William A. Tweed

Tussive effect of a fentanyl bolus

The aim of this study was to investigate the incidence of pre-induction coughing, after an iv bolus of fentanyl. The study sample was 250 ASA physical status I-II patients, scheduled for various elective surgical procedures. The first 100 were randomly allocated to recieve 1.5 μg · kg−1 fentanyl via a peripheral venous cannula (Group 1), or an equivalent volume of saline (Group 2). Twenty-eight per cent of patients who received fentanyl, but none given saline, coughed within one minute (P < 0.0001). The second 150 patients were then randomly assigned to three equal pretreatment groups. Group 3 received 0.01 μg · kg-1 atropine iv one minute before fentanyl. Groups 4 and 5 received 0.2 μg · kg-1 morphine im, and 7.5 mg midazolam po, respectively, one hour before fentanyl. Thirty per cent of patients in Group 3, 6% in Group 4, and 40% in Group 5, had a cough response to fentanyl. Fentanyl, when given through a peripheral cannula, provoked cough in a considerable proportion of patients. This was not altéréd by prémédication with atropine or midazolam, but was reduced after morphine (P < 0.01). Coughing upon induction of anaesthesia is undesirable in some patients, and stimulation of cough by fentanyl in unpremedicated patients may be of clinical importance.RésuméLe but de cette étude était d’investiguer l’incidence de la toux pré-induction après bolus intraveineux de fentanyl. La population de l’étude était de 250 patients ASA I–II cédulés pour des procédures chirurgicales électives variées. Les premiers 100 patients furent randomisés afin de recevoir 1.5 μg · kg−1 de fentanyl à trovers une canule veineuse périphérique (Groupe 1), ou un volume équivalent de salin (Groupe 2). Vingthuit pour cent des patients y ont reçu du fentanyl mais aucun de ceux qui ont reçu du salin, ont toussé a l’intérieur d’une minute (P < 0,0001). Les 150 autres patients furent ensuite randomises en trois groupes égaux de prétraitement. Le groupe 3 a reçu 0,01 μg · kg−1 d’atropine iv une minute avant le fentanyl et le groupe 4 et 5 ont reçu 0,2 mg · kg−1 de morphine im et 7,5 mg de midazolam po, respectivement, une heure avant le fentanyl. Trente pour cent des patients dans le Groupe 3, 6% dans le Groupe 4, et 40% dans le Groupe 5, ont présenté de la toux lors de l’injéction du fentanyl. Le fentanyl, lorsqu’administré dans une canule périphérique, a provoqué de la toux chez un grand nombre de patients. Ceci ne fut pas altéré par la prémédication avec l’atropine ou le midazolam mais fut réduit après morphine (P < 0,01). La toux lors de l’induction de l’anesthésie n’est pas désirée chez certains patients, et la stimulation de la toux par le fentanyl chez des patients nonprémédiqués peut être d’une importance clinique.

Explosive coughing after bolus fentanyl injection.

R eflex coughing after a preinduction IV bolus of fentanyl was observed in controlled studies reported by Böhrer et al. (1) in 1990 and by Phua et al. (2) in 1991, though neither reported morbidity. Bailey et al. in Miller’s Fifth Edition of Anesthesia (3) state that “Curiously, fentanyl, sufentanil and alfentanil elicit a brief cough in up to 50% of patients when injected by IV bolus.” However, fentanyl-induced coughing may not always be brief and benign. We report a case of explosive, spasmodic coughing after peripheral IV injection of fentanyl that was severe enough to produce periorbital petechiae and was only relieved after induction of general anesthesia.

Effect of halothane on cardiac output and regional flow in the fetal lamb in utero.

: We studied the effect of halothane on the fetal cardiovascular system of six lambs in utero by measuring fetal heart rate and femoral arterial blood pressure and by injecting labeled microspheres during a control period and again after 60 and 90 min of halothane anesthesia administered to six pregnant ewes at an inspired concentration of 1.5%. There were no significant effects on maternal cardiovascular function or acid-base balance, but fetal blood pressure decreased significantly by 27% after 8 min of halothane anesthesia and remained at this level for the duration of the experiment. However, there were no significant changes either in fetal regional blood flow to the vital organs or in fetal cardiac output. Fetal oxygenation and acid-base status remained stable. We conclude that in normal fetal lamb in utero the decrease in mean fetal arterial blood pressure associated with maternal halothane anesthesia is due to a decrease in peripheral vascular resistance because regional blood flow and acid-base status are well maintained.

