The effect of lidocaine on neutrophil respiratory burst during induction of general anaesthesia and tracheal intubation

BACKGROUND AND OBJECTIVE: Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst. METHODS: Twenty ASA I and II patients, aged 18-60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 microg kg-1), thiopental (4-6 mg kg-1), isoflurane (end-tidal concentration 0.5-1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg-1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline. RESULTS: Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 +/- 8.2% (group L) and 88.5 +/- 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 +/- 23.6%) and after (94.4 +/- 16.6%) tracheal intubation. CONCLUSION: Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.     

Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation

We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response.      

The effect of atracurium, vecuronium and pancuronium on heart rate and arterial pressure in normal individuals

Heart rate and rhythm (from ECG) and systolic, diastolic and mean arterial pressures (using an oscillotonometer) were measured for 30 min following administration of atracurium 0.5 mg kg-1 (n = 20), vecuronium 0.1 mg kg-1 (n = 20) or pancuronium 0.1 mg kg-1 (n = 20) during steady-state anaesthesia, with nitrous oxide, oxygen and either 0.75% halothane or fentanyl 4-5 micrograms kg-1, in the absence of any surgical stimulation. Whereas atracurium and vecuronium were associated with only small and clinically unimportant changes in heart rate, pancuronium produced a marked and significant increase associated with a junctional rhythm in four patients. Atracurium produced no significant changes in arterial pressure, vecuronium produced a significant fall (20 mmHg) in diastolic pressure during halothane anaesthesia and pancuronium a significant increase in mean arterial pressure with both anaesthetic techniques. No serious bradycardias were observed with either atracurium or vecuronium. Five patients showed cutaneous signs of histamine liberation after administration of atracurium.     

Does methylprednisolone potentiate the effects of dobutamine during thoracic epidural analgesia?

The cardiovascular effects of dobutamine (DOB) combined with methylprednisolone (MP) were studied during thoracic epidural analgesia (TEA) in 59 patients undergoing operations on upper abdomen. To establish TEA, 8-10 ml of lidocaine 20 mg.ml-1 was injected into the epidural space through the T8-T9 interspace. The patients was intubated after fentanyl 0.2 mg, thiopental 3 mg.kg-1 and vecuronium 0.2 mg.kg-1. Anesthesia was maintained with 67% N2O, 33% O2 and 0.6% enflurane and DOB was infused at a rate of 5 micrograms.kg-1.min-1 during the surgical operation. Systolic blood pressure and urinary output after TEA did not decrease in the two groups, pretreated with MP 5 mg.kg-1 one hour or immediately before TEA, but decreased in the control group without MP injection. Heart rate showed no significant changes after TEA in all groups. We conclude that MP may potentiate the cardiovascular effects of DOB during TEA.     

Propofol in urological endoscopy in elderly patients. Comparison with methohexital

Twenty patients undergoing cystoscopy (group A) and forty patients undergoing transurethral resection (group B), aged more than 65 years, were anaesthetized. Duration of anaesthesia was less than 15 min for cystoscopy, and more than 30 min for transurethral resection. No premedication was given. The patients were ASA I or ASA II. Group A patients were allocated randomly to receive either 1.5 mg . kg-1 propofol (n = 10) or 2 mg . kg-1 methohexitone (n = 10) for induction of anaesthesia. Anaesthesia was maintained using incremental doses of propofol or methohexitone and 60% N2O with a face-mask. Forty group B patients undergoing transurethral resection were randomly assigned to four equal groups (PB: propofol 1.5 mg . kg-1; MB: methohexitone 2 mg . kg-1; PF: propofol and 1.5 micrograms . kg-1 fentanyl; PFV: propofol, 2 micrograms . kg-1 fentanyl and 0.1 mg . kg-1 vecuronium). Suxamethonium (1 mg . kg-1; groups PB, MB and PF) and vecuronium (0.1 mg . kg-1; group PFV) were given to facilitate endotracheal intubation. Anaesthesia was maintained by infusion of propofol or methohexitone, using a calibrated pump started immediately after intubation. Ventilation was controlled only in group PFV. Induction with 1.5 mg . kg-1 propofol resulted in stopping counting after 62 s and loss of the eye-lash reflex after 84 s versus 47 and 67 s respectively with methohexitone. The anaesthesist's assessment was favourable for cystoscopy with propofol and methohexitone; recovery times were similar for the two drugs in cystoscopy lasting less than 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of intratracheal lidocaine spray on circulatory responses to endotracheal intubation

