Fiona E. Ralley

The effects of shivering on oxygen consumption and carbon dioxide production in patients rewarming from hypothermic cardiopulmonary bypass.

Oxygen consumption (VO2), carbon dioxide production (VCO2), end-tidal carbon dioxide partial pressure (PETCO2), mixed venous oxygen saturation (SvO2) and haemodynamic variables were recorded every 30 min for four hours in 15 patients recovering from hypothermic cardiopulmonary bypass (CPB). All patients had been anaesthetised with fentanyl 40 μg · kg-1, supplemented with isoflurane, and pancuronium 0.15 mg · kg-1 for muscle relaxation. Three of the 15 patients (20 per cent) shivered, defined as intermittent or continuous, vigorous movements of chest or limb muscles. Patients who shivered had a VO2 of 159 ±16.4 ml·min-1 ·m-2 on arrival in the ICU which rose to a maximum value of 254 ± 28.3 ml·min-1·m-2 by 150 min post-CPB. in contrast, patients who did not shiver had a significantly lower VO2 of 93.1 ± 6.9 ml·min-1 ·m-2 on arrival in the ICU which rose to a maximal value of only 168 ± 11.5 ml·min-1·m-2 by 180 min post-CPB. Maximal VO2 in both groups was reached when the nasopharyngeal temperature (NPT) was approaching normal. VCO2 paralleled the increase in VO2 in both groups. By four hours there was no significant difference between the two groups; however, the VO2 in both groupsRésuméLa consommation ďoxygène (VO2), la production de CO2 (VC02), la PCO2 en fin ďexpiration (PetCO2), la saturation ďoxygène du sang veineux mixte (SvO2) et les données hémodynamiques ont été enregistrées chaque 30 min pour quatre heures chez 15 patients ayant subi une CEC hypothermique (CPB). Tous les patients ont été anesthésiés avec du fentanyl 40 μg · kg-1 supplémenté ďisoflurane et de pancuronium 0.15 mg · kg-1 pour le reláchement musculaire. Trois des 15 patients (20 pour cent) ont présenté des frissons, définis comme étant des mouvements vigoureux intermittents ou continus des muscles thoraciques ou des muscles périphériques. Les patients ayant présenté des frissons avaient une VO2 de 159 ± 16.4 ml· min-1 · m-2 à ľarrivée aux soins intensifs augmentant à une valeur maximale de 254 ± 28.3 ml · min-1 · m-2 après 150 min de ľarrêt de la CEC. Par contre, les patients n’ayant pas présenté des frissons avaient des valeurs de VO2 significativement plus basses de 93.1 ± 6.9 ml· min-1 · m-2 à ľarrivée aux soins intensifs augmentant à une valeur maximale de 168 ± 11.5 ml· min-1 · m-2 180 min, après ľarrêt de la CEC. La valeur maximale de la VO2 dans les deux groupes était atteinte quand la température nasopnaryngée (NPT) s’est approchée de la normale. Les valeurs de VCO2 augmentèrent en parallèle avec celles de la VO2 dans les deux groupes. Après quatre heure il n’y avait aucune différence significative entre les deux groupes, cependant la VO2 dans les deux groupes (160.5 ± 21.3 ml·min-1 ·m-2 et 173.9 ± 12.3 ml · min-1 · m-2 respectivement) était approximativement le double de celle qu’on mesure habituellement chez des patients anesthésiés. Les patients ayant présenté des frissons avaient une fréquence cardiaque et un index cardiaque significativement plus élevés et une SvO2 significativement plus basse. On conclut que les valeurs élevées de la VO2 et de la VCO2 accompagnant les frissons amènent une augmentation du travail myocardique et peuvent être néfastes chez les patients ayant une fonction cardiaque diminuée après la chirurgie coronarienne (CAS).

Site of temperature monitoring and prediction of afterdrop after open heart surgery

To determine which of the commonly used “core” temperature sites, remote from the brain, best indicates total body rewarming, the temperatures in the rectum (RT), urinary bladder (UBT) and the pulmonary artery (PAT) at the termination of cardiopulmonary bypass (CPB) were correlated with the decrease in nasopharyn-geal temperature (NPT) after CPB (afterdrop) in 29 patients. The amount of afterdrop is inversely related to the adequacy of total body rewarming, smaller values indicating better rewarming. All patients had uncomplicated cardiac surgery and received high pump flows during rewarming on CPB. The UBT showed the best correlation with afterdrop (p < 0.001 ) compared with the other temperature sites, the durations of CPB and rewarming during CPB, and the time that the NPT was greater than 37° C during rewarming. The urinary bladder is a simple, non-invasive monitoring site when a urinary catheter is required and our results indicated that the UBT is a better monitor of the adequacy of total body rewarming on CPB than NPT alone. The study also suggested that rewarming to a UBT in excess of 36.2° C prior to the termination of CPB is unlikely to further reduce afterdrop.

