Fresh gas flow in the Bain circuit during laparoscopy

Twenty-two women were studied during laparoscopy with abdominal insufflation of carbon dioxide. A bain anaesthetic breathing circuit was used with a fresh gas flow (VFG) of 110 ml.min-1.kg-1, and controlled ventilation was applied with a minute ventilation (VE) of 175 ml.min-1.kg-1. Arterial blood gases were analysed at the end of the operation. Nineteen of the women (86 per cent) were found to have a PaCO2 within the range for normocapnia (i.e., 4.7-5.9 kPa (35-45 mmHg), two were hypocapnic with a PaCO2 of 4.4 and 4.5 kPa (33 and 34 mmHg) respectively and one was found to have a PaCO2 of 6.2 kPa (46.5 mmHg). It was concluded that the carbon dioxide absorbed from the abdomen during laparoscopy demands fresh gas flows that are higher than normally used in the Bain circuit if a PaCO2 within the normal range is to be obtained. A simultaneous increase in VFG and VE of about 45 per cent is sufficient to achieve normocapnia.     

A comparison of transcutaneous,end-tidal and arterial measurements of carbon dioxide during general anaesthesia

A randomized, prospective study was performed to evaluate the accuracy of a new transcutaneous carbon dioxide (CO2) monitor (Fastrac) during general anaesthesia. Twenty-two adult patients undergoing elective surgery were subjected to three different levels of minute ventilation by varying their respiratory rates in a randomized cross-over design. Simultaneous measurements of transcutaneous CO2 (PTCCO2) and arterial CO2 (PaCO2) were obtained at three levels of minute ventilation (low, medium and high). End-tidal CO2 (PETCO2) values were also recorded from a mass spectrometer (SARA) at each time period. A total of 66 data sets with PaCO2 ranging from 28-62 mmHg were analyzed. The PTCCO2 values demonstrated a high degree of correlation with PaCO2 over the range of minute ventilation (y = 0.904x + 6.36, r = 0.92, P less than 0.001). The PETCO2 measurement also demonstrated a generally good correlation with PaCO2 (y = 0.62x + 9.21, r = 0.89, and P less than 0.01). However, the PETCO2-PaCO2 gradients (mean 7.0 +/- 3.1 mmHg) were greater than the PTCCO2-PaCO2 gradients (mean 2.3 +/- 2.4 mmHg) at all three levels of minute ventilation (P less than 0.05). These differences were greatest when PaCO2 was in the high range (48-60 mmHg). We conclude that the new Fastrac CO2 monitor is accurate for monitoring carbon dioxide levels during general anaesthesia. The new transcutaneous devices provide an effective method for non-invasive monitoring of CO2 in situations where continuous, precise control of CO2 levels is desired.     

Vecuronium is more potent in montreal than in Paris

This study was undertaken to compare the potency of vecuronium in patients anaesthetized in Montreal or Paris. Anaesthesia was induced with thiopentone and maintained with N2O, and intermittent boluses of thiopentone and fentanyl in 18 patients in Paris and 19 in Montreal. Neuromuscular blockade was measured using train-of-four stimulation of the ulnar nerve. The force of contraction of the adductor pollicis muscle was measured. Single doses of vecuronium, 20, 30, or 40 micrograms.kg-1 were given by random allocation. Dose response curves were constructed by obtaining the linear regression of the logit of the first response (T1) neuromuscular blockade versus log dose. The patients in Paris required 27% more vecuronium (95% confidence limits 5-53%; P = 0.01) for the same intensity of blockade. In Montreal, the ED50 and ED90 (+/- SEE for the mean) values were 26.0 +/- 1.4 and 44.2 +/- 2.5 micrograms.kg-1 compared with 33.0 +/- 3.3 and 71.9 +/- 7.2 micrograms.kg-1 in Paris respectively. The patients were comparable with respect to age, sex, height and weight. These results confirm, for vecuronium, the transatlantic difference in potency of neuromuscular blocking drugs which was previously observed with d-tubocurarine between London and New York.     

Changes in the cerebral arteriovenous oxygen content difference by surgical incision are similar during sevoflurane and isoflurane anaesthesia

Purpose  

To investigate changes of cerebral arteriovenous oxygen content difference (AVDO₂) induced by surgical incision and to determine carbon dioxide (CO₂) reactivity of the cerebral circulation during sevoflurane and isoflurane anaesthesia.     