The effect of intratracheal lidocaine spray (0.5, 1.0, 2.0 mg.kg-1) on blood pressure and heart rate changes to endotracheal intubation was evaluated in 20 ASA I-II patients. After thiamylal induction, 15 patients received lidocaine spray with LTA kit. Mean arterial blood pressure and heart rate were recorded for 10 min every 30 sec and analysis of plasma lidocaine concentrations were also performed. In the control group, mean arterial blood pressure increased significantly compared with the pre-anesthetic values for one min, and with all spray groups at one min after intubation. Heart rate increased significantly at 30 sec after intubation only in the control group. Since the plasma lidocaine concentrations at intubation were below 1.5 micrograms.ml-1, we conclude that intratracheal lidocaine spray depresses the circulatory response to intubation by its local surface analgesic effect.     

Bolus dose remifentanil for control of haemodynamic response to tracheal intubation during rapid sequence induction of anaesthesia

The effect of three bolus doses of remifentanil on the pressor response to laryngoscopy and tracheal intubation during rapid sequence induction of anaesthesia was assessed in a randomized, double-blind, placebo- controlled study in four groups of 20 patients each. After preoxygenation, anaesthesia was induced with thiopental 5-7 mg kg-1 followed immediately by saline (placebo) or remifentanil 0.5, 1.0 or 1.25 micrograms kg-1 given as a bolus over 30 s. Cricoid pressure was applied just after loss of consciousness. Succinylcholine 1 mg kg-1 was given for neuromuscular block. Laryngoscopy and tracheal intubation were performed 1 min later. Arterial pressure and heart rate were recorded at intervals until 5 min after intubation. Remifentanil 0.5 microgram kg-1 was ineffective in controlling the increase in heart rate and arterial pressure after intubation but the 1.0 and 1.25 micrograms kg-1 doses were effective in controlling the response. The use of the 1.25 micrograms kg-1 dose was however, associated with a decrease in systolic arterial pressure to less than 90 mm Hg in seven of 20 patients.      

Neuromuscular and cardiovascular effects of pipecuronium

Pipecuronium bromide (Arduan) is a bisquaternary, steroid-type neuromuscular blocking agent in clinical use in Eastern Europe. Before its introduction into clinical practice in the USA, in the first phase of this study the neuromuscular potency of pipecuronium was determined under "balanced" and enflurance anaesthesia by the cumulative log dose-response method in 30 patients each. In the second phase the intubation and onset times, clinical duration of the first and repeated doses, spontaneous recovery index, reversibility of its residual neuromuscular effect by an anticholinesterase and its effect on heart rate and blood pressure was compared with the same variables observed in patients, anaesthetized with identical techniques but who had received vecuronium or pancuronium. The neuromuscular potency of pipecuronium was greater under enflurane (ED95 = 23.6 +/- 1.1 micrograms.kg-1 (mean +/- SEM)] than under balanced (ED95 = 35.1 +/- 17 micrograms.kg-1) anaesthesia. Pipecuronium was more potent than vecuronium under both balanced (ED95 = 45.8 micrograms.kg-1) and enflurane anaesthesia (ED95 = 27.4 micrograms.kg-1). Following the administration of 2 x ED95 doses there were no clinically significant differences in the intubation or onset times of pipecuronium, vecuronium and pancuronium. Under balanced anaesthesia the clinical duration of 2 x ED95 dose of pipecuronium (110.5 +/- 0.3 min) or pancuronium (115.8 +/- 8.1 min) were similar and about three times longer than that of vecuronium (36.3 +/- 2.1 min). The recovery indices of pipecuronium (44.5 +/- 8.2 min) and pancuronium (41.3 +/- 4.2 min) were also similar and about three times longer than that of vecuronium (14.3 +/- 1.4 min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Induction characteristics of thiopentone/suxamethonium, propofol/alfentanil or halothane alone in children aged 1-3 years.

