Edrophonium priming alters the course of neuromuscular recovery from a pipecuronium neuromuscular blockade

This study was designed to investigate the effect of divided administration of edrophonium on the course of neuromuscular recovery from a pipecuronium neuromuscular blockade. During thiopentone-nitrous oxide-halothane anaesthesia 48 patients were given pipecuronium 70 micrograms.kg-1. Patients were randomly assigned to one of four groups (n = 12 in each) to receive either edrophonium 1 mg.kg-1 (Groups I and II) or edrophonium 0.75 mg.kg-1 (Groups III and IV). In Groups I and III (single-dose groups), edrophonium was administered as a single bolus dose. In Groups II and IV (divided-dose groups) edrophonium was administered as an initial dose of 0.25 mg.kg-1 followed three minutes later by either 0.75 or 0.50 mg.kg-1 respectively. Reversal was attempted at 20% spontaneous recovery of twitch height. Administration of edrophonium in divided doses (Groups II and IV) accelerated the reversal of the pipecuronium neuromuscular blockade. At ten minutes post-reversal, train-of-four (TOF) ratio recovery reached 0.75 or more in 12 (100%) and in ten (83%) patients in Groups II and IV respectively. Similarly, times to attain a TOF of 0.75 (SEM) were shorter in the divided-dose groups than in the single-dose groups (P less than 0.05), being 354.5 (38.7) and 398.3 (49.1) sec in Groups II and IV vs 705.4 (66.6) and 651.2 (54.3) sec in Groups I and III respectively. Time was counted from the first administration of edrophonium. It is concluded that administration of edrophonium in divided doses produced a faster reversal of residual pipecuronium-induced neuromuscular blockade than single bolus administration. Also, administration in divided doses reduced the requirements of edrophonium needed for reversal of pipecuronium neuromuscular blockade.     

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.     

Edrophonium antagonism of vecuronium at varying degrees of fourth twitch recovery

The purpose of this study was to determine the optimal dose of edrophonium needed for successful antagonism (train-of-four ratio, or T₄/T₁ > 0.7) of vecuronium-induced blockade when all four twitches were visible in response to indirect train-offour (TOF) stimulation. Forty patients, scheduled for elective surgical procedures not exceeding 120 min, received vecuronium, 0.08 mg · kg^?1, during thiopentone-N₂O-isoflurane anaesthesia. Train-of-four stimulation was applied every 20 sec and the force of contraction of the adductor pollicis muscle was recorded. Increments of vecuronium, 0.015 mg · kg^?1, were given as required. At the end of surgery, and provided that neuro-muscular activity had recovered to four visible twitches, edrophonium, 0.1 mg · kg^?1, was given. Two minutes later, edrophonium, 0.1 mg · kg^?1, was given if T₄/T₁ did not reach 0.7. After another two minutes, edrophonium, 0.2 mg · kg^?1, was given if T₄/T₁ did not reach 0.7 or more. Finally, if T₄/ T₁ was still < 0.7, a dose of 0.4 mg · kg^?1 was given. Seventeen patients (42.5%) required 0.1 mg · kg^?1 of edrophonium for successful reversal, sixteen patients (40%) needed a cumulative dose of 0.2 mg · kg^?1 and six patients (15%) required 0.4 mg · kg^?1. Only one patient received 0.8 mg · kg^?1. There was a good correlation between T₄/ T₁ two minutes after the first dose of edrophonium and pre-reversal T₄/T₁ (r = 0.6; P = 0.00014). All patients with pre-reversal T₄/ T₁ > 0.23 required at most 0.2 mg · kg^?1 of edrophonium for successful reversal. We conclude that when all four twitches are clearly visible following train-of-four stimulation, small doses of edrophonium (0.1-0.2 mg · kg^?1) might be sufficient to antagonize vecuronium neuromuscular blockade.     

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).     

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.     

