J. Earl Wynands

Blood pressure response and plasma fentanyl concentrations during high- and very high-dose fentanyl anesthesia for coronary artery surgery.

We examined whether different plasma fentanyl concentrations could maintain hemodynamic stability during coronary artery surgery. Two randomly selected groups of 10 patients were studied. Patients in group 1 received a single 75-μg/kg intravenous dose of fentanyl; patients in group 2 received the same dose but it was followed by an infusion of fentanyl at a rate of 0.75 μg/kg/min. The total dose of fentanyl in group 2 was 162 ± 6.5 μg/kg (mean ± SEM). At some point during surgery, all 10 patients in group 1 and 7 of 10 patients in group 2 had a hypertensive response. Plasma fentanyl concentrations in the two groups were not significantly different in the period 10–45 min after induction of anesthesia. At 60 min, corresponding to the time of aortic root dissection, mean plasma fentanyl concentration was statistically significantly lower in group 1 than in group 2 (13.5 ± 1.4 ng/ml and 24 ± 2.3 ng/ml, respectively, P < 0.01). However, no significant difference was observed in the frequency of hypertensive response between the two groups in the period before cardiopulmonary bypass. During cardiopulmonary bypass, plasma fentanyl concentrations in group 1 were 2–3 times lower than those in group 2, and hypertension was observed in all 10 patients in group 1 but in only 2 patients in group 2 (P < 0.05). Patients in group 1 were ventilated for 16.6 ± 1.5 h, and those in group 2 for 19.1 ± 1.8 h, postoperatively (P > 0.05). Six patients in group 1 required vasodilating drugs, whereas eight patients in group 2 required alpha-adrenergic agonists. Although the plasma fentanyl concentrations achieved were not successful in totally suppressing a hypertensive response, this study suggests that a plasma fentanyl concentration might be attainable to effect this.

Amrinone and dobutamine as primary treatment of low cardiac output syndrome following coronary artery surgery: A comparison of their effects on hemodynamics and outcome

This study was undertaken in order to compare the effectiveness of amrinone and dobutamine as primary treatment of a low cardiac output (CO) after coronary artery bypass graft (CABG) surgery. Thirty patients with preoperative left ventricular dysfunction participated in this open-label randomized study. Patients were included if they failed to separate from cardiopulmonary bypass (CPB) without inotropic support or if they had a cardiac index (CI) less than 2.4 L/min/m2 after CPB regardless of the blood pressure, in the presence of adequate filling pressures. The treatment objectives were to separate from CPB and achieve a CI > or = 2.4 L/min/m2 and a mean arterial pressure > or = 70 mmHg. Patients treated with amrinone received 0.75 mg/kg followed by 10 micrograms/kg/min; when the objectives were not achieved within five minutes, another 0.75 mg/kg was given. Patients treated with dobutamine received an initial infusion of 5 micrograms/kg/min increased stepwise to 15 micrograms/kg/min if necessary. Eleven of 15 amrinone versus 6 of 15 dobutamine patients achieved the predefined treatment objectives with the test drug alone (P = NS). Comparisons of hemodynamics in patients treated solely with amrinone (n = 7) or dobutamine (n = 6) after CPB showed no significant differences between the treatment groups. The incidence of myocardial ischemia as detected by Holter monitor was 36% with amrinone and 33% with dobutamine. Two patients suffered ventricular fibrillation and two had significant supraventricular tachyarrhythmias (heart rate > 130/min) during treatment with dobutamine alone, whereas no significant arrhythmias occurred in the amrinone group (P = NS). Six dobutamine patients (40%) had postoperative myocardial infarction (MI) as opposed to none among the amrinone patients (P = 0.017). These results indicate that amrinone compares favorably with dobutamine as a primary treatment of low CO after CABG. Further study in a larger number of patients will be required in order to determine if the lower incidence of MI in the amrinone group was due to the treatment drug.