Neostigmine decreases heart rate in heart transplant patients

PurposeThis study evaluated the effect of neostigmine on heart rate in cardiac transplant patients.MethodsNeostigmine (2.5–50 μg · kg−1) was administered to ASA 1 or 2 patients with normally innervated hearts (controls), and to patients who had undergone recent (<six months before study) or remote (> six months before study) cardiac transplantation.ResultsBaseline heart rate was 66 ± 3 beats · min−1 in controls (n = 10, mean ± SEM), which was slower than that observed in recently (95 ± 4 beats · min−1, n = 15, P < 0.001) and in remotely (88 ± 3 beats · min−1, n = 16, P < 0.001) transplanted patients. Neostigmine produced a dose-dependent decrease in heart rate in all patients. Controls were the most sensitive to neostigmine, with a 10% decrease in heart rate produced by an estimated dose of 5.0 ± 1.0 μg · kg−1. The recently transplanted group was the least sensitive, with the maximum dose producing only an 8.3 ± 0.9% reduction. The response to neostigmine of the remotely transplanted patients was variable. The estimated dose to produce a 10% decrease in heart rate in this group was 24 ± 6 μg · kg−1 which was greater than that for controls (P = 0.008). Administration of atropine (1.2 mg) reversed the neostigmine-induced bradycardia in all three groups. Reversal of the bradycardia consisted of a transient peak increase in heart rate in controls to 145 ± 6% of baseline, a value which was greater than that observed in recent (103 ± 1%, P < 0.001) and in remote (109 ± 3%, P < 0.001) transplants.ConclusionsNeostigmine produces a dose-dependent brady-cardia in heart transplant patients. Some remotely transplanted patients may be particularly sensitive to the bradycardic effects of neostigmine.RésuméObjectifEvaluer les effets de la néostigmine sur les transplantés cardiaques.MéthodesDe la néostigmine (2,5–50 μg · kg−1) a été administrée à des patients ASA 1 ou 2 dont le coeur était innervé normalement (contrôles) et à des patients qui avaient subi une transplantation cardiaque récente (<six mois) ou plus ancienne.RésultatsLa fréquence cardiaque de base était de 66 ± 3 b · min−1 (n = 10, moyenne ± SEM) laquelle était inférieure à celle des transplantés récents (95 ± 4 b · min−1, n = 15, P < 0,001). La néostigmine a produit une baisse de la fréquence proportionnelle à la dose chez tous les patients. Les contrôles ont été plus sensibles à la néostigmine, avec une baisse de 10% produite par une dose estimée de 5,0 ± 1,0 μg · kg−1. Les transplantés récents ont été les moins sensibles, alors que la dose maximale ne produisait qu’une baisse de 8,3 ± 0,9%. La réponse à la néostigmine des transplantés plus anciens a été variable. La dose estimée, pour produire une baisse de 10% de la fréquence cardiaque, plus élevée que pour les contrôles, était de 24 ± 6 μg · kg−1 (P = 0,008). L’administration d’atropine a neutralisé la bradycardie induite par le néostigmine chez les trois groupes. L’antagonisme de la bradycardie a été caractérisé par une augmentation transitoire de la fréquence cardiaque à 145 ± 6% de la valeur initiale dans le groupe contrôle, valeur plus importante que chez les transplantés récents (103 ± 1%, P < 0,001) et anciens (108 ± 3%, P < 0,001).ConclusionsLe néostigmine produit une bradycardie proportionnelle à la dose chez le transplanté cardiaque. Quelques uns des transplantés plus anciens peuvent être plus particulièrement sensibles aux effets bradycardisants de la néostigmine.

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 role of intrathecal morphine in the anesthetic management of patients undergoing coronary artery bypass surgery

The study was undertaken to assess the effects of intrathecal morphine (ITM) on perioperative hemodynamics, and anesthetic and postoperative analgesic requirements in patients anesthetized with fentanyl/enflurane undergoing coronary artery bypass surgery. Forty patients were randomized in a double-blind fashion to receive either intrathecal morphine or saline. Nineteen patients received ITM, 0.02 mg/ kg, and 21 intrathecal saline (ITS) after induction of anesthesia. Anesthesia included fentanyl, 40 microg/kg, and pancuronium, 0.15 mg/kg, and was supplemented with enflurane when systolic blood pressure was 20% higher than ward pressure. Intrathecal morphine did not improve hemodynamic stability or reduce enflurane requirements perioperatively. No significant difference was found between ITM and ITS groups for postoperative requirements of morphine (3.5 +/- 0.5 v 4.5 +/- 0.6 mg), diazepam (5.6 +/-1.25 v 3.9 +/- 1.26 mg), and vasodilators (6 v 13 patients), respectively. Comparable and significant reductions of peak expiratory flow rates (PEFR), forced vital capacity (FVC), and forced expiratory volume (FEV1) occurred in both groups postextubation when compared with preoperative values. Intrathecal morphine at the dose of 0.02 mg/kg does not offer any clear benefit to patients anesthetized with fentanyl, 40 microg/kg, for coronary artery bypass surgery.

