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 receive 1.5 micrograms.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 less than 0.0001). The second 150 patients were then randomly assigned to three equal pretreatment groups. Group 3 received 0.01 mg.kg-1 atropine iv one minute before fentanyl. Groups 4 and 5 received 0.2 mg.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 altered by premedication with atropine or midazolam, but was reduced after morphine (P less than 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.     

Randomized comparison of outcome after propofol-nitrous oxide or enflurane-nitrous oxide anaesthesia in operations of long duration

A randomized, prospective, comparative study was performed to evaluate induction characteristics, haemodynamic changes and recovery in 60 ASA I-II patients undergoing mainly gynaecological laparotomies with either propofol or thiopentone-enflurane anaesthesia. The propofol group (n = 30) received 2 mg.kg-1 propofol for induction of anaesthesia followed by propofol infusion. The thiopentone-enflurane group (n = 30) received thiopentone 4 mg.kg-1 for induction followed by enflurane (0.5-2 per cent). All patients received nitrous oxide (66 per cent] in oxygen begun one minute after tracheal intubation, and fentanyl (1.5 micrograms.kg-1) four minutes prior to induction. Other drugs administered during or after anaesthesia were similar among the groups. Haemodynamic measurements were similar between propofol and enflurane groups except after tracheal intubation when the mean arterial pressure was lower in the propofol group (P less than 0.05). The propofol group had significantly less (P less than 0.01) emesis in the recovery room than the enflurane group. The propofol group experienced significantly less (P less than 0.05) dizziness, depression/sadness and hunger than the enflurane group in the postoperative period as assessed with a visual analogue questionnaire. We conclude that propofol provided better outcome than enflurane in terms of these nonvital but annoying outcome measures after relatively long intra-abdominal operations.     

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.     

Metabolic and endocrine responses to surgery during caudal analgesia in children

Plasma concentrations of glucose, lactate, epinephrine, norepinephrine, insulin, cortisol and growth hormone were measured in 28 healthy children, three to six years of age, before, during, and after lower abdominal surgery. The children received premedication with secobarbital, 6 mg.kg-1, pentazocine, 0.5 mg.kg-1, and atropine, 0.01 mg.kg-1 im. Fourteen children received general anaesthesia with nitrous oxide and halothane, and 14 others received caudal analgesia with 1.5% mepivacaine. Plasma glucose, epinephrine and norepinephrine concentrations remained unchanged in the general anaesthesia group, but decreased during and after surgery in the caudal analgesia group (P less than 0.05). During surgery, these concentrations were different between the two groups (P less than 0.05). Plasma insulin and cortisol concentrations increased after surgery (P less than 0.05), and growth hormone concentration increased during and after surgery in the general anaesthesia group (P less than 0.05), but the concentrations of these hormones remained unchanged during and after surgery in the caudal analgesia group. Plasma lactate concentrations were unchanged in both groups. These results indicate that caudal analgesia suppresses the metabolic and endocrine responses to stress associated with lower abdominal surgery in children.     

Butorphanol compared with fentanyl in general anaesthesia for ambulatory laparoscopy

Butorphanol was compared with fentanyl as the narcotic component of general anaesthesia for ambulatory laparoscopic surgery. This double-blind, randomized study enrolled 60 healthy women who received equianalgesic doses of fentanyl 1 microgram.kg-1 (F, n = 30) or butorphanol 20 micrograms.kg-1 (B, n = 30) prior to induction of anaesthesia. Tracheal anaesthesia was maintained with nitrous oxide/oxygen, isoflurane, and succinylcholine by infusion. Intraoperatively, patients who received B demonstrated lower pulse rate before and after intubation (P less than 0.05, P less than 0.01) and lower diastolic blood pressure after intubation (P less than 0.01). Anesthesiologists judged the maintenance phase as satisfactory more often with B (P less than 0.05). Postoperatively, there were no differences in analgesic need. No major side-effects occurred in either group. Among minor side-effects, patients who received B reported postoperative sedation more often, 77% vs 37% (P less than 0.01), which occurred during the first 45 min of recovery (P less than 0.05). Discharge times were not different. On the first postoperative day, more subjects who received B were satisfied with their anaesthesia experience (P less than 0.05). Butorphanol 20 micrograms.kg-1 is an acceptable alternative analgesic in general anaesthesia for ambulatory laparoscopy.     