Catheter-induced pulmonary artery false aneurysm and rupture: Case report and review

REAS MANY believe that information derived from the pulmonary artery catheter (PAC) is crucial for the diagnosis and quantification of cardiovascular dysfunction, there are those who think it contributes to morbidity and mortality.lJ Persons performing pulmonary artery (PA) catheterization must therefore be cognizant of iatrogenic problems related to the catheter in order to avoid preventable adverse outcomes.3 The most feared complication is perforation of the PA, which is estimated to occur in 0.06% to 0.2% of cases but which carries a mortality rate of 45% to 65%.4,5 Delayed hemorrhage resulting from rupture of catheter-induced pulmonary artery false aneurysms (PAPAs) has been described but reported to be rare.6 A Medline search of virtually all cases reported in the English literature through August 1992 indicates that the high morbidity and mortality associated with this delayed complication have not been fully appreciated. A case is reported of catheter-induced PAPA and rupture and the current knowledge of this complication is reviewed.

Fentanyl Infusion Anesthesia for Aortocoronary Bypass Surgery: Plasma Levels and Hemodynamic Response

Plasma fentanyl concentrations were measured by radioimmunoassay in patients during aortocoronary bypass surgery and correlated with hemodynamic responses to surgical stimulation. Thirty patients scheduled for aortocoronary bypass surgery were divided into three groups of 10. Patients in group 1 received fentanyl, 30 μg/kg, as a loading dose followed by an infusion of 0.3 μg/kg/min; those in group 2 received 40 μg/kg as a loading dose followed by an infusion of 0.4 μg/kg/min; and those in group 3 received 50 mg/kg as the loading dose followed by an infusion of 0.5 μg/kg/min. The total dose of fentanyl administered to each group up to the time of rewarming on cardiopulmonary bypass was 60 jug/kg, 90 μg/kg, and 100 μg/kg, respectively. Each of the dose regimens produced stable plasma concentrations starting approximately 20 minutes after induction and continuing until the infusion was discontinued. Patients in group 1 had a mean plasma concentration of 10 to 12 ng/ml in the stable period compared with 12 to 14 ng/ml in group 2 and 15 to 18 ng/ml in group 3. Fewer patients in group 3 responded to intubation and surgical stimulation than in the other groups, although the differences between groups were not statistically significant. Response to stimulation was treated by the administration of droperidol or volatile anesthetic agents. At a plasma concentration of 15 ng/ml, 50% of patients had an increase in systolic blood pressure which required treatment. This minimal intra-arterial concentration, analogous to MAC, can be achieved by the administration of fentanyl as a loading dose of 50 μg/kg followed by an infusion of 0.5 μg/kg/min.

Effect of heated humidified gases on temperature drop after cardiopulmonary bypass.

In an attempt to prevent the decrease in nasopharyngeal temperature (NPT) (“afterdrop”) after cardiac surgery, 30 patients undergoing hypothermic cardiopulmonary bypass (CPB) were randomly assigned to receive humidified heated inspired gases at 45°C at the proximal end of the endotracheal tube (group I) or dry gases at room temperature (group II), from the time of termination of CPB. All patients received high flow rates on CPB during the rewarming period with the use of vasodilator drugs when necessary. Both groups were comparable with respect to total bypass time, rewarming time, and temperature at termination of CPB. In addition, the NPT was compared with the tympanic membrane temperature (TMT) in group I to assess the validity of the NPT under these conditions. The results indicate that heating and humidifying inspired gases do not prevent afterdrop and do not falsely increase the nasopharyngeal temperature. The reasons for the ineffectiveness of heated humidified gases may include a large heat deficit at termination of CPB despite a normal NPT, and the very small heat content of heated gases. Monitoring the temperature of a site that reflects the heat deficit, and a more complete rewarming during CPB are suggested as a better approach to the prevention of afterdrop.