Pure opioid versus opioid-volatile anesthesia for coronary artery bypass graft surgery: a prospective, randomized, double-blind study.

This study was designed to assess, in a prospective, randomized, blinded fashion, the hemodynamic effects of different anesthetics used in the prebypass period during coronary artery bypass grafting (CABG) and the effect on incidence of ischemia. Seventy-five patients were randomly assigned to receive sufentanil increments, isoflurane, or enflurane after a standard premedication and anesthetic induction with sufentanil 5 micrograms/kg. Myocardial ischemia was monitored intraoperatively by the anesthesiologist with electrocardiogram (ECG) leads V5(CB5) and II, and by a Holter monitor of the same leads from which recordings were analyzed postoperatively by a cardiologist. A continuous recording of the blood pressure was analyzed to determine the duration of hypertensive responses. Arterial blood pressure control was best in the patients supplemented with anesthetic vapors; patients receiving beta-adrenergic blockers or those receiving isoflurane were less likely to require treatment for tachycardia. All episodes of myocardial ischemia occurred within 5 min of induction-intubation and were diagnosed more frequently by the anesthesiologist than on the Holter monitor (29% vs 9%), with no difference between groups. There were five perioperative myocardial infarctions with no difference between groups. After anesthetic induction with sufentanil 5 micrograms/kg, isoflurane or enflurane given during CABG provides better hemodynamic control than increments of sufentanil and is associated with a similar incidence of prebypass ischemia and perioperative infarction.

The incidence of myocardial ischemia during anesthesia for coronary artery bypass surgery in patients receiving pancuronium or vecuronium

This study was performed to compare the incidence of prebypass myocardial ischemia in patients receiving fentanyl and enflurane for anesthesia along with either pancuronium or vecuronium. Ninety-eight patients with normal left ventricular function were randomly allocated to receive either pancuronium 0.15 mg.kg-1 or vecuronium 0.15 mg.kg-1 in a double-blind manner after fentanyl 40 micrograms.kg-1 for induction of anesthesia for elective coronary artery bypass grafting (CABG). Premedication included diazepam 0.15 mg.kg-1 po, morphine 0.10 mg.kg-1, and scopolamine 0.005 mg.kg-1 im. Two lead Holter monitor recordings (leads V6 and V9) from the time of arrival in the operating suite to institution of cardiopulmonary bypass were analyzed for ischemia by a cardiologist blinded to the choice of muscle relaxant. Intraoperatively, heart rates greater than 90 beats.min-1 and systolic blood pressure +/- 20% of ward values were treated with propranolol, enflurane, or phenylephrine. Nitroglycerin was infused for ECG signs of ischemia or pulmonary hypertension. After induction of anesthesia the heart rate and cardiac index were consistently decreased in patients receiving vecuronium and also lower in these patients compared with those receiving pancuronium. Thirty-two per cent of patients receiving pancuronium received propranolol for heart rates greater than 90 beats.min-1 versus 7% of those who received vecuronium (P approximately 0.01). Eight patients developed 13 episodes of ischemia after administration of the muscle relaxant: four who received pancuronium (n = 44; 9%) and four receiving vecuronium (n = 54; 7%). Four episodes occurred at induction or tracheal intubation, two in each group. There were four perioperative myocardial infarctions as determined by ECG and CPK-MB levels, two in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Neostigmine-induced bradycardia following recent vs remote cardiac transplantation in the same patient

PurposeThis report describes the effects of neostigmine on heart rate in the same patient following recent and remote cardiac transplantation.Clinical featuresEighty-six months following the first transplant, neostigmine 5.0 μg · kg−1 iv produced a 10% reduction in heart rate which was reversed by atropine 1.2 mg. For 24 months prior to this initial study, the patient experienced angina, suggesting cardiac afferent reinnervation. Three months after the second heart transplant, a second study showed that a six-fold increase in the dose of neostigmine, 30.0 μg · kg−1, only produced a 3.5% reduction in heart rate which was reversed by atropine 1.2 mg.ConclusionsThese observations indicate that neostigmine produces bradycardia following cardiac transplantation, and suggest that a greater response may be observed in remotely than in recently transplanted patients.RésuméObjectifCette observation décrit les effets de la néostigmine chez le même patient entre une première et une deuxième transplantations cardiaques.Caractéristiques cliniquesQuatre-vingt-six mois après une première transplantation, de la néostigmine 5,0 μg · kg−1 iv a provoqué une baisse de la fréquence cardiaque de 10% neutralisée par l’atropine 1,2 mg. Vingt-quatre mois après le début de cette étude, le patient souffrait d’angine, ce qui suggérait une réinnervation cardiaque afférente. Trois mois après la seconde transplantation, une autre étude a révélé que six fois la dose initiale de neostigmine, 30,0 μg · kg−1, ne produisait qu’une baisse de 3,5% de la fréquence cardiaque laquelle a été neutralisée par l’atropine 1,2 mg.ConclusionsCette observation montre que la néostigmine produit de la bradycardie après une transplantation cardiaque et suggère que cette réponse peut être plus importante chez le patient dont la transplantation est de plus longue date.