Stability of the intra-operative arterial to end-tidal carbon dioxide partial pressure difference in children with congenital heart disease

The purpose of this study was to evaluate the stability of the arterial PCO2 (PaCO2) to end-tidal PCO2 (PETCO2) partial pressure difference (Pa-ETCO2) during surgery using PETCO2 monitoring, in children with congenital heart disease (CHD). Forty children with CHD were studied: ten children with no interchamber communication and normal pulmonary blood flow (PBF) (normal group); ten acyanotic children with increased PBF (acyanotic-shunting group); ten cyanotic children with mixing type lesions and normal or increased PBF (mixing group), and ten cyanotic children with right-to-left intracardiac shunts demonstrating decreased and variable PBF (cyanotic-shunting group). Simultaneous PaCO2 recordings and PETCO2 measurements were obtained for each patient during five intraoperative events: (1) control time, arterial line placement under anaesthesia; (2) time 1, patient preparation; (3) time 2, immediately after sternotomy; (4) time 3, after heparin administration; and (5) time 4, immediately after aortic cannulation. Initially, cyanotic children demonstrated a greater Pa-ETCO2 compared with acyanotic children (P less than 0.05). There was no difference in the Pa-ETCO2 over time in the control, acyanotic-shunting, or mixing groups. The Pa-ETCO2 in the children with cyanotic-shunting lesions at times 2 and 3 was greater (P less than 0.05) than at their control times. We conclude that the Pa-ETCO2 of children with acyanotic-shunting and mixing congenital heart lesions is stable intraoperatively, although patients with mixing congenital heart lesions may demonstrate large individual variations. In children with cyanotic-shunting congenital heart lesions, the Pa-ETCO2 is not stable. The PETCO2 cannot be used during surgery to estimate reliably the PaCO2 in children with cyanotic CHD.     

A comparison of the cerebral pressure-flow relationship for halothane and isoflurane at haemodynamically equivalent end-tidal concentrations in the rabbit

The cerebral pressure-flow relationship for halothane and isoflurance was studied at end-tidal concentrations which resulted in similar baseline mean arterial pressure (MAP). Two groups of New Zealand white rabbits (n = 8; each group) were studied with five regional blood flow determinations in each animal. Blood flow was determined by injecting radioactive microspheres during the following conditions: injection 1: after stable 2.05 per cent end-tidal isoflurane (1.0 MAC) Group I; or after stable 0.74 +/- 0.04 per cent end-tidal halothane (0.53 MAC) Group H. Injections 2-5: after MAP was increased 20, 40, 60, and 80 per cent respectively above baseline MAP by phenylephrine infusion. Baseline MAP was the same for both groups (64.3 +/- 3.1 vs 67.2 +/- 2.0 mmHg; mean +/- SEM; Group I and H respectively). Baseline total CBF (tCBF; 0.68 +/- 0.03 vs 0.86 +/- 0.05) and hemispheric CBF (hCBF; 0.64 +/- 0.03 vs 0.96 +/- 0.06) were significantly greater in Group H; no significant difference between groups was seen for baseline posterior fossa CBF (pCBF; 0.79 +/- 0.06 vs 0.75 +/- 0.04). For each experiment a pressure-flow curve was generated by curvilinear regression analysis. Significantly greater phenylephrine concentrations were required for injections 2-5 in Group H. Mean slopes and intercepts were derived for each group. Within each group comparison of the pressure-flow curves for hCBF vs MAP and pCBF vs MAP showed autoregulation was less impaired in posterior fossa structures (cerebellum and brain stem) for both anaesthetic agents (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Carbon dioxide reactivity and local cerebral blood flow during prostaglandin E1 — or nitroglycerine-induced hypotension

The aims of this randomized study were to determine the effect of prostaglandin-(PGE1) or nitroglycerin-(TNG) induced hypotension on local cerebral blood flow (LCBF) and carbon dioxide reactivity during isoflurane anaesthesia in 20 patients after subarachnoid haemorrhage (SAH) scheduled for aneurysm clip ligation. Mean arterial blood pressure decreased immediately, after giving either PGE1 or TNG. The LCBF, measured using a thermal gradient blood flowmeter, was unchanged after PGE1, while the LCBF increased after TNG infusion (control; 47.6 + 10.0, 60 min after infusion; 55.1 +/- 6.5 (P < 0.05), before clipping; 55.5 +/- 7.8 (P < 0.05)) but returned to control values after its discontinuation. Carbon dioxide reactivity, calculated from % delta LCBF/delta PaCO2 was unchanged during PGE1- or TNG-induced hypotension (PGE1; 2.13 +/- 0.9, 2.48 +/- 0.68 and 2.31 +/- 0.79%/mmHg for before, during and after hypotension respectively) (TNG; 2.08 +/- 0.68, 2.17 +/- 0.64 and 2.02 +/- 0.69%/mmHg for before, during and after hypotension respectively). Carbon dioxide reactivity correlated with presurgical neurological status (rs = -0.7, -0.648 and -0.458 for before, during and after hypotension respectively) and the initial LCBF (rs = -0.605). These results suggest that both PGE1 and TNG are useful drugs for induced hypotension for cerebral aneurysm surgery, because neither decreased LCBF.     

Induction reflex actions with intravenous nalbuphine as an adjunct to isoflurane

Ninety unpremedicated patients undergoing mask anaesthesia were assigned to one of three groups according to the volatile anaesthetic and the acute intravenous premedication administered. Group I received saline placebo as premedication and halothane by inhalation. Group II received saline placebo and isoflurane by inhalation. Group III received nalbuphine 0.1 mg.kg-1 IV as premedication and isoflurance by inhalation. Mean time to loss of consciousness (71 sec) did not differ among groups. The dosage of thiopentone required to induce loss of consciousness was decreased by 15 per cent (from 3.9 to 3.3 mg.kg-1) by nalbuphine premedication (P less than 0.05), and time to induction of surgical anaesthesia using isoflurane was decreased by 15 per cent (P less than 0.05). The incidence of reflex actions (coughing, laryngospasm, breath holding, hiccoughs and movement) during induction was no different in the saline-premedicated halothane or isoflurane groups. Acute intravenous nalbuphine premedication decreased significantly the incidence of reflex actions during induction of isoflurane anaesthesia from 77 per cent to 37 per cent (P less than 0.02). Desaturation episodes (SaO2 less than 90 per cent) were more frequent with isoflurane inductions compared with halothane (55 per cent vs 17 per cent, P less than 0.01). Apnoeic episodes accounted for the majority of desaturations associated with nalbuphine premedication, while excitatory reflexes (coughing and laryngospasm) accounted for more desaturations with isoflurane alone.     

Analgesic efficacy and safety of a caudal bupivacaine-fentanyl mixture in children

The analgesic efficacy and safety of a single caudal injection of a bupivacaine-fentanyl mixture was investigated in this prospective, controlled, triple-blinded study of 34 children, aged 1-11 yr and of ASA physical status I-II undergoing urological surgery. After induction of anaesthesia and before surgery, the children were randomly assigned to receive a caudal injection of 1.0 ml.kg-1 bupivacaine 0.125% with epinephrine 1:400,000 and either fentanyl 1.0 microgram.kg-1 in 1.0 ml of normal saline or 1.0 ml of normal saline. After completion of surgery, patients were assessed in the recovery room for six hours from the time of the caudal injection and for a further 18 hr on the ward. While in the recovery room arterial oxygen saturation and respiratory rate were monitored continuously and recorded hourly together with end-tidal carbon dioxide, pain and sedation scores. Other complications were also recorded. While on the ward, pain and sedation scores, respiratory rate and side effects were recorded every two hours. Postoperative analgesia was provided by intravenous morphine. Analgesic requirements were recorded for the 24-hr study period. Pain and sedation scores did not differ between groups. Respiratory depression or hypoxia did not occur. The incidences of other side effects did not differ. There were no differences in the numbers of patients requiring morphine within eight hours, the time to first morphine administration or the total morphine requirements. We conclude that a single caudal injection of a bupivacaine-fentanyl mixture with epinephrine administered prior to surgery, while safe, offers no advantage over an injection of bupivacaine 0.125% with epinephrine for paediatric urological surgery.     

Factors influencing the R-R interval during central venous injection in newborn swine

Seven Yorkshire swine, ages 7-11 days and weighing 1.4-2.8 kg were studied to determine the effects of temperature and volume of injectate, depth of anaesthesia, position of the central venous catheter tip and vagotomy on the R-R interval after central venous injection of saline. The swine were anaesthetized with halothane in 100 per cent oxygen and their lungs ventilated to normocapnia. The length of the R-R varied inversely with the temperature of the injectate between 0 and 20 degrees C reaching a maximum prolongation of 152 per cent above control values with 0 degrees C saline. Injecting saline at 37 degrees C did not affect the R-R interval. The length of the R-R interval varied directly with the volume of injectate between 1.5 and 4.5 ml.kg-1 (P less than 0.05). The R-R interval response also varied directly with the depth of anaesthesia: the post-injection R-R interval increased from 185 per cent to 341 per cent as the end-tidal halothane concentration increased from 0.45 to 1.20 per cent. The position of the tip of the central venous catheter that produced the maximum increase in the R-R interval, as determined radiographically, was at the junction of the superior vena cava and the right atrium. Neither bilateral vagotomy nor atropine (50 micrograms.kg-1) affected the R-R interval after injecting 3 ml.kg-1 saline 0 degrees C. We conclude that the increases in R-R interval after injection of fluid into the right atrium are due to direct effects on the nerve conduction system of the heart, possibly on the sino-atrial node.     

Low-dose sufentanil in major surgery

The purpose of this study was to assess the efficacy of sufentanil 1 micrograms.kg-1 during N2O-O2 and intermittent isoflurane anaesthesia in major non-cardiac surgery. Thirty-one patients (18 females, 13 males; mean age 47 yr), undergoing cholecystectomy received a 1 microgram.kg-1 bolus of sufentanil before the induction of anaesthesia with thiopentone. On average, three sufentanil increments were administered, to a total (bolus + maintenance) dose of 1.5 micrograms.kg-1. Cardiovascular stability was not achieved in eleven patients who then were given isoflurane. The arterial pressure decreased after sufentanil (P less than 0.05), reaching a nadir (mean 108/65 mmHg, heart rate 63 bpm) at one minute post-incision. Clinically important hypertension or hypotension did not occur in any patient. One patient, receiving beta-blocker therapy, required atropine to control bradycardia. Postoperative respiratory depression did not occur in patients who received less than one micrograms.kg-1.hr-1 with the last increment being given more than 20 minutes before the end of anaesthesia. Slight respiratory depression in the recovery room was reported in one patient, who had received a total of 1.3 micrograms.kg-1.hr-1 of sufentanil, and the last sufentanil increment 24 min before the end of surgery. The most frequently reported side-effects were nausea (35 per cent) and vomiting (23 per cent). Induction, maintenance and recovery from anaesthesia were rated as "good" in 87, 87, and 74 per cent of the cases, respectively, and "satisfactory" in the remainder. We conclude that this technique is valuable to assure good protection of the cardiovascular system without undue respiratory depression during recovery.     

Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.     

Secondary hyperparathyroidism shortens the action of vecuronium in patients with chronic renal failure

The authors studied the duration of action of vecuronium in 15 patients with normal renal function and 40 patients with chronic renal failure to evaluate the effect of secondary hyper-parathyroidism on the action of vecuronium. The patients were divided into four groups: 15 patients with normal renal function (Group A); nine patients with chronic renal failure who did not need haemodialysis (Group B); 15 anephric patients who did not require parathyroidectomy (Group C); and 16 anephrenic patients who underwent parathyroidectomy because of severe secondary hyperparathyroidism (Group D). The ratio of the height of the first twitch (T₁) to the baseline value before vecuronium administration was measured by an electromyogram. Baseline T₁ was obtained after anaesthesia induction with thiamylal iv. The time to 10% recovery of the first twitch (REC 10) after administration of vecuronium 0.12 mg · Kg^?1 iv was measured in each group. Anaesthesia was maintained with isoflurane and nitrous oxide in oxygen, and supplemented with fentanyl iv. Patients in Group D showed shorter REC 10 (51 ± 4 min) than those in Groups B (71 ± 6 min) and C (80 ± 10 min) (P < 0.05), but similar REC 10 to patients in Group A (37 ±4 min). These results suggest that the duration of action of vecuronium in anephric patients with secondary hyperparathyroidism is shorter than in those without secondary hyperparathyroidism.     

Neuromuscular and cardiovascular effects of mivacurium chloride in surgical patients receiving nitrous oxide-narcotic or nitrous oxide-isoflurane anaesthesia

The neuromuscular and cardiovascular effects of mivacurium chloride were studied during nitrous oxide-oxygen narcotic (fentanyl) (n = 90) and nitrous oxide-oxygen isoflurane (ISO) anaesthesia (n = 45). In addition, a separate group (n = 9) received succinylcholine during fentanyl anaesthesia to compare its neuromuscular effects with mivacurium. Mivacurium was initially administered as a single bolus in doses from 0.03 mg.kg-1 to 0.25 mg.kg-1 to study the dose-response relationships, as well as the cardiovascular effects of mivacurium. Neuromuscular block (NMB) was measured by recording the twitch response of the adductor pollicis muscle following ulnar nerve stimulation (0.15 Hz, 0.2 ms supramaximal voltage). The ED95 values for mivacurium were estimated to be 0.073 mg.kg-1 and 0.053 mg.kg-1 in the fentanyl and ISO groups respectively. The duration of block (time from injection to 95 per cent recovery) for a dose of 0.05 mg.kg-1 mivacurium was 15.3 +/- 1.0 min and 21.5 +/- 1.3 min for fentanyl and ISO anaesthesia, respectively. The recovery index (25-75 per cent) between initial bolus dose (6.1 +/- 0.5 min), repeat bolus doses (7.6 +/- 0.6 min), mivacurium infusion (6.7 +/- 0.7 min) and succinylcholine infusion (6.8 +/- 1.8 min) were not significantly different. There was minimal change in mean arterial pressure (MAP) or heart rate (HR) following bolus doses of mivacurium up to 0.15 mg.kg-1. Bolus administration of 0.20 mg.kg-1 or 0.25 mg.kg-1 of mivacurium decreased MAP from 78.2 +/- 2.5 to 64.0 +/- 3.2 mmHg (range 12-59 per cent of control) (P less than 0.05). The same doses when administered slowly over 30 sec produced minimal change in MAP or HR.     

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg⁻¹ IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32 ± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent) following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children is the result of increases in HR alone. Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement, deux minutes après l’injection IV de 0.02 mg·kg⁻¹ d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC) et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection (FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5 pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18 ± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse de la FC.

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Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA.     

A comparison of the area of histochemical dysfunction after focal cerebral ischaemia during anaesthesia with isoflurane and halothane in the rat

The investigations that have thus far evaluated the cerebral protective properties of isoflurane have provided conflicting results. Protection would be most likely to occur in the circumstances of incomplete cerebral ischaemia in which there is a penumbral zone of marginal perfusion. The present investigation sought to evaluate further the protective properties of isoflurane in that circumstance. Middle cerebral artery occlusion (MCAO) was performed in Sprague-Dawley rats anaesthetized with 1.2 MAC concentrations of either halothane or isoflurane. At the end of four hours of MCAO, the brains were removed, sectioned and incubated in the histochemical stain 2-3-triphenyltetrazolium (TTC). An image analysis system was used to measure the area of reduced or absent TTC staining in four coronal planes spanning the distribution of the middle cerebral artery. There was no difference between halothane and isoflurane anaesthetized animals with respect to the area of brain with evidence of histochemical dysfunction. It is concluded that isoflurane is not protective (relative to the status of halothane anaesthetized control animals) when administered at 1.2 MAC concentration during four hours of focal (incomplete) cerebral ischaemia in the rat.     

Intraocular pressure in anaesthetized dogs given flumazenil with and without prior administration of midazolam

This study examined the effect of flumazenil, a benzodiazepine antagonist, on aqueous humour pressure in dogs receiving either midazolam or no benzodiazepine. Twenty-four halothane-anaesthetized dogs were assigned to one of four groups. Group I (n = 6) received saline iv at 0, 45 and 90 min. Group 2 (n = 6) received saline at 0 min, flumazenil 0.0025 mg.kg-1 iv at 45 min and flumazenil 0.16 mg.kg-1 at 90 min. Group 3 (n = 6) received midazolam 1.6 mg.kg-1 at 0 min followed by continuous iv infusion (1.25 mg.kg-1.hr-1). Flumazenil was given at 45 and 90 min as in Group 2. In Group 4 (n = 6) aqueous humour pressure was elevated to about 35 mmHg then midazolam and flumazenil were given as in Group 3. Aqueous humour pressure was determined using a 30-gauge needle placed into the anterior chamber. Saline or flumazenil produced no change in aqueous humour pressure in Groups 1 and 2. In Groups 3 and 4, midazolam decreased aqueous humour pressure from 18 +/- 2 mmHg (mean +/- SD) to 14 +/- 3 mmHg (P less than 0.001) and from 34 +/- 5 mmHg to 31 +/- 3 mmHg (P less than 0.01) respectively. Flumazenil given during continuous infusion of midazolam produced increases of aqueous humour pressure of 2 +/- 1 (P less than 0.01) to 5 +/- 2 mmHg (P less than 0.01) that lasted less than or equal to 12 min. It is concluded that at both normal and elevated aqueous humour pressures flumazenil produces statistically significant but clinically unimportant increases of aqueous humour pressure in anaesthetized dogs receiving midazolam, but not in dogs given no benzodiazepine.     

Pharmacokinetics and cardiovascular dynamics of pipecuronium bromide during coronary artery surgery

The haemodynamic effects of 200 micrograms.kg-1 pipecuronium and pancuronium were compared under etomidate/piritramide anaesthesia in 20 patients scheduled for elective coronary artery surgery. Following the completion of the haemodynamic measurements (ten minutes), anaesthesia was maintained by etomidate/sufentanil infusion. The mean changes in cardiac output were approximately -19 and -2 per cent and in heart rate -1 and +26 per cent for pipecuronium and pancuronium respectively. Plasma and urine concentrations of pipecuronium were also measured and the pharmacokinetic variables obtained indicated rapid initial decrease in plasma concentration (t1/2 = 7.6 minutes) followed by a longer terminal phase (t1/2 = 161 minutes). The central compartment volume was 102 +/- 24 ml.kg-1 and plasma clearance was 1.8 +/- 0.4 ml.kg-1 min-1. Approximately 56 per cent of the dose was recovered from the urine within 24 hours of administration and about 25 per cent of this was the metabolite, 3-desacetyl pipecuronium. High-dose pipecuronium administration under the anaesthetic regimen employed did not produce deleterious haemodynamic effects. The pharmacokinetic variables after bolus injection of pipecuronium did not deviate from those reported under normothermic conditions.     

A comparison of the myocardial metabolic and haemodynamic changes produced by propofol-sufentanil and enflurane-sufentanil anaesthesia for patients having coronary artery bypass graft surgery

The purpose of this study was to compare propofol-sufentanil with enflurane-sufentanil anaesthesia for patients undergoing elective coronary artery bypass graft (CABG) surgery with respect to changes in (1) haemodynamic variables; (2) myocardial blood flow and metabolism; (3) serum cortisol, triglyceride, lipoprotein concentrations and liver function; and (4) recovery characteristics. Forty-seven patients with preserved ventricular function (ejection fraction greater than 40%, left ventricular end diastolic pressure less than or equal to 16 mmHg) were studied. Patients in Group A (n = 24) received sufentanil 0.2 microgram.kg-1 and propofol 1-2 mg.kg-1 for induction of anaesthesia which was maintained with a variable rate propofol (50-200 micrograms.kg-1.min-1) infusion and supplemental sufentanil (maximum total 5 micrograms.kg-1). Patients in Group B (n = 23) received sufentanil 5 micrograms.kg-1 for induction of anaesthesia which was maintained with enflurane and supplemental sufentanil (maximum total 7 micrograms.kg-1). Haemodynamic and myocardial metabolic profiles were determined at the awake-sedated, post-induction, post-intubation, first skin incision, post-sternotomy, and pre-cardiopulmonary bypass intervals. Induction of anaesthesia produced a larger reduction in systolic blood pressure in Group A (156 +/- 22 to 104 +/- 20 mmHg vs 152 +/- 26 to 124 +/- 24 mmHg; P less than 0.05). No statistical differences were detected at any other time or in any other variable including myocardial lactate production (n = 13 events in each group), time to tracheal extubation and time to discharge from the ICU. We concluded that, apart from hypotension on induction of anaesthesia, propofol-sufentanil anaesthesia produced anaesthetic conditions equivalent to enflurane-sufentanil anaesthesia for CABG surgery.