ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundDespite evidence that regional anesthesia may be associated with fewer perioperative complications than general anesthesia, most studies that have compared cardiac outcome after general or regional anesthesia alone have not shown major differences. This study examines the impact of anesthetic choice on cardiac outcome in patients undergoing peripheral vascular surgery who have a high likelihood of associated coronary artery disease.MethodsFour hundred twenty‐three patients, between 1988 and 1991, were randomly assigned to receive general (n = 138), epidural (n = 149), or spinal anesthesia (n = 136) for femoral to distal artery bypass surgery. All patients were monitored with radial artery and pulmonary artery catheters. Postoperatively, patients were in a monitored setting for 48–72 h and had daily electrocardiograms for 4–5 days and creatine phosphokinase/isoenzymes every 8 h x 3, then daily for 4 days. Cardiac outcomes recorded were myocardial infarction, angina, and congestive heart failure.ResultsBaseline clinical characteristics were not different between anesthetic groups. Overall, the patient population included 86% who were diabetic, 69% with hypertension, 36% with a history of a prior myocardial infarction, and 41% with a history of smoking. Cardiovascular morbidity and overall mortality were not significantly different between groups when analyzed by either intention to treat or type of anesthesia received. In the intention to treat analysis, incidences of cardiac event or death for general, spinal, and epidural groups were 16.7%, 21.3%, and 15.4%, respectively. The absolute risk difference observed between general and all regional anesthesia groups for cardiac event or death was ‐1.6% (95% confidence interval ‐9.2%, 6.1%) This reflected a nonsignificant trend for lower risk of postoperative events with general anesthesia.ConclusionsThe choice of anesthesia, when delivered as described, does not significantly influence cardiac morbidity and overall mortality in patients undergoing peripheral vascular surgery.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundSurgically induced ischemia and reperfusion is frequently accompanied by local and remote organ injury. It was hypothesized that this procedure may produce injurious oxidants such as hydrogen peroxide (H2O2), which, if unscavenged, will generate the highly toxic hydroxyl radical (*symbol* OH). Accordingly, it was proposed that tourniquet‐induced exsanguination for limb surgery may be a useful ischemia‐reperfusion model to investigate the presence of oxidants, particularly H2O2.MethodsIn ten patients undergoing knee surgery, catheters were placed in the femoral vein of the limb operated on for collection of local blood and in a vein of the arm for sampling of systemic blood. Tourniquet‐induced limb exsanguination was induced for about 2 h. After tourniquet release (reperfusion), blood samples were collected during a 2‐h period for measurement of H2O2, xanthine oxidase activity, xanthine, uric acid (UA), glutathione, and glutathione disulfide.ResultsAt 30 s of reperfusion, H2O2concentrations increased ([nearly equal] 90%) from 133+/‐5 to 248+/‐8 nmol *symbol* ml sup ‐1 (P < 0.05) in local blood samples, but no change was evident in systemic blood. However, in both local and systemic blood, xanthine oxidase activity increased [nearly equal] 90% (1.91+/‐ 0.07 to 3.93+/‐0.41 and 2.19+/‐0.07 to 3.57+/‐ 0.12 nmol UA *symbol* ml sup ‐1 *symbol* min sup ‐1, respectively) as did glutathione concentrations (1.27+/‐0.04 to 2.69+/‐0.14 and 1.27+/‐0.03 to 2.43+/‐0.13 micro mol *symbol* ml sup ‐1, respectively). At 5 min reperfusion, in local blood, H2O2concentrations and xanthine oxidase activity peaked at 796+/‐38 nmol *symbol* ml sup ‐1 ([nearly equal] 500%) and 11.69+/‐1.46 nmol UA *symbol* ml sup ‐1 *symbol* min sup ‐1 ([nearly equal] 520%), respectively. In local blood, xanthine and UA increased from 1.49 +/‐0.07 to 8.36+/‐0.33 nmol *symbol* ml sup ‐1 and 2.69 +/‐0.16 to 3.90+/‐0.18 micro mol *symbol* ml sup ‐1, respectively, whereas glutathione and glutathione disulfide increased to 5.13+/‐0.36 micro mol *symbol* ml sup ‐1 and 0.514+/‐ 0.092 nmol *symbol* ml sup ‐1, respectively. In systemic blood, xanthine oxidase activity peaked at 4.75+/‐0.20 UA nmol *symbol* ml sup ‐1 *symbol* min sup ‐1. At 10 min reperfusion, local blood glutathione and UA peaked at 7.08+/‐0.46 micro mol *symbol* ml sup ‐1 and 4.67 +/‐0.26 micro mol *symbol* ml sup ‐1, respectively, while the other metabolites decreased significantly toward pretourniquet levels. From 20 to 120 min, most metabolites returned to pretourniquet levels; however, local and systemic blood xanthine oxidase activity remained increased 3.76+/‐0.29 and 3.57+/‐0.37 nmol UA *symbol* ml sup ‐1 *symbol* min sup ‐1, respectively. Systemic blood H2O2was never increased during the study. During the burst period ([nearly equal] 5–10 min), local blood H2O2concentrations and xanthine oxidase activities were highly correlated (r = 0.999).ConclusionsThese studies suggest that tourniquet‐induced exsanguination for limb surgery is a significant source for toxic oxygen production in the form of H2O2and that xanthine oxidase is probably the H2O2‐generating enzyme that is formed during the ischemia‐reperfusion event. In contrast to the reperfused leg, the absence of H2O2in arm blood demonstrated a balanced oxidant scavenging in the systemic circulation, despite the persistent increase in systemic xanthine oxidase activity.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundPropofol and alfentanil frequently are administered together for intravenous sedation. This study investigated pharmacokinetic and pharmacodynamic interactions between propofol and alfentanil, at sedative concentrations, with specific regard to effects on ventilation, analgesia, sedation, and nausea.MethodsTen male volunteers underwent steady‐state infusions on 3 separate days consisting of propofol alone, alfentanil alone, or a combination of the two. Target plasma concentrations for propofol were 150, 300, and 600 ng/ml for 1 h at each concentration; for alfentanil it was 40 ng/ml for 3 h. Assessment included serial measurements of (1) ventilatory function (minute ventilation, carbon dioxide production, end‐tidal carbon dioxide, ventilatory response to rebreathing 7% CO2); (2) analgesia (subjective pain report in response to graded finger shock and evoked potential amplitude); (3) sedation (subjective rating, observer scores, and digit symbol substitution test); (4) nausea (visual analog scale, 0–100 mm).ResultsDuring combination treatment, propofol plasma concentration was 22% greater than during propofol alone using replicate infusion schemes (P < 0.009). End‐tidal carbon dioxide was unchanged by propofol, and increased equally by alfentanil and alfentanil/propofol combined (Delta end‐tidal carbon dioxide 7.5 and 6.2 mmHg, respectively). Analgesia with propofol/alfentanil combined was greater than with alfentanil alone. (Pain report decreased 50% by PA vs. 28% for alfentanil, P < 0.05). Sedation was greater with propofol/alfentanil combined than with alfentanil or propofol alone (digit symbol substitution test 30 for propofol/alfentanil combined vs. 57 for alfentanil, and 46 for propofol, P < 0.05). Nausea occurred in 50% of subjects during alfentanil, but in none during propofol/alfentanil combination treatment.ConclusionsThe combination of propofol and alfentanil produced greater sedation and analgesia than that with either drug alone. Propofol offset the emetic effects of alfentanil. Equivalent depression of the carbon dioxide response curve, and elevation of end‐tidal carbon dioxide occurred with propofol/alfentanil combined and alfentanil.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundAn appropriate measure of performance is needed to identify anesthetic depth indicators that are promising for use in clinical monitoring. To avoid misleading results, the measure must take into account both desired indicator performance and the nature of available performance data. Ideally, anesthetic depth indicator value should correlate perfectly with anesthetic depth along a lighter‐deeper anesthesia continuum. Experimentally, however, a candidate anesthetic depth indicator is judged against a "gold standard" indicator that provides only quantal observations of anesthetic depth. The standard anesthetic depth indicator is the patient's response to a specified stimulus. The resulting observed anesthetic depth scale may consist only of patient "response" versus "no response," or it may have multiple levels. The measurement scales for both the candidate anesthetic depth indicator and observed anesthetic depth are no more than ordinal; that is, only the relative rankings of values on these scales are meaningful.MethodsCriteria were established for a measure of anesthetic depth indicator performance and the performance measure that best met these criteria was found.ResultsThe performance measure recommended by the authors is prediction probability PK, a rescaled variant of Kim's dy*symbol* x measure of association. This performance measure shows the correlation between anesthetic depth indicator value and observed anesthetic depth, taking into account both desired performance and the limitations of the data. Prediction probability has a value of 1 when the indicator predicts observed anesthetic depth perfectly, and a value of 0.5 when the indicator predicts no better than a 50:50 chance. Prediction probability avoids the shortcomings of other measures. For example, as a nonparametric measure, PKis independent of scale units and does not require knowledge of underlying distributions or efforts to linearize or to otherwise transform scales. Furthermore, PKcan be computed for any degree of coarseness or fineness of the scales for anesthetic depth indicator value and observed anesthetic depth; thus, PKfully uses the available data without imposing additional arbitrary constraints, such as the dichotomization of either scale. And finally, PKcan be used to perform both grouped‐ and paired‐data statistical comparisons of anesthetic depth indicator performance. Data for comparing depth indicators, however, must be gathered via the same response‐to‐stimulus test procedure and over the same distribution of anesthetic depths.ConclusionsPrediction probability PKis an appropriate measure for evaluating and comparing the performance of anesthetic depth indicators.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundMovement in response to painful stimulation is the end point classically used to assess the potency of anesthetic agents. In this study, the ability of modeled propofol effect‐site concentration to predict movement in volunteers during propofol/nitrous oxide anesthesia was tested, then it was compared with the predictive abilities of the Bispectral Index and 95% spectral edge frequency of the electroencephalogram, pupillary reflex amplitude, and systolic arterial blood pressure. In addition, the relationships between simple end points of loss and recovery of consciousness, and pupillary, hemodynamic, and propofol concentration indicators were studied.MethodsTen healthy volunteers were anesthetized with an infusion of propofol, which was increased in three equal steps to 21 mg *symbol* kg lean body mass sup ‐1 *symbol* h sup ‐1. After loss of the ability to hold a syringe and of the eyelash reflex, 60% nitrous oxide was introduced and the trachea was intubated without the use of muscle relaxants. The propofol infusion rate then was decreased to 15.4 mg *symbol* kg lean body mass sup ‐1 *symbol* h sup ‐1. Ten minutes later, tetanic electrical stimulation was administered to the thigh via needle electrodes: if movement was observed within 1 min, the propofol infusion rate was increased by 1.75 mg *symbol* kg lean body mass sup ‐1 *symbol* h sup ‐1 5 min after the stimulus; if not, it was similarly decreased. This 15‐min sequence was repeated until volunteers "crossed over" from movement to no movement (or vice versa) four times. The propofol infusion rate then was increased to 21 mg *symbol* kg lean body mass sup ‐1 *symbol* h sup ‐1, nitrous oxide was discontinued, the trachea was extubated, and the infusion rate was decreased in five equal steps over 50 min. The times at which the eyelash reflex returned and the birth date was recalled were recorded. The electroencephalogram was monitored continuously (FP1, FP2, ref: nasion, ground: mastoid). Measurements of the pupillary response, arterial blood pressure, and heart rate were recorded during induction and awakening, just before and for 5 min after each stimulation. Arterial blood samples were obtained for propofol assay, and propofol effect‐site concentrations were calculated at each time. The predictive value of indicators was compared using a new statistic, the prediction probability (PK).ResultsLoss