The Management of Temperature During Cardiopulmonary Bypass: Effect on Neuropsychological Outcome

Laboratory studies demonstrate that mild degrees of brain cooling (2°C to 5°C) confer substantial protection from ischemic brain injury, and that mild elevation of brain temperature can be markedly deleterious. During hypothermic cardiopulmonary bypass (CPB) patients are made hypothermic and then rewarmed at a time when they are exposed to neurological insults. Our studies show that during rewarming, peak brain temperatures near 39°C often are achieved inadvertently. We hypothesize that maintaining brain temperature ≤ 34°C during and after CPB will reduce the incidence of postoperative neuropsychological deficits. We present safety data from a study of 30 patients assigned either to conventional hypothermic CPB with rewarming or a protocol where brain temperature is raised only to 34°C at the time of separation from CPB. There was no difference in bleeding, cardiac morbidity, or time to extubation between groups. We designed a neuropsychological test battery to detect postoperative neuropsychological deficits and tested its usefulness in a preliminary sample of 15 patients undergoing hypothermic CPB. We found patient acceptability and compliance were good. Sensitivity also seemed adequate in that 30% of patients were identified as having deteriorated at 1 week postoperatively compared to preoperatively, a result similar to that reported by others. Clinical trials of the efficacy of mild hypothermia in modulating brain injury in humans are needed before techniques of CPB can be designed to optimize neuroprotection.

Amrinone: Is it the inotrope of choice?

In the treatment of acute heart failure, conventional therapy with epinephrine, norepinephrine, dopamine, and dobutamine may be used effectively to treat inotropic abnormalities. However, the addition of a vasodilator to catecholamine therapy may be needed to help improve lusitropic function. Because it seems to exert positive inotropic and lusitropic effects, the phosphodiesterase inhibitor amrinone may be a valuable addition to the anesthesiologists armamentarium for the treatment of acute heart failure. When used as adjunctive therapy with catecholamines, amrinone has been shown to exert a significant additive and synergistic effect. Amrinone may also be the inotrope of choice in patients who are refractory to therapy with conventional inotropes, due to its positive inotropic and lusitropic effects, combined with its vasodilating effects. Because of its broad pharmacodynamic spectrum, amrinone may effectively control all of the major elements involved in myocardial performance--preload, afterload, contractility, and heart rate.

Profound hypoxemia during treatment of low cardiac output after cardiopulmonary bypass.