The aim of this study was to compare the effect of three different induction techniques, with or without neuromuscular block, on tracheal intubation, haemodynamic responses and cardiac rhythm. Ninety children, aged 1-3 years, undergoing day-case adenoidectomy were randomly allocated to three groups: group TS received thiopentone 5 mg kg-1 and suxamethonium 1.5 mg kg-1, group H 5 Vol.% halothane and group PA alfentanil 10 micrograms kg-1 and propofol 3 mg kg-1 for induction of anaesthesia. No anti-cholinergics were used. Holter-monitoring of the heart rate and rhythm was started at least 15 min before induction of anaesthesia and continued until 3 min after intubation. Tracheal intubation was performed by an anaesthetist blinded to the induction method and judged as excellent, moderate or poor according to ease of laryngoscopy, position of vocal cords and incidence of coughing after intubation. Tracheal intubation was successful at the first attempt in all children in groups TS and H and but only in 80% in group PA (P = 0.001). Intubating conditions were excellent in 22 (73%), 22 (73%) and one (3%) of the patients in groups TS, H and PA, respectively (P = 0.001). Cardiac dysrhythmias (supraventricular extrasystole or junctional rhythm) occurred in two (7%) patients in groups PA and H each (NS). Bradycardia occurred in 0 (0%), four (14%) and six (21%) children in groups TS, H and PA, respectively (P = 0.007 PA vs. TS, P = 0.03 H vs. TS). In conclusion, induction of anaesthesia with propofol 3 mg kg-1 and alfentanil 10 micrograms kg-1 without neuromuscular block did not provide acceptable intubating conditions in children 1-3 years, although it preserved arterial pressure better than thiopentone/suxamethonium or halothane. Cardiac dysrhythmias were few regardless of the induction method.     

Use of diltiazem in the anesthetic management of epinephrine predominant pheochromocytoma]

This report describes a case of epinephrine predominant pheochromocytoma successfully managed intraoperatively with an infusion of diltiazem. A 50-yr-old woman with a 10-yr history of diabetes mellitus was admitted to the hospital because of thirst and general fatigue. A cystic left adrenal tumor was found on computed tomographic scan. Although resting plasma catecholamine levels were normal, plasma norepinephrine and epinephrine levels obtained from the left adrenal vein were 1.6 ng.ml-1 (normal, 0.04-0.35) and 6.2 ng.ml-1 (normal, less than 0.12), respectively. Diltiazem was administered i. v. at a rate of 3 micrograms.kg-1.min-1 before induction of anesthesia. Anesthesia was induced with enflurane 2-3% and nitrous oxide in oxygen, followed by tracheal intubation facilitated with vecuronium. Anesthesia was maintained with enflurane 1-3% and nitrous oxide in oxygen. Paralysis was maintained with vecuronium. Hypertension during the manipulation of the tumor was controlled by increasing the inspired concentration of enflurane or by increasing the infusion rate of diltiazem to 5 micrograms.kg-1.min-1. There was no tachyarrhythmia. The infusion of diltiazem was continued until the draining vein from the tumor had been ligated. Hypotension, after removal of the tumor, was treated by the rapid infusion of fluid. Plasma norepinephrine and epinephrine levels during tumor manipulation were 1.18 ng.ml-1 and 6.57 ng.ml-1, respectively.     