Preservation of fetal brain blood flow relative to other organs during hypovolemic hypotension.

Summary: The asphyxiated newborn is particularly vulnerable to hypotension, which contributes to hypoxic brain damage by reducing cerebral perfusion. During asphyxia, cerebral blood flow (CBF) is pressure passive, that is, CBF autoregulation is abolished. It is important to know if the nonasphyxiated fetus and newborn are similarly vulnerable to hypotension. In the present study, we have measured acute responses of organ blood flow to a hypovolemic/hypotensive stress in the normoxic near term sheep fetus. Changes in brain flow were compared to changes in other organs.Eight chronically prepared fetal lambs were studied. Organ blood flows were measured by the microsphere technique during a control period, after a 20% blood volume reduction, and again after reinfusion of that volume.Hypovolemia was accompanied by a 21% decrease in blood pressure and a 4 torr increase in Pco2; after reinfusion blood pressure increased 16% above control. Control measurements of organ perfusion were similar to those reported by other investigators. Cardiac output and flow to all organs, with the exception of the brain, were reduced 30–56% during hypovolemia. Brain blood flow was insignificantly reduced by 9%. If a correction is applied for the increase in Pco2, CBF corrected to control Pco2 would have been significantly reduced by 18%. After reinfusion, flow to all organs increased to near control levels.We conclude that the normoxic fetal lamb shows evidence of CBF autoregulation, and is able to preserve relative constancy of CBF within a blood pressure range of ± 20% of normal. However, the evidence presented in this study suggests that autoregulation may be less effective in response to a hypotensive stress, even though CBF is better preserved than flow to most other organs.Speculation: The brain of the lamb is more mature than that of the human at to changing blood pressure was of particular interest. birth. Although the normoxic fetal lamb shows evidence of cerebral blood flow autoregulation, these studies suggest that even unde normal physiologic conditions in utero, the fetal brain may not be fully protected against acute hypotension. This may be because the normal fetal blood pressure is close to the lower limit of autoregulation. Previous work by ourselves and others has also demonstrated the vulnerability of autoregulation to hypercapnea, hypoxia, and acidosis. Since these are common manifestations of fetal and newborn asphyxia, and even to some extent of the normal birth process, it is reasonable to speculate that autoregulation is generally impaired when there is fetal or newborn distress. There- fore, cerebral blood flow of even the nonasphyxiated neonate may be vulnerable to marked deviations of blood pressure.

Hydroxylation and glucuronidation of various xenobiotics by hepatic microsomes from the fetal lamb, pregnant ewe and human fetus.

The ability of microsomes isolated from liver of pregnant ewes and their fetuses at near term to catalyze the biotransformation of benzo[a]pyrene, hexobarbital, meperidine, methadone and morphine was investigated. Cytochromes P-450 and b5, NADPH and NADH cytochrome c reductase, methadone and meperidine N-demethylase and morphine glucuronyltransferase activities were detected in microsomes from both maternal and fetal livers. Fetal hepatic microsomes however, lacked the ability to catalyze the hydroxylation of hexobarbital and benzo[a]pyrene.

Oxygen consumption and carbon dioxide elimination after release of unilateral lower limb pneumatic tourniquets