Onset of vecuronium neuromuscular block is more rapid in patients undergoing Caesarean section

This investigation was carried out in ten patients undergoing elective Caesarean section and the results were compared with those of a control group of ten nonpregnant females of the same age group. The study investigated the onset of vecuronium neuromuscular block and the conditions of tracheal intubation when ketamine (1.5 mg.kg-1)-vecuronium 100 micrograms.kg-1) sequence was used for rapid-sequence induction of anaesthesia. The ulnar nerve was stimulated supra-maximally at the wrist with train-of-four stimuli every 20 sec, and the electromyographic response of the adductor pollicis muscle was displayed. The onset of 50% neuromuscular block as monitored by electromyography was shorter in the Caesarean group (80 +/- 30 sec) than in the control group (144 +/- 43 sec). The conditions of intubation at 50% block were adequate in both groups. Also, the onset of 90% block was shorter in the Caesarean group. The time of recovery to T1/control ratio of 25% was longer in the Caesarean group (46 +/- 10 min) than in the control patients (28 +/- 10 min). The results show that administration of vecuronium according to body weight results in a more rapid onset and delayed recovery of neuromuscular block in pregnant women undergoing Caesarean section than in the nonpregnant control patients.     

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.     

Decreased glucose utilization during prolonged anaesthesia and surgery

We studied the influence of prolonged anaesthesia and surgery on glucose metabolism by means of the euglycaemic insulin clamp method in eight patients who underwent prolonged surgery. Eleven patients who underwent surgery of short duration served as a control group. Plasma concentrations of catabolic hormones were measured simultaneously. Glucose utilization during prolonged anaesthesia, (PA) group, was lower than that in the control group (P less than 0.01) (glucose utilization 7.59 +/- 0.73 mg.kg-1.hr-1 in the control group vs 4.03 +/- 0.71 mg.kg-1.hr-1 in PA group respectively). There were no significant differences in plasma catecholamine and glucagon concentrations between the PA and control groups. Plasma-free fatty acid levels increased significantly in the PA group before the euglycaemic insulin clamp (free fatty acid level: 0.496 +/- 0.053 mmol.L-1 in the control group, vs 0.834 +/- 0.103 mmol.L-1 in the PA group at the pre-clamp period, P less than 0.01). Tissue resistance to exogenous insulin increased during prolonged anaesthesia and surgery although there were no significant changes in plasma catabolic hormone levels.     

Residual curarization in the neonate after Caesarean section

The transplacental transfer and the neonatal effects of atracurium 0.3 mg.kg-1 (ED95) were compared with those of d-tubocurarine at the usual clinical dose of 0.3 mg.kg-1 (ED90) in 46 patients undergoing elective Caesarean section. The atracurium group (25 patients) was similar to the d-tubocurarine group (21 patients) as far as age, parity and time intervals between precurarization, induction, skin incision, muscle relaxant administration, hysterotomy and birth. The transplacental transfer of atracurium was lower than that of d-tubocurarine, with a feto-maternal ratio of 9 +/- 3% for atracurium and 12 +/- 5% for d-tubocurarine (P less than 0.05). The transplacental transfer of laudanosine was low at 14 +/- 5%, with blood levels of 0.101 +/- 0.032 microM.L-1 in the umbilical vein. Newborns in the two groups were comparable in terms of Apgar scores at one, five and ten minutes, as well as for NACS scores (neurological and adaptive capacity scoring test) at two and 24 hours after birth. However, at 15 min after birth, only 55% of newborns in whom the mothers received atracurium had a normal NACS score (greater than or equal to 35/40) compared with 83% of newborns in whom the mothers received d-tubocurarine (P less than 0.05). Further analysis of the five variables related to active muscle tone revealed that the modal score for active extension of the neck of newborns from the atracurium group was lower than for newborns from the d-tubocurarine group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clindamycin-induced neuromuscular blockade

The purpose of this article is to report the case of a patient who developed prolonged neuromuscular block after a large dose of clindamycin (2400 mg). A 58-yr-old, 65 kg woman with severe rheumatoid arthritis was admitted for wrist arthrodesis. After d-tubocurarine (3 mg) and fentanyl (1.5 μg · kg^?1), anaesthesia was indúced with thiopentone (4 mg · kg^?1) followed by succinycholine (1.5 mg · kg^?1) and was maintained with N₂O in O₂ and isoflurane (0.75-1.0% end tidal) and ventilation was controlled. No further neuromuscular relaxants were given although full return of neuromuscular activity in response to train-of-four and 100 Hz tetanic stimulation was observed after succinylcholine. An overdose of clindamycin (2400 mg, instead of the intended 600 mg) was given iv soon after the start of surgery. At the end of surgery, 75 min later, the patient made no attempt at spontaneous ventilation, was unresponsive to painful stimuli and naloxone (0.2 mg iv) was ineffective. Controlled ventilation was continued in the Recovery Room where neuromuscular testing showed a train-of-four ratio of 0.27 which improved to only 0.47 five minutes after calcium chloride (1.5 mg · kg^?1 iv), and to 0.62 after edrophonium (20 mg) and neostigmine (2 mg). Nine hours later the patient began to cough, the TOF had returned to 1.0 and two hours later the trachea was extubated and spontaneous ventilation was resumed. Large doses of clindamycin can induce profound, long-lasting neuromuscular blockade in the absence of non-depolarizing relaxants and after full recovery from succinylcholine has been demonstrated.     