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 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.     

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.     

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.     

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)     

Postoperative neuromuscular block following atracurium or alcuronium in children

Postoperative neuromuscular block (NMB) was evaluated in 60 children who received randomly either atracurium or alcuronium to induce and maintain an 85-95 per cent NMB during balanced anaesthesia. The EMG-monitor was turned away from the anaesthetist 10-15 min before the end of surgery. The average NMB was comparable between the groups at the time of reversal with neostigmine 50 micrograms.kg-1 (84 +/- 9 per cent, mean +/- SD) as were the NMB and the train-of-four ratio when the tracheas were extubated on a clinical basis (32 +/- 20 per cent and 50 +/- 18 per cent, respectively). Patients who had been paralyzed with atracurium arrived at the recovery room earlier and on arrival had greater train-of-four ratios than the patients paralyzed with alcuronium (P less than 0.01). Time to a train-of-four ratio of greater than 90 per cent was significantly shorter in the atracurium group (10 +/- 5 min vs 26 +/- 15 min, P less than 0.001). Thus, an intermediate-acting muscle relaxant offers a safer recovery profile of the NMB than a long-acting muscle relaxant in paediatric patients.     

A defasciculating dose of d-tubocurarine causes resistance to succinylcholine

Forty-four patients, ASA physical status I or II, undergoing thiamylal, fentanyl, N2O/O2 anaesthesia were studied to determine the dose-response to succinylcholine (Sch) without prior defasciculation (24 pt - Group 1), or three minutes following d-tubocurarine (dTC), 0.043 mg.kg-1 (20 pt - Group 2). The individual log dose-logit response curve for each patient was determined using a cumulative dose plus infusion technique and integrated EMG monitoring of the first dorsal interosseous muscle. The mean (+/- SEM) ED50, ED90 and ED95 values for Sch in Group 1 were 0.13 +/- 0.01, 0.19 +/- 0.01 and 0.22 +- 0.01 mg.kg-1, and in Group 2 were 0.16 +/- 0.01, 0.25 +/- 0.01 and 0.29 +/- 0.02 mg.kg-1, respectively. The mean ED values in Group 2 were significantly greater than the equivalent values in Group 1 (P less than 0.05). Compared with values in Group 1, ED values in Group 2 represented mean increases of 23, 32, and 32 per cent, respectively. These pharmacodynamic data indicate that the dose of Sch needs to be increased by 32 per cent following a defasciculating dose of dTC 3 mg.70 kg-1 (0.043 mg.kg-1).     

Disposition of propofol infusions for caesarean section

The disposition of propofol was studied in women undergoing elective Caesarean section. Indices of maternal recovery and neonatal assessment were correlated with venous concentrations of propofol. After induction of anaesthesia with propofol 2.0 mg.kg-1, ten patients received propofol 6 mg.kg-1.hr-1 with nitrous oxide 50 per cent in oxygen (low group) and nine were given propofol 9 mg.kg-1.hr-1 with oxygen 100 per cent (high group). Pharmacokinetic variables were similar between the groups. The mean +/- SD Vss = 2.38 +/- 1.16 L.kg-1, Cl = 39.2 +/- 9.75 ml.min-1.kg-1 and t1/2 beta = 126 +/- 68.7 min. At the time of delivery (8-16 min), the concentration of propofol ranged from 1.91-3.82 micrograms.ml-1 in the maternal vein (MV), 1.00-2.00 micrograms.ml-1 in the umbilical vein (UV) and 0.53-1.66 micrograms.ml-1 in the umbilical artery (UA). Neonates with high UV concentrations of propofol at delivery had lower neurologic and adaptive capacity scores 15 minutes later. The concentrations of propofol were similar between groups during the infusion but they declined at a faster rate in the low group postoperatively. Maternal recovery times did not depend on the total dose of propofol but the concentration of propofol at the time of eye opening was greater in the high group than the low group (1.74 +/- 0.51 vs 1.24 +/- 0.32 micrograms.ml-1, P less than 0.01). The rapid placental transfer of propofol during Caesarean section requires propofol infusions to be given cautiously, especially when induction to delivery times are long.     