Oxygen consumption (&OV0312;o2, carbon dioxide elimination (&OV0312;co2, and respiratory exchange ratio (RQ) were continuously measured in 15 male and 15 female adults during knee surgery, with the leg exsanguinated by an inflatable tourniquet around the thigh. Arterial blood was also intermittently sampled for blood gas analysis, electrolytes, and lactate content before and after tourniquet deflation. There was a significant increase in &OV0312;o2 and &OV0312;co2 after tourniquet deflation, which was more pronounced in the male (aged 29.5 ± 14.8 yr, mean ± SD) than the female (aged 56.9 ± 15.6 yr) patients, both in terms of maximal increase (P < 0.001) and percent of increase from values before deflation (P < 0.001 and P = 0.01). The body weights and tourniquet inflation times were not significantly different between the male and female patients. Excess &OV0312;o2 (O2 debt) and excess &OV0312;co2 over 12 min after deflation of the tourniquet were also significantly higher for male (593.5 ± 222.9 mL and 714.9 ± 463.8 mL, respectively) than for female patients (302 ± 73.3 mL and 196 ± 162.22 mL, respectively; P < 0.01). There was no correlation between the duration of tourniquet inflation time and peak increase in &OV0312;o2, peak increase in &OV0312;co2, and O2 debt over 12 min after deflation of the tourniquet; however, tourniquet time was weakly correlated with excess &OV0312;co2 over 12 min after tourniquet deflation (r = 0.55, P = 0.002). There was a significant decrease in pHa (P < 0.001) from release of Paco2 and lactate after tourniquet deflation. Plasma potassium levels also increased significantly after tourniquet release (P < 0.01). All of these biochemical changes did not cause any adverse effects in the study patients. In view of the predictable increase in &OV0312;o2 and &OV0312;co2, we recommend monitoring of end-tidal CO2 and a transient increase in minute ventilation to maintain normocapnea.

The effect of halothane anaesthesia on the asphyxiated foetal lambin utero

In a previous study, we examined the effects of halothane on the normal foetal lamb in utero. The most significant finding was a 33 per cent fall infoeial mean arterial blood pressure (MABP). Cardiac output and placental blood flow were not affected. To determine if the asphyxiated foetus would respond similarly, the following study was performed. Seven pregnant ewes were surgically prepared two days prior to study with maternal and foetal indwelling arterial and venous cannulas. An inflatable occlusion loop was secured around the umbilical cord.On the day of study, a tracheostomy was performed on each ewe. Microspheres were injected into the foetal circulation during the control period. The occlusion loop was inflated to produce foetal asphyxia and microspheres were again injected. The ewe was then anesthetized with halothane; and after 15 minutes, microspheres were injected into the asphyxiated foetus and halothane levels were measured.The asphyxiated foetuses showed a significant rise in MABP, fall in heart rate and fail in cardiac output from control. Blood flow to the brain was significantly increased and flow to the placenta and gut decreased. Exposure of the asphyxiated foetus to haiothane resulted in a fall of MABP to control but no significant change in cardiac output or brain blood flow. The mean haltithane level in the foetus was 46.0 mg.l-1 or 0.32 vol%. Exposure of the asphyxiated foetus to halothane for 15 minutes does not produce significant further deterioration of the foetal lamb in utero.RésuméLors d’une étude antérieure, les auteurs avaient étudié les effets de l’halothane sur le fœtus de brebis in utero. La constatation la plus significative a été une chute de 33 pour cent de la pression artérielle moyenne. Le débit cardiaque et le débit placentaire n’ont pas été affectés. Pour déterminer si le fœtus asphyxié répondrait de façon similaire, l’étude suivante a été réalisée. Sept brebis gravides ont subi une préparation chirurgicale comprenant l’insertion de sondes maternelles et fœtales à demeure tant du côté artériel que veineux. Un lacet insufflable a été installé autour du cordon ombilical.Le jour de l’étude on a trachéotomisé chacune des brebis. On a ensuite injecté des microsphères dans la circulation fœtale pendant la période de contrôle. Le lacet fut insufflé pour produire l’asphyxie fœtale et des microsphères ont été réinjectées. La brebis fut ensuite anesthésiée à l’haiothane; après 15 minutes, on a injecté de nouveau des microsphères dans la circulation du fœtus asphyxié et on a mesuré la concentration de i’halothane dans le sang.Les fœtus asphyxiés ont montré une élévation significative de la pression artérielle majeure, une chute de la fréquence et du débit cardiaque comparativement aux contrôles. Le débit sanguin cérébral a été augmenté de façon significative et les débits sanguins placentaire et intestinal diminués. L’exposition à l’haiothane des fœtus asphyxiés a causé une baisse de la pression artérielle moyenne comparativement aux contrôles mais pas de changement significatif du débit cardiaque et du débit cérébral. La concentration sanguine de l’haiothane dans le fœtus a été de 46.0 mg.l-1 ou 0.32 vol. pour cent.L’exposition du fœtus en étal d’asphyxie pendant 15 minutes ne produit pas de façon significative une détérioration plus marquée du fœtus de la brebis in utero.