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.     

Alfentanil infusion for sedation in infants and small children during cardiac catheterization

We have analyzed several sedation techniques for paediatric cardiac catheterization which offer stable conditions for a few hours investigation, and maintain spontaneous breathing. In the present study, after premedication with oral flunitrazepam 0.1 mg.kg-1, 14 children aged 1-17 mo were sedated with an individually titrated alfentanil infusion. Every patient was sedated to a level which produced no reaction to pain or any discomfort. The induction dose and the maintenance requirement of alfentanil were 24 +/- 8 micrograms.kg-1 and 32 +/- 8 micrograms.kg-1.hr-1 (mean +/- SD), respectively. These doses were less in cyanotic than in acyanotic patients: 21 +/- 6 vs 28 +/- 8 micrograms.kg-1 and 29 +/- 10 vs 34 +/- 3 micrograms.kg-1.hr-1, respectively (P less than 0.05). The mean plasma concentration of alfentanil during maintenance of sedation was 79 +/- 23 ng.ml-1. Ventilation of two children was assisted for a short time after an incremental bolus of alfentanil. It is concluded that an alfentanil infusion technique with close monitoring of breathing is a practical sedation method for paediatric cardiac catheterization.     

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.     

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.     

Epidural morphine reduces halothane MAC in the dog

Morphine, 0.1 mg.kg-1 was administered epidurally on two different occasions to ten dogs to determine the effect of two different volumes of saline dilution, 0.13 and 0.26 ml.kg-1, on the minimum alveolar concentration (MAC) of halothane as determined by subcutaneous electrical current applied to the fore and hind limbs in a random order. Following MAC determination with halothane alone, epidural morphine was administered and MAC was redetermined. Epidural morphine significantly reduced, P less than 0.001, the MAC of halothane for fore and hind legs in both volume groups; from 1.04 +/- 0.038 to 0.68 +/- 0.034 and 0.60 +/- 0.017 for for and hind limbs, respectively, in the large volume group, and from 0.96 +/- 0.038 to 0.66 +/- 0.088 and 0.60 +/- 0.030 for fore and hind limbs, respectively, in the small volume group. The reduction in MAC was significantly greater, P less than 0.025, in the hind limb. This study indicates that epidural morphine reduces the halothane requirements in the dog in a segmental manner. The volume of administration was not shown to be critical. Epidural morphine, 0.1 mg.kg-1, diluted in 0.13 to 0.26 ml.kg-1 saline produces significant analgesia in the dog as far forward as the fore limb and will reduce the halothane requirement to permit surgery.     

Continuous oxygen saturation monitoring following rectal methohexitone induction in paediatric patients

Rectal methohexitone has been used to induce anaesthesia in paediatric patients for a number of years. This study was conducted in order to confirm the safety of this method of induction for uncomplicated routine paediatric patients. Children between the ages of six months and six years were considered candidates for induction with methohexitone (10%, 25-30 mg.kg-1). Patients were monitored with a continuous oxygen saturation recording. Forty-nine patients participated in this study and anaesthesia was induced successfully in 44. The mean age of the patients was 2.7 +/- 1.6 yr. The mean weight was 13.8 +/- 4.3 kg and the mean dose of methohexitone for successful induction was 27.0 +/- 3.0 mg.kg-1. Continuous oximeter recordings were available in 31 of the 42 patients who allowed oximeter placement prior to administration of methohexitone. No major desaturation events were noted in any patient. Two brief episodes of desaturation occurred. One with a nadir of 90% which lasted for 45 sec and another with a nadir of 86% which lasted for 26 sec. Both children had their heads flexed over their parents' shoulders at the time of the event resulting in partial airway obstruction. Both of these episodes were the result of upper airway obstruction which was clinically diagnosed by the anesthetist and readily corrected by repositioning the head. This study confirms the efficacy and safety of rectal methohexitone for induction of general anaesthesia in children. Mechanical obstruction of the airway following induction seems to be the most likely cause for oxygen desaturation. Monitoring of pulse oximetry does not appear necessary provided the child is carefully observed for adequacy of air exchange.     