Benzodiazepines and neuromuscular blocking drugs in patients

The interaction between four benzodiazepines (diazepam, lorazepam, lormetazepam and midazolam) and two nondepolarizing neuromuscular blocking drugs (vecuronium and atracurium) was investigated in 113 patients during general anaesthesia. Neuromuscular function was monitored by recording the mechanical twitch tension of the adductor pollicis muscle of the thumb in response to ulnar nerve stimulation with single supramaximal stimuli of 0.2 ms at 0.1 Hz. In the first group of patients a benzodiazepine (diazepam 20 mg, lorazepam 5 mg, lormetazepam 2 mg or midazolam 15 mg), was injected i.v. 15 min before a single bolus of vecuronium 45 micrograms kg-1. In the second group of patients suxamethonium 1 mg kg-1 was given for endotracheal intubation, and 30 min later the patients received atracurium 200 micrograms kg-1. Fifteen min before injection of atracurium one of the same benzodiazepines as in the first group was injected i.v. Comparisons were made with control patients receiving thiopentone. Neither benzodiazepine caused significant potentiation of neuromuscular blocking agents in comparison with control. With midazolam, however, the duration to 25% and to 75% recovery of the twitch height after vecuronium was significantly longer than with diazepam. The time to 25% recovery of the twitch height after atracurium was significantly longer in patients receiving midazolam than in those receiving diazepam. The recovery index was not influenced by the four benzodiazepines.     

Effects of urapidil on the cardiovascular response to intratracheal intubation]

The effects of urapidil on the haemodynamic response to endotracheal intubation were compared to that of placebo in two groups of 25 patients scheduled for general surgery. Normal saline solution or 0.4 mg.kg-1 urapidil were injected 3 min before induction of anaesthesia with 3 micrograms.kg-1 fentanyl, 0.3 mg.kg-1 etomidate and 0.1 mg.kg-1 vecuronium. Blood pressure (Pasys, Padia, Pa) and heart rate were measured continuously by servoplethysmomanometry before giving the test drug (T0), at the time when the lowest blood pressure was recorded during the three minute period between giving the drug and induction (T1), at the time when the lowest blood pressure was recorded during the three minute period between induction and endotracheal intubation (T2), at the time when the highest blood pressure was recorded immediately after intubation (T3), three minutes after intubation (T4), five minutes after intubation (T5), and at the time when the lowest blood pressure was recorded after surgery had been started (T6). It was planned to give a 25 mg urapidil dose to any patient, from either group, who had a Pasys greater than 200 mmHg for more than 60 sec. Giving urapidil lowered Pasys (T1) by 16%, whilst heart rate increased by 12%. The blood pressure peak due to endotracheal intubation was lower in those patients who had been given urapidil than in the placebo group (T3; p less than 0.05). Six patients in the latter group required the 25 mg urapidil dose, versus 2 in the urapidil group. The preventive effects of urapidil seem to be similar to those obtained with other antihypertensive agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of remifentanil on the haemodynamic response to orotracheal intubation

We have examined the effect of remifentanil on the haemodynamic response to orotracheal intubation in a randomized, double-blind study. We studied 40 patients allocated to one of four groups of 10 each, to receive the following immediately before induction of anaesthesia: remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; saline placebo only; glycopyrrolate 200 micrograms and remifentanil 1 microgram kg-1 bolus over 30 s, followed by an infusion of 0.5 microgram kg-1 min-1; or glycopyrrolate 200 micrograms only. Anaesthesia was induced with propofol, vecuronium and 1% isoflurane with 66% nitrous oxide in oxygen. The trachea was intubated under direct laryngoscopy 3 min after induction of anaesthesia. Arterial pressure and heart rate were measured non- invasively, immediately before induction of anaesthesia and then at 1- min intervals. Remifentanil was found to effectively attenuate the pressor response to intubation (P < 0.05 for the increase in mean arterial pressure; P < 0.01 for the increase in heart rate). In the absence of a concurrent vagolytic agent, remifentanil was associated with bradycardia or hypotension, or both, in five of 10 patients, compared with one patient who received remifentanil and glycopyrrolate.      

Thoracic epidural anaesthesia combined with enflurane anaesthesia reduces atrioventricular conduction in dogs