Amrinone before termination of cardiopulmonary bypass: haemodynamic variables and oxygen utilization in the postbypass period

One hundred patients were randomly allocated to receive saline or amrinone, 0.75 mg · kg−1, ten minutes before separation from cardiopulmonary bypass (CPB) after elective coronary artery bypass grafting, in order to determine the effects of this agent on haemodynamic variables and O2 utilization. Anaesthesia and CPB were managed in a standard fashion. Before induction of anaesthesia, at pericardiotomy, then at 1, 10, 20 and 30 min after CPB, haemodynamic profiles, haematocrit, and O2 saturation of arterial and mixed venous blood were measured. Incremental doses of ephedrine or phenylephrine, or an infusion of norepinephrine with phentolamine were administered when required. The groups were demographically similar and surgical variables were also similar. Haemodynamic measurements were similar between groups at all times; however, a higher dose of phenylephrine was given immediately before weaning from CPB in the amrinone group, and more patients in this group received phenylephrine in the first 30 min after CPB. Mixed venous saturation (S− vO2) was higher in the amrinone patients at all times after CPB, leading to lower calculated oxygen consumption (VO2) (P < 0.05). Insufficient dosage may explain the lack of haemodynamic effect, while possible reasons for the higher S− vO2 and lower VO2 are either reduced whole body VO2 or peripheral shunting.RésuméAfin de déterminer les effets de l’amrinone sur les paramètres hémodynamiques et sur l’utilisation de l’oxygène, 100 patients ont été désignés au hasard à recevoir soit du soluté physiologique, soit de l’amrinone 0,75 mg · kg− 1 dix minutes avant l’arrêt de la circulation extracorporelle (CEC) pour une chirurgie de revascularisation coronarienne nonurgente. L’anesthésie et la CEC ont été réalisées de la manière habituelle. Les paramètres hémodynamiques, l’hématocrite, et la saturation en O2 du sang artériel et veineux mêlé ont été mesurés avant l’induction de l’anesthésie, lors de la péricardectomie et à 1, 10, 20 et 30 minutes après la CEC. Des doses progressives d’éphédrine ou de phényléphrine, ou une perfusion de norépinéphrinephentolamine étaient administrees au besoin. Les groupes étaient identiques sur la plan de la démographie ainsi que des variables chirurgicales. Les mesures hémodynamiques ont été comparables en tout temps entre les deux groupes. Cependant, dans le groupe amrinone, une dose plus élevée de phényléphrine a dû être administrée immédiatement avant le sevrage de la CEC et un plus grand nombre de patient ont dû recevoir ce médicament pendant les 30 minutes qui ont suivi la CEC. Après celleci, la saturation oxyhémoglobinée du sang veineux mêlé (S−vO2) a toujours été plus élevée chez les patients du groupe amrinone, ce qui a fait baisser la valeur calculée de la consommation d’oxy gène (VO2) (P < 0,05). Une dose insufflsante d’amrinone peut expliquer l’absence d’action hémodynamique, alors que la diminution de VO2 systémique ou un effet shunt périphérique pourrait expliquer l’augmentation de la S−vO2 et la diminution de la VO2.

The diabetic patient: a challenge or just routine?

ConclusionBy understanding basic physiological and endocrinological principles the anaesthetist can make rational decisions regarding the metabolic care of the diabetic patient. Good perioperative management of these patients often with complex multiple pathology due to end-organ dysfunction can have a considerable effect in reducing the morbidity and mortality associated with this disease. Therefore it is behovent to maintain euglycaemia in these complex and often unexpectedly high risk patients.RésuméC’est par la connaissance des principes physiologiques et endocrinologiques de base que l’anesthésiste pourra prendre des décision rationnelles en vue de la prise en charge du diabétique. La gestion périopératoire appropriée de ces patients souffrant de plusieurs pathologies complexes par dysfonctionnement organique peut réduire considérablement la morbidité et la mortalité associées à cette maladie. Notre devoir est donc de maintenir une glycémie normale chez ces malades complexes et qui présentent souvent un haut risque insoupçonné.