Bolus doses of esmolol for the prevention of perioperative hyper-tension and tachycardia

The effectiveness of esmolol, an ultra short-acting cardioselective beta blocker, in the prevention and treatment of post-intubation haemodynamic perturbations, was investigated. Forty-eight ASA physical status I and II patients undergoing hysterectomy were randomly assigned to receive a single intravenous bolus of placebo, esmolol 100 mg, or esmolol 200 mg in a double-blind fashion. This was administered over 15 sec, and immediately followed by thiopentone 3-5 mg.kg-1, succinylcholine 1.5 mg.kg-1, and tracheal intubation 90 sec later. The heart rate following induction of anaesthesia was lower in the esmolol 200 mg group (P less than 0.01); following intubation, the increase in heart rate in the placebo group was greater than in the esmolol groups (P less than 0.05). The systolic blood pressure post-induction was lower in the esmolol 200 mg group (P less than 0.05); following intubation, however, no significant differences were seen among groups in systolic, diastolic, or mean blood pressures. Following tracheal intubation, the incidence of ventricular arrhythmias was lower in the esmolol groups (P less than 0.05). In summary, esmolol in 100 mg and 200 mg doses was effective in mitigating the haemodynamic response following tracheal intubation.     

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.     

Cumulative dose-response curves for atracurium in patients with myasthenia gravis

The potency of atracurium was determined in five patients with moderate to severe generalized myasthenia gravis undergoing thymectomy. Train-of-four stimulation was applied to the ulnar nerve and the force of contraction of the adductor pollicis was measured. Cumulative dose-response curves were obtained during thiopentone-nitrous oxide-fentanyl anaesthesia. The average time to complete the dose-response studies was 12.7 +/- 1.5 minutes. The ED50, ED90 and ED95 of atracurium were (mean +/- SEM) 0.07 +/- 0.01, 0.12 +/- 0.22, and 0.14 +/- 0.04 mg.kg-1, respectively. The time to 25 per cent first twitch recovery was 35 +/- 4 min following maximum blockade. Ten normal patients were studied in the same manner. Their ED50, ED90 and ED95 were 0.13 +/- 0.01, 0.21 +/- 0.02 and 0.24 +/- 0.03 mg.kg-1, respectively. These results demonstrated that, in patients with moderate to severe generalized myasthenia gravis, atracurium was 1.7-1.9 times as potent as in normal individuals.     

Systemic lidocaine and human somatosensoryevoked potentials during sufentanil-isoflurane anaesthesia

The effect of systemically administered lidocaine on somatosensory evoked potentials (SSEPs) during general anaesthesia has not been widely reported. Knowledge of the influence of anaesthetic agents on evoked potentials assists in interpreting evoked potential waveforms. Accordingly, we studied the behaviour of cortical and subcortical (recorded at the second cervical vertebra) SSEPs after administration of intravenous lidocaine (3 mg.kg-1 bolus followed by infusion at 4 mg.kg-1.hr-1) during a sufentanil-based anaesthetic regimen in 16 patients undergoing abdominal or orthopaedic surgery. When compared to awake baseline recordings, the sufentanil-nitrous oxide, low-dose isoflurane anaesthetic depressed N1 amplitude by approximately 40% and prolonged latency by 10%. Fifteen minutes after establishment of this anaesthetic, the amplitude and latency of N1 were 1.13 +/- 0.56 microV and 19.81 +/- 1.63 msec, respectively. Within five minutes of adding lidocaine, amplitude decreased further to 0.84 +/- 0.39 microV (P = 0.001), while latency was extended to 20.44 +/- 1.48 msec (P = 0.01). Lidocaine did not affect cervical amplitude and prolonged latency only minimally. Despite the observed effects on amplitude and latency, SSEP waveforms were preserved and interpretable. Plasma lidocaine levels obtained at 5, 20, and 40 minutes after lidocaine were 5.17 +/- 1.33, 3.76 +/- 1.14, and 3.66 +/- 0.9 micrograms.dl-1, respectively. Our results indicate that systemically administered lidocaine at therapeutic plasma levels acts synergistically with a sufentanil-based anaesthetic to depress the amplitude and prolong the latency of SSEPs.