Preservation of renal blood flow during hypotension induced with fenoldopam in dogs

The introduction of drugs that could induce hypotension with different pharmacological actions would be advantageous because side effects unique to a specific drug could be minimized by selecting appropriate therapy. Specific dopamine-1, (DA1) and dopamine-2 (DA2) receptor agonists are now under clinical investigation. Fenoldopam mesylate is a specific DA1 receptor agonist that lowers blood pressure by vasodilatation. The hypothesis that fenoldopam could be used to induce hypotension and preserve blood flow to the kidney was tested. Systemic aortic blood pressure and renal blood flow were measured continuously with a carotid arterial catheter and an electromagnetic flow probe respectively, in order to compare the cardiovascular and renal vascular effects of fenoldopam and sodium nitroprusside in ten dogs under halothane general anaesthesia. Mean arterial pressure was decreased 30 +/- 8 per cent from control with infusion of fenoldopam (3.4 +/- 2.0 micrograms.kg-1.min-1) and 34 +/- 4 per cent with infusion of sodium nitroprusside (5.9 micrograms.kg-1.min-1) (NS). Renal blood flow (RBF) increased during fenoldopam-induced hypotension 11 +/- 7 per cent and decreased 21 +/- 8 per cent during sodium nitroprusside-induced hypotension (P less than 0.01). Sodium nitroprusside is a non-selective arteriolar and venous vasodilator that can produce redistribution of blood flow away from the kidney during induced hypotension. Fenoldopam is a selective dopamine-1 (DA1) receptor agonist that causes vasodilatation to the kidney and other organs with DA1 receptors and preserves blood flow to the kidney during induced hypotension.     

Spinal tetracaine decreases central nervous system metabolism during somatosensory stimulation in the rat

The influence of spinal tetracaine on central nervous system (CNS) metabolism was determined during nociceptive stimulation. Rats were divided into a halothane group in which the sciatic nerve was stimulated during 0.5 per cent halothane anaesthesia, a tetracaine group in which the sciatic nerve was stimulated during a simultaneous tetracaine spinal and 0.5 per cent halothane anaesthetic, or an awake group. Autoradiographic determination of local spinal cord and cerebral glucose utilization was performed using 14C-2-deoxyglucose. Central nervous system metabolism was greater in the halothane group than the tetracaine and awake groups (P less than 0.05). The only meaningful differences between the tetracaine and awake groups were in two lumbar grey areas at the site of drug administration where metabolism was decreased in the tetracaine/stimulated group. These results indicate that spinal tetracaine effects a decrease in metabolism locally, and attenuates increases in metabolism throughout the CNS observed during somatosensory stimulation.     