PurposeTo illustrate the multiple causes of hypoxemia to be considered following cardiopulmonary bypass and how therapy given to improve oxygen delivery may have contributed to a decrease in arterial oxygen saturation to life-threatening levels.Clinical featuresA 61 yr old man with severe mitral regurgitation and chronic obstructive lung disease underwent surgery for mitral valve repair. A pulmonary artery catheter with the capacity to measure cardiac output and mixed venous oxygen saturation (SvO2) continuously was used. Two unsuccessful attempts were made to repair the valve which was finally replaced, requiring cardiopulmonary bypass of 3 17 min. Dobutamine 5 μg·kg−1·min−1 and sodium nitroprusside I μg·kg−1·min−1 were used to increase cardiac output. Soon after, the SvO2 decreased progressively from 55 to 39%. The patient became cyanotic with a RaO2 of 39 mmHg. Sodium nitroprusside was stopped and amrinone 100 mg bolus followed by 10 μg·kg−1·min−1 was given in addition to adding PEEP to the ventilation. With these measures PaO2 could be maintained at safe levels but PEEP and high inspired oxygen concentrations were needed postoperatively until the trachea could be extubated on the third postoperative day.ConclusionThe profound hypoxemia in this case was likely due to a combination of intra-and extrapulmonary shunt, both augmented by sodium nitroprusside. The desaturation of mixed venous blood amplified the effect of these shunts in decreasing arterial oxygen saturation. The interaction of these factors are analyzed in this report.RésuméObjectifIllustrer les multiples causes de l’hypoxémie dont il faut tenir compte après une circulation extracorporelle et montrer comment la thérapie qui vise à améliorer la livraison d’oxygène peut avoir contribué à baisser la saturation artérielle en oxygène à des niveaux dangereux.Aspects cliniquesUn homme de 61 ans souffrant de régurgitation mitrale sévère et de bronchopneumopathie chronique obstructive devait subir une chirurgie réparatrice de la valvule mitrale. On a utilisé une sonde artérielle pulmonaire, ayant la capacité de mesurer de façon continue le débit cardiaque et la saturation en oxygène du sang veineux mêlé (SvO2). La réparation ayant été tentée deux fois sans succès, on a finalement remplacé la valve, ce qui a nécessité 317 min de circulation extracorporelle. Pour augmenter le débit cardiaque, on a administré 5 μg·kg−1min−1 de dobutamine et I μg·kg−1min−1 de nitroprussiate de sodium. Peu après, la SvO2 a diminué progressivement de 55 à 39%. Le patient est devenu cyanosé et présentait une PaO2 de 39 mmHg. Le nitroprussiate de sodium a été stoppé et on a administré un bolus de 100 mg d’amrinone suivi de 10 μg·kg−1min−1 en plus de l’addition d’une PEP à la ventilation. Ces interventions ont permis de maintenir la PaO2 à des niveaux de sécurité, mais la PEP et de fortes concentrations d’oxygène inspiré ont été nécessaires après la chirurgie jusqu’à ce que l’extubation de la trachée soit possible le troisième jour postopératoire.ConclusionDans ce cas, l’importante hypoxémie était probablement causée par une combinaison de shunts intra et extrapulmonaire qui ont été accentués par le nitroprussiate de sodium. La désaturation du sang veineux mêlé a amplifié l’effet de ces shunts en diminuant la saturation artérielle en oxygène. L’interaction de ces facteurs est analysée dans l’article qui suit.

Simulation-based education in Canada: will anesthesia lead in the future?

It is remarkable that 40 years have elapsed since Denson and Abrahamson first introduced high fidelity simulation (Sim One) to facilitate the teaching of endotracheal intubation and the induction of anesthesia. The concept of utilizing a simulator for clinical training was far ahead of its time and not immediately embraced by anesthesiologists or other educators. Simulation technology for medical education underwent a revival in the mid-1980s when computer-generated screen based simulation programs made their appearance, focusing primarily on pharmacology and physiology applications relevant to anesthesia. The anesthesiologist could choose one of many scenarios that might be encountered by a clinical anesthesiologist. These programs allowed the learner to interpret information and make pharmacological and therapeutic decisions. Such simulators were novel and afforded a meaningful learning experience, especially for novice learners; however, they did not duplicate the application of practical skills and knowledge in a clinical environment in real time. In 1986, Gaba et al. at Stanford University developed a full-scale, high fidelity simulator (‘‘The Comprehensive Anesthesia Simulation Environment [CASE]’’) which allowed the anesthesiologist to manage critical situations. With Jeff Cooper in Boston, they developed an organized program called ‘‘Anesthesia Crisis Resource Management’’ (ACRM), applying principles from the airline industry where pilots and airline crew use ‘‘Crew Resource Management’’ programs to elicit human responses in a realistic environment. The objective of ACRM is to teach participants the importance of non-technical skills such as team working, task management, decision-making and situation awareness, focusing on communication and leadership skills. In the late 90s, several simulation centres appeared in Canada, led by anesthesiologists, to allow learners to practice difficult and rare scenarios without placing patients at risk. Today, simulation centres have been developed in over 50 centres across Canada, including many community colleges, in addition to hospitals and universities. In spite of the exponential growth of simulation, many professions and disciplines have been slow to recognize that simulationbased education is more than a teaching tool—it is a novel form of ‘‘experiential education’’, with which non-technical skills required in professional practice can be learned. Educators know that these are difficult (if not impossible) to teach in the clinical environment. Most Canadian academic departments of anesthesia have been progressive in integrating simulation into the undergraduate and/or postgraduate curricula. Undergraduate medical students who are given time in an anesthesia simulator, enthusiastically compete with each other to manage the airway, and pharmacologically treat simple hemodynamic problems. It is often their first opportunity to independently treat a ‘‘patient problem’’ and the majority find it very enjoyable and a great learning experience. At the postgraduate level, simulators are used to teach firstyear residents how to ‘‘troubleshoot’’ the anesthesia gas machine through clinically relevant scenarios, and manage common intraoperative anesthetic problems. Postgraduate years 2–5 often spend at least two, three-hour sessions each year in the simulation center. They usually share this experience in a small group and are usually not in the same R. J. Byrick, MD (&) V. N. Naik, MD Department of Anesthesia, St. Michael’s Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada e-mail: robert.byrick@utoronto.ca