PRE-HOSPITAL ANALGESIA WITH ENTONOX

Pre-hospital self-administered analgesia using a 50:50 mixture of nitrous oxide and oxygen (Entonox) was evaluated in 240 patients. Of these, 93.4 per cent experienced either complete or partial relief from traumatic, chest, abdominal or back pain. Drowsiness was the most common side effect noted. No complications occurred during delivery of the mixture. Attention is drawn to the effect of extreme temperatures on the Entonox mixture and recommendations are made with respect to its use in below-freezing climates. Because of its ease of use and short duration of action, Entonox appears to be well suited for the treatment of pre-hospital pain by Emergency Medical Technicians.RésuméL’analgésie procurée par un mélange égal de protoxyde d’azote et d’oxygène (Entonox) a été évaluée en auto-administration sur 240 patients. Parmi ceux-ci, 93.4 pour cent ont été complètement ou partiellement soulagés d’une douleur d’origine traumatique située au thorax, à l’abdomen ou au dos. La somnolence a été l’effet secondaire le plus fréquent. Il n’y a eu aucune complication lors de l’administration du mélange. Les effets des températures excessives sur le mélagne Entonox sont décrits et des recommandations pour son utilisation dans les climats où la température descend sous le point de congélation. Etant donné sa grande facilité d’emploi et sa courte durée d’action, l’Entonox nous semble un bon analgésique qui a l’avantage de pouvoir être utilisé par des paramédicaux à la période qui précède l’hospitalisation.

The experiential curriculum: an alternate model for anaesthesia education

The shift to direct entry into residency training from medical school for all graduates will offer new challenges for anaesthesia training programmes. In this paper we argue that it also offers us an opportunity to re-evaluate our current approach to anaesthesia education. Emphasis in the residency programmes should be to provide trainees with clinical experiences and stimulation that will develop the required traditional competencies. It should also cultivate competency in clinical decision-making, intuition and judgement. Our purpose is to generate discussion by proposing an alternate curriculum model, the experiential curriculum. The basic premise is that learning is a process and outcome is to a large extent related to what the learner does. The process begins with an experience that provides for observation and reflection. Integration of the thoughts provides the basis for executing either existing or new actions. In the experiential curriculum residency training and learning are enhanced by documenting and critically evaluating the experiences to which the resident is exposed. Included within such a structured programme are the methodologies of problem-based and evidence-based learning. Faculty development will be required to help the resident pursue these skills of self-evaluation and efficient learning. We believe that incorporation of an experiential curriculum into the residency training programme will achieve the goals listed above and allow maturation of the process of lifelong learning. It will also allow greater achievement of the application of new information to one’s practice.RésuméL’évolution de la formation vers l’accès direct à la résidence à partir de l’école de médecine pour tous les diplômés représente une nouveau défi pour les programmes d’enseignement de l’anesthésie. Cet article nous offre l’opportunité de réévaluer notre attitude actuelle vis-à-vis la formation en anesthésie. Les programmes d’anesthésie doivent fournir à leurs étudiants en formation des expériences cliniques et les stimuler dans le but de les faire assimiler les compétences traditionnelles. Ils devraient aussi se former à prendre les décisions cliniques appropriées et à acquérir de l’intuition et du jugement. Notre objectif est de susciter la discussion en proposant un modèle de curriculum de rechange, le curriculum expérientiel. La prémisse initiale consiste en ce que l’éducation est un processus et que ses résultats dépendent largement de l’apprentissage. Le processus débute avec une expérience qui fournit observation et réflexion. L’intégration des idées constitue la base de l’exécution d’actions existantes ou nouvelles. Dans le curriculum expérientiel pour la résidence en l’anesthésie, la formation et l’acquisition de connaissances sont consolidées par la documentation et l’évaluation critique des expériences auxquelles le résident est exposé. Les méthodes d’enseignement basées sur l’étude de problèmes et sur la démonstration sont comprises dans ce genre de programme. Le corps enseignant doit évoluer et permettre au résident de poursuivre ces aptitude d’autocritique et d’apprentissage. Nous croyons que l’incorporation du curriculum expérientiel au programme de formation du résident atteindra les objectifs décrits plus haut et permettra la maturation du processus perpétuel de l’acquisition des connaissances. Elle permettra de plus réaliser plus facilement l’application de nouvelles connaissance à sa pratique.