Low-dose sufentanil and lidocaine supplementation of general anaesthesia

This randomized double-blind study compared the effects of: (1) saline infusion (C); (2) sufentanil alone (1.0 micrograms.kg-1) (S); and (3) low-dose sufentanil (0.5 micrograms.kg-1) in combination with lidocaine (1.5 mg.kg-1) (LS): on the cardiovascular responses to tracheal intubation and on postoperative ventilation as monitored by respiratory inductive plethysmography in day-care surgical procedures of approximately 60 min duration. Thirty healthy, unpremedicated patients were studied. Thiopentone requirements were reduced by 40 and 28 per cent in the S and LS groups respectively compared with control (P less than 0.001). Both treatments suppressed HR and BP responses (P less than 0.005) to intubation. Postoperatively, PaCO2 was elevated (P less than 0.05) in group S. Dose-related respiratory depression was observed. The incidence of postoperative apnoea was significantly higher in both S and LS groups than compared with control (P less than 0.05). However, only patients in group S showed higher apnoea index and mean apnoea duration over the initial 10-20 min after surgery compared with control (P less than 0.005). In addition, group S showed slower respiratory frequency and prolonged expiratory time (P less than 0.005). In conclusion, an induction dose of sufentanil (1 microgram.kg-1) used in balanced anaesthesia of less than 70 min duration was associated with significant respiratory depression, particularly during the initial 10-20 min after surgery, whereas low-dose sufentanil (0.5 micrograms.kg-1) with lidocaine (1.5 mg.kg-1) had minimal postoperative respiratory depression and comparable attenuation of pressor responses to intubation.     

Clinical and pharmacokinetic aspects of the combination of meperidine and prilocaine for spinal anaesthesia

The aim of this study was to determine whether the addition of a small dose of prilocaine could augment the spinal block induced by meperidine and affect intrathecal meperidine pharmacokinetic behaviour. Spinal anaesthesia was performed in 60 men scheduled for endoscopic resection of a prostatic adenoma or bladder tumour under spinal anaesthesia. They were allocated randomly to receive either 1 mg.kg-1 meperidine (Group 1, n = 30), or 1 mg.kg-1 meperidine plus 0.5 mg.kg-1 prilocaine (Group 2, n = 30). Blood samples were collected prior to and for 24 hr after spinal injection in 24 patients (12 in each group). Plasma meperidine levels were assayed by gas chromatography. Complete motor block was achieved in all Group 2 patients, but was incomplete in seven of Group 1 (P less than 0.05). The onset of both motor and sensory blocks was shorter (P less than 0.01) in Group 2 and the duration was longer (P less than 0.05). Coadministration of prilocaine modifies meperidine pharmacokinetic behaviour. The area under curve was 48% greater (P less than 0.01) and Cmax was higher in Group 2 than in Group 1, 145.8 +/- 42.2 vs 107 +/- 20.5 ng.ml-1 (P less than 0.001). No evidence of respiratory depression was noted in any of the patients. Despite the increase in plasma meperidine concentrations, no side effects were observed. The plasma concentrations remained at one third to one sixth the levels reported to induce a respiratory depression. It is concluded that the addition of prilocaine to meperidine improves motor and sensory block during surgery and alters meperidine kinetics without producing major side effects.     

Haemodynamic interactions of muscle relaxants and sufentanil in coronary artery surgery

The haemodynamic interactions between sufentanil (S) and muscle relaxants (MR) were studied in 40 ASA physical status III or IV patients (four groups of ten) scheduled for coronary artery bypass grafting (ABG). Group I received pancuronium (P) 0.08 mg.kg-1, Group II received vecuronium (V) 0.1 mg.kg-1, Group III received atracurium (A) 0.5 mg.kg-1 and Group IV metocurine 0.1 mg.kg-1 plus pancuronium 0.02 mg.kg-1 (M-P). Sufentanil, 20 micrograms.kg-1 was administered before sternotomy, 10 micrograms.kg-1 being injected before tracheal intubation and 10 micrograms.kg-1 afterwards. Heart rate (HR), ECG leadII and V5, systolic, diastolic and mean arterial and pulmonary blood pressures, central venous pressure (CVP) and pulmonary capillary wedge pressure (W) were measured and recorded at the time of seven strategic events between the pre-induction of anaesthesia period and sternotomy. Cardiac output (CO) and systemic vascular resistances (SVR) were also measured before induction of anaesthesia and after the administration of S 10 micrograms.kg-1 plus the MR. The HR decreased from baseline values in the post-tracheal intubation period in all groups except in P group. The mean arterial pressure also decreased significantly in all groups except in the P group. The CO did not change from baseline values but SVR decreased in all groups. There was no evidence of new myocardial ischaemia according to the ECG monitoring and there was no significant difference in the HR changes between patients who had or who had not received beta-blockers in any group. We conclude that within the present study conditions and design, HR and blood pressure changed least with pancuronium.     