Clinical application of cardiac risk indices: How to avoid misleading numbers

Perioperative cardiac complications are associated with a high mortality rate. During the preoperative assessment the anaesthetist must determine if the patient is at risk so that appropriate interventions can be made to ensure the best possible outcome. Over the past three decades several indices have been proposed to identify the surgical patient at risk of cardiac morbidity or mortality. These indices can be thought of as diagnostic tests which determine the likelihood of perioperative cardiac complication. In this article the authors review the epidemiological basis of diagnostic tests and apply this theory to three currently available indices of perioperative risk: the American Society of Anesthesiologists physical status classification, the Goldman multifactorial cardiac, risk index and a modified version devised by Detsky. A case history describing a surgical patient with unstable angina is first presented to show how different indices can lead to different predictions. These indices are then analysed as if they were diagnostic tests to predict cardiac complications after surgery. The characteristics of diagnostic tests such as sensitivity, specificity, positive and negative predictive values, and receiver operating characteristic curves are described and applied to the indices. Basic principles such as odds ratio, likelihood ratio and their relation to prevalence and post-test probability are also presented. This overview will help the anaesthetist to understand the limitations of risk indices as predictors of adverse cardiac outcome and to apply these scales more effectively to individual patients at different institutions.RésuméLes complications cardiaques durant la période périopératoire sont associées à une mortalité élevée. Au cours de l’évaluation préopératoire, l’anesthésiste doit déterminer les risques d’un patient afin de pouvoir prendre les mesures qui favoriseront la meilleure évolution possible après la chirurgie. Plusieurs échelles d’évaluation de risque cardiaque ont été proposées afin d’améliorer la prédiction de la morbidité et de la mortalité périopératoires. Ces échelles peuvent être considérées comme des tests diagnostiques déterminant la probabilité de complications cardiaques. Dans cet article, les auteurs présentent les principes épidémiologiques essentiels à la compréhension et l’utilisation de tout test diagnostique et ils appliquent ces concepts à trois échelles d’évaluation de risque périopératoire: la classification de l’ état physique telle que définie par la Société Américaine des Anesthésistes, l’échelle multifactorielle de risque cardiaque décrite par Goldman ainsi que sa version modifiée proposée par Detsky. Une histoire de cas décrivant un patient chirurgical avec angine instable est d’abord présentée afin de démontrer comment différentes échelles donnent des prédictions différentes. Ces échelles sont par la suite analysées comme si elles étaient des tests diagnostiques de prédiction de complications cardiaques périopératoires. Certaines notions propres aux tests diagnostiques telles la sensibilité, la spécificité, la valeur prédictive positive et négative, ainsi que les courbes de rapport vrai positifs sur faux positif sont décrites et appliquées à ces échelles. Les principes de base des rapports de probabilité et leur relation avec la prévalence et la prédiction d’un test sont aussi présentées. Cette révision permettra à l’anesthésiste de mieux comprendre les limites des échelles d’évaluation du risque de complications cardiaques et l’aidera dans l’application clinique de ces échelles.