Fresh gas flow and carbon dioxide rebreathing in a low pressure semi-open anaesthesia system.

We have constructed a simple system for field anaesthesia by using a Farman entrainer and a semi-open circuit to convert a draw-over apparatus to a continuous flow air/O2 system. Compressed O2 was the driving gas for the entrainer; fresh gas (FG) delivered to the semi-open circuit was a mixture of O2, entrained air and anaesthetic vapour. The purpose of this study was to examine FG flow rate and CO2 rebreathing during intermittent positive pressure ventilation (IPPV). A nonrebreathing inflation valve (Laerdal) placed at the end of the expiratory (efferent) limb of the circuit vented both expiratory gas and excess FG. Ambient air IPPV was applied through the Laerdal valve from a self-inflating bag or ventilator. Since this circuit is functionally similar to a T-piece, the gas from the efferent limb (340 ml, containing FG) entered the lungs first. If tidal volume was larger than 340 ml the balance was ambient air. Minute ventilation of the lungs with efferent limb gas was defined as Veff. Respiratory gas was sampled at the endotracheal tube and the CO2 tension was measured with a NIHON-KOHDEN CO2 analyzer. Thirty-seven adult patients having intra-abdominal or pelvic surgery under general tracheal anaesthesia were studied. Four FG flow rates (5.7, 8.0, 9.3, and 10.4 L · mm−1), corresponding to driving gas pressures of 40, 60, 80, and 100 mmHg, were introduced in random order. Although inspired CO2 was detected at FG flow rates of 5.7–9.3 L · min−1, there were no differences inPetCO2 among the four groups. We conclude that clinically important rebreathing does not occur when VFG is 1.67 times Veff For general use we recommend a VFG of more than twice the Veff which for this circuit configuration would be about 8 L · min−1. This requires a minimum O2 flow of 1.6 L · min−1 or driving gas pressure of 60 mmHg.RésuméNous avons fabriqué un appareil de campagne pour l’anesthésie avec un entraîneur Farman et un circuit semi-ouvert pour convertir un appareil à débit intermittent en débit continu air/ O2. De l’O2 comprimé constitue la force motrice de l’appareil. Le gaz frais (GF) délivré à l’appareil consiste en un mélange d’O2, d’air entraîné et de vapeur anesthésique. L’objectif de l’étude consiste à déterminer le débit de GF et l’importance du rebreathing pendant la ventilation mécanique. Une valve sans rebreathing (Laerdal) installée à l’extrémité du circuit élimine les gaz expiratoires et l’excédent de gaz frais. A la valve de Laerdal, la ventilation mécanique fonctionne à l’air ambiant mû par un ballon réservoir auto-insufflé ou un ventilateur. Le circuit fonctionne comme une pièce en T et le gaz de la branche expiratoire (tube réservoir contenant 340 ml de gaz frais) pénètre d’abord dans le poumon. Si le volume courant est plus grand que 340 ml, le reste est constitué d’air ambiant. La ventilation-minute par la branche expiratoire est appelée Veff. Les gaz respiratoires sont prélevés au niveau du tube endotrachéal et la pression partielle du CO2 est mesurée par un analyseur Nihon-Kohden. Trente-sept adultes soumis à une chirurgie viscérale ou pelvienne sous anesthésie générale endotrachéale sont étudiés. Quatre débits de G F (5,7, 8,0, 9,3, et 10,4 L · min−1) correspondant à une pression motrice de 40, 60, 80 et 100 mmHg, sont introduits de façon aléatoire. Bien qu’on puisse détecter du CO2 à des débits de GF de 5,7 à 9,3 L · min−1, on ne trouve pas de différence dePetCO2 entre les quatre groupes. Nous concluons qu’il n’existe pas de rebreathing cliniquement important avec des GF de 1,67 fois le volume courant. Pour usage général, nous recommandons un VGF doubles du Veff qui avec la configuration du circuit équivaut à environ 8 L · min−1. Ceci requiert un débit minimum d’O2 de 1,6 L · min−1 ou une pression motrice de 60 mmHg.