Purpose: In response to the Royal College's request to improve the validity and reliability of oral examinations, the Examination Board in anesthesia proposed a structured oral examination format. Prior to its introduction, we studied this format in two residency programs to determine reliability of the examiners.Methods: Twenty faculty and 26 residents from two Canadian residency programs participated (Sites A and B). Pairs of examiners scored five or six residents examined consecutively on two standardized questions using global rating scales with anchored performance criteria. Residents' performances were scored independently during the examination (Time 1) and later from a videotaped recording (Time 2). Correlations between scores of the pairs of examiners and between scores of each examiner were determined.Results: Correlations demonstrating inter-rater agreement between examiners at Site A ranged from -.324 to .915 (mean .506) at Time 1. At Time 2, correlations ranged from .64 to .887 (mean .791). At Site B correlations ranged from .279 to .989 (mean .707) at Time 1 and at Time 2 correlations ranged from -.271 to .924 (mean .477). Correlations demonstrating intra-rater agreement of examiners at Site A ranged from .054 to .983 (mean .723) and at Site B correlations ranged from -.055 to .974 (mean .662).Correlations >0.4 were seen in 80% of the scores and >0.7 in 50% indicating fair to good intra-rater and inter-rater reliability using this format.Conclusions: Despite the limitations of our study our results compare favourably with those previously reported in anesthesia. We recommend the adoption of this format to the Royal College of Physicians and Surgeons of Canada Examination Board. Objectif : C'est à la demande du Collège royal, d'améliorer la validité et la fiabilité des examens oraux, que le Bureau des examinateurs en anesthésie a proposé un modèle d'examen oral structuré. Avant sa mise en application, nous l'avons testé dans deux programmes de rési-dence afin de déterminer la fiabilité des examinateurs. Méthode : Vingt facultés et 26 résidents de deux programmes canadiens ont participé à l'étude (Sites A et B). Des paires d'examinateurs ont utilisé une échelle de notation globale comportant des critères de rendement définis pour évaluer cinq ou six résidents appelés à répon-dre consécutivement à deux questions normalisées. Les résultats des résidents ont été cotés séparément pendant l'examen (Temps 1) puis, à partir d'un enregistrement vidéo (Temps 2). Les corrélations entre les scores des paires d'examinateurs et entre les scores de chaque examinateur ont été établies.Résultats : Les corrélations démontrant une concordance interexaminateurs au Site A sont 324 à 0,915 (moyenne de 0,506) au Temps 1. Au Temps 2, de 0,64 à 0,887 (moyenne de 0,791). Au Site B, elles sont de 0,279 à 0,989 (moyenne 0,707) au Temps 1,271 à 0,924 (moyenne de 0,477

INTRQDUCTION: Opiates are hypothesized to cause a vasodepressor effect by acting on the rostral vantrolateral medulla (RVLM) wherein lie neurons which control sympathetic tone. Using voltammetry which measures catecholamine oxidation currents (CA.OC) generated by adrenergic activity in these neurons, our objective was to demonstrate the in vivo effect of morphine on the RVLM. METHODS: Halothane anaesthetized rats were implanted stereotaxically with carbon-fibre electrodes to monitor CA-OC by differential normal pulse voltammetry. Mean arterial pressure (MAP) was monitored by a femoral arterial line. After stabilization, rats received either intracerebroventricular (icy) morphine 10/zg (n =5) followed 45 minutes later by intravenous (iv) naloxone 1 mg-kg" or icy saline 5/Jl (n=5) followed by iv saline 0.45 ml. Changes in MAP and CA. OC were compared to baseline. RESULTS: The CA-OC was maximally depressed by 39 percent 45 minutes following morphine (Fig 1). Naloxone reversed the effects of morphine and produced a significant 21 percent rebound increase in the CA.OC. MAP was maximally depressed by 21 percent 45 minutes following morphine (Fig 1). This decrease in MAP was reversed by naloxone. Saline treatment had no significant effect on the CA.OC (ANOVA, p=0.321) or MAP (ANOVA, p=.531). Fig 1 40 30 Change 20 from lO Baseline o (percent)-lO-20-3O-40 n CA'OC naloxone 9 MAP r (mean + SEM) 9 , , , Y '* ,p < 0.05; Dunnstt's 0 15 30 45 60 75 90 Time (rain) DISCUSSION: An increase in the CA.OC in the RVLM accompanies induced hypotension possibly by way of a baroreceptor reflex. However, our results suggest that morphine depresses adrenergic neurons in the RVLM to produce a vasodepressor effect. The rebound effect following the antagonism of morphine with iv naloxone is analogous to the observation of excessive sympathetic activity in post-operative patients receiving naloxone. This acute opiate withdrawal phenomenon is possibly mediated through the RVLM and if so, it may be prevented by attenuation of activity in this area. REFERENCES= i.