Esmolol bolus and infusion attenuates increases in blood pressure and heart rate during electro-convulsive therapy

To determine whether a standardized dose of esmolol can effectively attenuate the cardiovascular response to electroconvulsive therapy (ECT), 17 ASA physical status I-II patients were studied in a randomized within-patient, crossover design. Each patient received "no esmolol" during one ECT and three to five days later crossed over to the alternative treatment receiving an esmolol 80 mg bolus followed by 24 mg.min-1 infusion two minutes prior to induction of anaesthesia and continued for five minutes after induction. Esmolol blunted the maximum increases in heart rate (HR) by 26 per cent, mean arterial pressure (MAP) by 14 per cent, and rate pressure product by 37 per cent with significant differences (P less than 0.05) noted at one, two, three and four minutes after ECT (minutes five, six, seven, and eight of the esmolol infusion). There was no significant difference in seizure duration between the two groups and no adverse reactions occurred.     

Airway irritation produced by volatile anaesthetics during brief inhalation: comparison of halothane,enflurane, isoflurane and sevoflurane

Eleven male volunteers were studied to compare the airway irritation produced by the four anaesthetic agents: halothane, enflurane, isoflurane and sevoflurane at two concentrations, equivalent to one and two MAC. Tidal volume, respiratory frequency and functional residual capacity changes induced by 15 sec inhalation of the anaesthetics were measured using respiratory inductive plethysmograph. Appearance of the cough reflex was also observed. The order of subjective airway irritation was evaluated by the volunteers. Inhalation of the anaesthetic agents induced a decrease in tidal volume, increase in respiratory frequency and decrease in functional residual capacity. Significant changes were considered to have occurred if tidal volume and respiratory frequency changed by more than 30% from the resting values for at least ten seconds, or if functional residual capacity changed by more than 30% of the value at resting tidal volume, for at least ten seconds. Each change was induced most frequently by isoflurane followed by enflurane, halothane and, least frequently, by sevoflurane. The orders of appearance of the cough reflex and of subjective airway irritation were similar. Sevoflurane did not elicit a cough reflex. It is concluded that sevoflurane was the least irritant anaesthetic and is considered to be the most suitable for inhalational induction of anaesthesia. Sept volontaires du sexe masculin font partie dune étude visant à comparer les ejfets irritants de quatre agents anesthésiques sur les voies respiratoires: l’halothane, l’enflurane, l’ isoflurane et le sévoflurane, à deux concentration qui équivalent soit à MAC 1, soit à MAC 2. On mesure les changements de volume courant, de fréquence respiratoire et de capacité résiduelle fonctionnelle à l’aide d’un pléthysmographie à induction. On note l’apparition du réflexe de toux. De plus, on évalue le degré subjectif d’irritation éprouvé par les sujets. L’inhalation d’agents anesthésiques cause une baisse du volume courant, une augmentation de la fréquence respiratoire et une diminution de la capacité résiduelle fonctionnelle. On considère significatifs les changements de volume courant et de fréquence respiratoire de plus de 30% des valeurs de repos pour au moins dix secondes, les changements de capacité résiduelle fonctionnelle de plus de 30% de sa valeur au volume courant de repos pour au moins dix secondes. Les changements sont initiés principalement par l’isoflurane, suivi par l’enflurane, l’halothane et moins fréquemment par le sévoflurane. L’ordre d’apparition du réflexe de toux et de l’impression subjective d’irritation des voies aériennes est identique. Le sévoflurane ne provoque pas de réflexe de toux. On conclut que le sévoflurane est le moins irritant des anesthesiques et qu’on peut le considerer comme celui qui convient le mieux à l’induction de l’anesthésie par inhalation.