ionized calcium in the absence of hepatic function. When hypocalcemia (Ca++< 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7). Serum concentrations of ionized calcium and citrate, hematocrit, arterial blood gas tensions, acid-base state, and hemodynamic profiles were determined before and up to 10 min after calcium therapy. In both groups of patients initial similar and rapid increases in Ca++(0.98 ± 0.14 mM in the calcium chloride group and 1.05 ± 0.10 mM in the calcium gluconate group) were followed by gradual decreases over the next 10 min. Measured hemodynamic values were similar in the two groups, and neither group showed improvement in cardiovascular function after calcium therapy, possibly because of the decrease in preload that occurred during the anhepatic stage. Equally rapid increases in Ca++after administration of calcium chloride and gluconate in the anheptic state suggest that calcium gluconate does not require hepatic metabolism for the release of Ca++and is as effective as calcium chloride in treating ionic hypocalcemia in the absence of hepatic function.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID