Emeritus Faculty-Med Ctr Line, Anesthesiology, Perioperative and Pain Medicine
Neurological dysfunction after cardiopulmonary bypass;, metabolism of inhalation anesthetics.
: Anesthesiologists' cognitive resources such as their attention, knowledge, and strategies play an important role in the prevention and correction of critical events. In this paper, we examined anesthesiologists' responses to the anesthesia machine (AM) in the "off" position during a simulated emergent cesarean section scenario.: All simulations were videotaped which allowed for offline review. At the beginning of the scenario, the AM system switch was purposefully turned to the off/standby position. The responses of 14 anesthesia residents at the Veterans Affairs Palo Alto Health Care System and Stanford University Simulation Center for Crisis Management Training in Health Care (VASC) and 11 anesthesia residents at the Boston Center for Medical Simulation (CMS) were analyzed.: Nine subjects at VASC restored the AM system switch to the "on" position on their own, whereas five subjects required help from another clinician. The median response time (RT) for all 14 subjects was 149.5 seconds. At CMS, five subjects restored the AM system switch to the "on" position on their own (median RT = 207 seconds), whereas two subjects received help from another anesthesia resident. There were four cases where the AM system switch problem was not corrected.: Factors that could have contributed to subjects' difficulty in detecting and correcting the AM system switch included the unusual nature of the problem, the human factors design of the AM front panel and system switch, and inadequate training by the subjects. Improving the appearance of the AM's system switch and training of clinicians to recognize the location and functionality of the AM system switch could be useful in correcting such an event in a timely manner and reducing patient risk.
View details for PubMedID 19088570
Techniques are needed to assess anesthesiologists' performance when responding to critical events. Patient simulators allow presentation of similar crisis situations to different clinicians. This study evaluated ratings of performance, and the interrater variability of the ratings, made by multiple independent observers viewing videotapes of simulated crises.Raters scored the videotapes of 14 different teams that were managing two scenarios: malignant hyperthermia (MH) and cardiac arrest. Technical performance and crisis management behaviors were rated. Technical ratings could range from 0.0 to 1.0 based on scenario-specific checklists of appropriate actions. Ratings of 12 crisis management behaviors were made using a five-point ordinal scale. Several statistical assessments of interrater variability were applied.Technical ratings were high for most teams in both scenarios (0.78 +/- 0.08 for MH, 0.83 +/- 0.06 for cardiac arrest). Ratings of crisis management behavior varied, with some teams rated as minimally acceptable or poor (28% for MH, 14% for cardiac arrest). The agreement between raters was fair to excellent, depending on the item rated and the statistical test used.Both technical and behavioral performance can be assessed from videotapes of simulations. The behavioral rating system can be improved; one particular difficulty was aggregating a single rating for a behavior that fluctuated over time. These performance assessment tools might be useful for educational research or for tracking a resident's progress. The rating system needs more refinement before it can be used to assess clinical competence for residency graduation or board certification.
View details for Web of Science ID 000074710800004
View details for PubMedID 9667288
The authors have developed a course in Anesthesia Crisis Resource Management (ACRM) analogous to courses in Crew (Cock-pit) Resource Management (CRM) conducted in commercial and military aviation. Anesthesiologists do not typically receive formal training in crisis management although they are called upon to manage life-threatening crises at a moment's notice. Two model demonstration courses in ACRM were conducted using a realistic anesthesia simulation system to test the feasibility and acceptance of this kind of training. Anesthesiologists received didactic instruction in dynamic decision-making, human performance issues in anesthesia, and in the principles of anesthesia crisis resource management. After familiarization with the host institution's operating rooms and with the simulation environment, they underwent a 2-h simulation session followed by a debriefing session which used a videotape of their simulator performance. Participants rated the course as intense, helpful to their practice of anesthesiology, and highly enjoyable. Several aspects of the course were highly rated, including: videotapes of actual anesthetic mishaps, simulation sessions, and debriefing sessions. Scores on written tests of knowledge about anesthesia crisis management showed a significant improvement following the first course (residents) but not the second course (experienced anesthesiologists). Although the ultimate utility of this training for anesthesiologists cannot easily be determined, the course appeared to be a useful method for addressing important issues of anesthesiologist performance which have previously been dealt with haphazardly. The authors believe that ACRM training should become a regular part of the initial and continuing education of anesthesiologists.
View details for Web of Science ID A1992JK72800001
View details for PubMedID 1524531
Halothane is metabolized by an oxidative pathway to stable, nonvolatile end products, trifluoroacetic acid (TFAA) and bromide (Br-), and by reductive pathways to Br-and inorganic fluoride (F-). There is evidence that both oxidatively and reductively formed intermediates may produce hepatotoxicity, although the exact etiology of the fulminant hepatic necrosis seen in humans is unproven. Obese patients receiving volatile anesthetics exhibit higher serum anesthetic metabolite concentrations than do normal-weight patients, and thus might be at greater risk of hepatotoxicity because of higher concentrations of reactive intermediates from halothane metabolism. To eliminate the variables inherent in human clinical studies leading to confounding interpretation of data, this study determined the contributions of oxidative and reductive pathways to halothane metabolism in an animal model of human hypertrophic obesity, the most common form of human obesity. Eight pairs of obese (high-fat diet) and normal-weight (standard chow), male Fischer 344 rats were anesthetized with halothane for 4 h at an inspired concentration of 0.78%. Serum and urinary concentrations of TFAA, Br-, and F-were measured. Thirty-six hours following halothane anesthesia, mean serum TFAA concentrations peaked at 7.3 +/- 1.1 mM in obese rats and 4.7 +/- 0.7 mM in nonobese rats. TFAA urinary excretions during the 180-h period postanesthesia were 519 +/- 69 and 336 +/- 22 mumol, respectively. Peak serum Br- concentrations were 9.1 +/- 1.0 and 6.9 +/- 0.6 mM for obese and nonobese rats, respectively, and Br-urinary excretions were 127 +/- 30 and 79 +/- 14 mumol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1989AM76600020
View details for PubMedID 2774271
The mechanism for enhanced metabolism of inhaled anesthetics in obese rats and humans is unknown. In this study, hepatic microsomes from normal-weight chow-fed rats and rats fed a high fat diet for approximately 54 weeks to induce obesity were examined for their ability to metabolize fluorinated inhalation anesthetics. Body composition of rats on diet for 54 weeks revealed a significantly elevated lipid content of both the whole body and liver in obese compared to normal-weight rats. Protein per g liver was not significantly different. The hepatic microsomal content of cytochromes b5 and P-450 per mg protein was not different between obese and normal-weight rats. Hepatic microsomal defluorination rates of the anesthetics, methoxyflurane, enflurane and isoflurane, were not altered by high fat diets of 54 weeks duration. The activity rate of aminopyrine N-demethylase was not changed by the diet; however, p-nitroanisole O-demethylase activity was significantly increased in microsomes from obese rats to approximately 150% of control activity. Thus the enhanced in vivo anesthetic metabolism of obese Fischer 344 rats does not appear to be the result of an increase in the specific activity of anesthetic metabolizing enzymes.
View details for Web of Science ID A1989AJ88800026
View details for PubMedID 2774769
This study was designed to investigate the effects of etomidate and its solubilizing agent (propylene glycol) upon enflurane metabolism and adrenal steroidogenesis in Fischer 344 rats. A central venous catheter was placed using pentobarbital anesthesia, and rats were randomized to one of four groups for treatment several days later. Group 1 animals received normal saline, 3 ml/kg, given via the central venous catheter. The other three groups were administered equivalent volumes of either: crystalline etomidate (group 2), 0.4 mg/ml, in saline and 1.1% ethanol; propylene glycol (group 3), 7%, in saline; or etomidate (group 4), 0.4 mg/ml in saline with 7% propylene glycol. In the first part of this study, after an intravenous bolus of one of these four solutions, animals were immediately placed in a 200-liter chamber and received 1 h of 2% enflurane. Serum and urine were assayed for inorganic fluoride (F-) before and after anesthesia. Two hours after enflurane anesthesia, groups 1 and 2 had the highest mean peak serum F- concentrations (13.2 and 13.5 uM, respectively). Groups 3 and 4 had significantly lower mean peak serum F- concentrations (4.7 and 4.5 uM, respectively). In the second part of this study, additional animals were randomized into four groups and received the same intravenous medications as above. Thirty minutes later, they received an intravenous bolus of ACTH. Blood samples were drawn and serum aldosterone levels were measured. Animals in groups 1 and 3 had significantly greater increases in peak serum aldosterone levels 30 minutes after ACTH (peak levels: 0.80 and 0.77 ng/ml, respectively) than animals in groups 2 and 4 (peak levels: 0.60 and 0.58 ng/ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1988L961800003
View details for PubMedID 2829658