and return of the eyelash reflex occurred at greater propofol effect‐site concentrations than either dropping the syringe or recall of the birthday. The propofol effect‐site concentration (in the presence of 60% nitrous oxide) predicted to prevent movement after a supramaximal stimulus in 50% of volunteers was 1.80 micro gram/ml (95% confidence limits: 1.40–2.34 micro gram/ml). The Bispectral Index (PK= 0.86), 95% spectral edge frequency (PK= 0.81), pupillary reflex amplitude (PK= 0.74), and systolic arterial blood pressure (PK= 0.78) did not differ significantly from modeled propofol effect‐site concentration (PK= 0.76) in their ability to predict movement.ConclusionsIndicators of pharmacodynamic effect, such as the electroencephalogram, pupillary light reflex, and systolic arterial blood pressure, predict movement as well as effect‐site concentration during propofol/nitrous oxide anesthesia. Loss and return of the eyelash reflex correspond to a deeper level of anesthesia than syringe‐dropping or recall of the birth date.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundThe electroencephalogram (EEG) has been used to study the effects of anesthetic and analgesic drugs on central nervous system function. A prospective study was designed to evaluate the accuracy of various EEG parameters for assessing midazolam‐induced sedation during regional anesthesia.MethodsTwenty‐six consenting adult patients were administered 4.5–20 mg intravenous midazolam (in increments of 0.5–1‐mg bolus doses every 6–10 min) until they became unresponsive to tactile stimulation (i.e., mild prodding or shaking). The EEG was continuously recorded from a bifrontal montage (FP1‐Czand FP2‐Cz) to obtain the bispectral index (BI), 95% spectral edge frequency (SEF), median frequency (MF), and delta, theta, alpha, and beta power bands. Sedation was assessed clinically at 6–10‐min intervals using the Observers' Assessment of Alertness/Sedation (OAA/S) scale, with 1 = no response (unconsciousness) to tactile stimulation to 5 = wide awake. The EEG parameters were correlated with the OAA/S scores using nonparametric Spearman's rank‐correlation analysis. Kruskal‐Wallis analysis of variance was used to determine significant changes in EEG parameters during the onset of and recovery from midazolam‐induced sedation.ResultsOf the EEG parameters studied, the BI exhibited the best correlation with OAA/S scores during both the onset (Spearman's Rho = 0.815) and recovery (Spearman's Rho = 0.596) phases. With increasing sedation, there was a progressive decrease in the BI (OAA/S score of 5: BI = 95.4+/‐2.3; 4:90.3+/‐4.5; 3:86.6+/‐4.6; 2:75.6+/‐9.7; 1:69.2+/‐13.9). A similar pattern was found for the 95% SEF as the OAA/S score decreased from 4 to 1. Similarly, EEG‐BI increased with recovery from the sedative effects of midazolam (OAA/S score = 2: BI = 75.2+/‐10.2; 3:82.3+/‐7.3; 4:90.8 +/‐6). However, no consistent changes were found with the other EEG parameters. The mean EEG values between OAA/S scores 3 and 2 and between OAA/S scores 2 and 1 during the onset and recovery phases from midazolam‐induced sedation, defined as EEG50values for response to verbal command (EEG50‐VC) and to shaking of the head (EEG50‐SH), were 79.3+/‐8 and 70.8+/‐14.3, respectively, for EEG‐BI. The EEG‐BI displayed the smallest coefficients of variation for the EEG sub 50‐VC and EEG50‐SH values.ConclusionsThe EEG‐BI appears to be a useful parameter for assessing midazolam‐induced sedation and can predict the likelihood of a patient responding to verbal commands or to shaking of the head during midazolam‐induced sedation.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundAnimal studies show that airway receptors responsible for eliciting respiratory protective reflexes are not uniformly distributed in the airways. Based on this information, it is possible that the protective reflex responses to airway irritation in humans may vary, depending on the site of stimulation. The purpose of this study is to examine whether the protective reflex responses evoked from the larynx are different from those evoked from the lower airways and to see how change in depth of anesthesia modifies the protective reflex responses evoked from individual sites.MethodsThe airway mucosa of the larynx, tracheal carina, and bronchi were stimulated by injection of distilled water (0.5 ml) at two different depths of sevoflurane anesthesia (1.2 and 1.8 MAC) in 11 female subjects breathing spontaneously through the laryngeal mask airway. The respiratory responses were monitored by measuring ventilatory flow and airway pressure.ResultsAt 1.2 MAC of sevoflurane anesthesia, both laryngeal and tracheal stimulation caused protective responses, such as forceful expiratory efforts, apnea, and spasmodic panting, whereas bronchial stimulation caused little or no such responses. There was no significant difference in the incidence of different types of reflex responses between the larynx and the trachea. At 1.8 MAC of sevoflurane, the nature of the elicited responses was very similar to that observed at 1.2 MAC of sevoflurane, showing little dose‐dependence of anesthetic effect.ConclusionsThe respiratory reflex responses evoked by injection of water vary, depending on the site of stimulation. The incidence of various reflex responses was not affected by the changing depth of anesthesia. The sensitivity to airway irritation seems to be greater at the larynx and trachea than at the more peripheral airways.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundA rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses.MethodsTo test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg *symbol* kg sup ‐1 propofol, anesthesia was maintained with 4% end‐tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg *symbol* kg sup ‐1 propofol was administered either 2 or 5 min before increasing end‐tidal desflurane concentration from 4% to 8%.ResultsWithout propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63+/‐3 beats/min to 108 +/‐5 beats/min, mean+/‐SEM; P < 0.01), mean arterial pressure (from 73+/‐1 mmHg to 118+/‐6 mmHg; P < 0.01), and epinephrine concentration (from 14+/‐1 pg *symbol* ml sup ‐1 to 279+/‐51 pg *symbol* ml sup ‐1; P < 0.05). There was no significant change in norepinephrine concentration (from 198+/‐37 pg *symbol* ml sup ‐1 to 277+/‐46 pg *symbol* ml sup ‐1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158+/‐35 pg *symbol* ml sup ‐1, propofol given 2 min before, and 146 + 41 pg *symbol* ml sup ‐1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses.ConclusionsAlthough able to blunt the increase in epinephrine concentration, propofol 2 mg *symbol* kg sup ‐1 propofol does not attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

BackgroundEpidural anesthesia is sometimes initiated during general anesthesia, yet few data exist concerning efficacy of epinephrine‐containing test doses.MethodsThirty‐six patients were randomized to receive either 0.5 MAC isoflurane, 1 MAC isoflurane, or 0.5 MAC each (1 MAC total) of isoflurane and nitrous oxide. Each subject received intravenous saline followed by three test doses containing 45 mg lidocaine with 7.5, 15, and 30 micro gram epinephrine in a randomized, double‐blind fashion. Heart rate and systolic, diastolic, and mean blood pressures were measured for 5 min after injection. Positive hemodynamic criteria identifying intravascular injection were determined from peak increases in hemodynamics during administration of saline. Dose‐effect relationships between epinephrine and peak increases in hemodynamics were assessed with linear regression. Minimum required doses of epinephrine to produce peak positive hemodynamic increases on average were determined from linear regression.ResultsPositive hemodynamic criteria were identified as increases in heart rate greater or equal to 8 beats/min, systolic blood pressure greater or equal to 13 mmHg, diastolic blood pressure greater or equal to 7 mmHg, and mean blood pressure greater or equal to 9 mmHg. Significant dose‐effect relationships were observed for epinephrine and peak increases in hemodynamics (correlation coefficients ranged from 0.61–0.91). Minimum required doses of epinephrine ranged from 6 to 19 micro gram depending on hemodynamic measurement and anesthetic group.ConclusionsHemodynamic responses to intravascular injection of test doses vary with dose of epinephrine and depth and type of general anesthetic used. Thus, the 15 micro gram epinephrine contained in the standard test dose may not be sufficient during all anesthetic conditions.

ISSN:0003-3022    

出版商:OVID    

年代:1996

数据来源: OVID