Cardiac electrophysiological variables during thoracic epidural lidocaine (TEL) were compared with those during continuous intravenous lidocaine (IVL) infusion in 14 mongrel dogs anaesthetized with enflurane in order to investigate the combined effects of thoracic epidural anaesthesia (TEA) and enflurane anaesthesia on intracardiac conduction. Thoracic epidural lidocaine suppressed intracardiac conduction. Sinus cycle length (SCL) and Atrium-His (AH) interval increased by 9 and 11 per cent respectively (P less than 0.05), 30 min after TEL. Intravenous lidocaine did not increase either SCL or AH. The functional refractory period of the atrioventricular node increased five per cent above the control value 15 min after TEL (P less than 0.05), while it was unchanged in the IVL group. The mean plasma concentrations of lidocaine ranged from 0.48 +/- 0.07 to 1.00 +/- 0.14 micrograms.ml-1 in the TEL group and from 0.98 +/- 0.13) to 1.21 +/- 0.15 micrograms.ml-1 in the IVL group. There were no significant differences in plasma concentrations of lidocaine in both groups during the observation period. Therefore, it is concluded that the depressant effects of TEA on intracardiac conduction were caused by blocking of the sympathetic efferent activity. Caution may be advised in administering TEA when cardiac conduction is already compromised.     

Plasma determination of lidocaine and bupivacaine after caudal anesthesia in children

Serum concentrations of lidocaine and plasma concentrations of bupivacaine were measured so as to assess the risk of systemic toxicity following their administration by the caudal route in children, and study their pharmacokinetic profiles according to age. The serum concentrations of lidocaine were measured by immuno-enzymology in 37 children (23 +/- 13 kg) during the first hour after administration of 7 mg . kg-1. The plasma concentrations of bupivacaine were measured by high performance liquid chromatography in 40 children (18.03 +/- 8.90 kg) during the first hour after administration of 2.5 mg . kg-1. The greatest concentrations observed between 15 and 30 min after the injection were of 2.40 +/- 0.86 micrograms . ml for lidocaine and 0.93 +/- 0.44 microgram . ml-1 for bupivacaine. Higher values were observed in infants weighing less than 12 kg where they reached 2.89 +/- 0.72 and 1.52 +/- 0.68 micrograms . ml-1 respectively. These results showed that caudal anaesthesia with lidocaine (7 ml . kg-1) and bupivacaine (2.5 ml . kg-1) was a safe technique for children, giving average plasma concentrations inferior to toxic values. However, it seemed prudent not to give more than the prescribed doses in the small infant.     

Pharmacokinetics of vecuronium during acute isovolaemic haemodilution

To evaluate the effect of acute isovolaemic haemodilution on the pharmacokinetics of vecuronium, we studied 13 patients undergoing haemodilution during surgery and 13 control patients. General anaesthesia was induced with thiopentone 4-6 mg kg-1 and fentanyl 2-4 micrograms kg-1, and maintained with enflurane and 60% nitrous oxide in oxygen. The haemodilution patients underwent major elective plastic surgery with an anticipated surgical loss of more than 600 ml. Haemodilution was achieved by drainage of venous blood and i.v. infusion of lactated Ringer's solution and 6% dextran, during which the packed cell volume and haemoglobin concentration decreased from 45% to 28.1% and from 14.7 g dl-1 to 9.1 g dl-1, respectively. After administration of a bolus of vecuronium 100 micrograms kg-1, an improved fluorimetric assay was used to measure the plasma concentrations of vecuronium for 5 h. The results showed that the disposition kinetics of vecuronium were best described mathematically by a three-compartment open model in the two groups. The mean volume of the central compartment and volume of distribution at steady state were 42.3 (SD 11.8) ml kg-1 and 168.4 (31.5) ml kg-1, respectively, in control patients, and significantly greater (55.2 (13.4) ml kg-1 and 225.9 (53.3) ml kg-1) in the haemodilution patients (P < 0.05). The elimination half-life was 50.3 (11.5) min in control patients and significantly greater (68.2 (15.1) min) in the haemodilution patients (P < 0.05). The half-lives of fast distribution and distribution, mean residual time, area under the plasma concentration curve and plasma clearance were unchanged in patients who underwent haemodilution compared with the control group.      

Oral premedication with clonidine: effects on stress responses during general anaesthesia

The effect of clonidine (4.5 micrograms kg-1) on haemodynamics and hormonal stress responses was evaluated in 21 female patients undergoing breast surgery. The standardized general anaesthesia included diazepam as premedicant, thiopentone, enflurane, N2O, fentanyl and vecuronium. Venous plasma concentrations of noradrenaline, adrenaline, growth hormone, vasopressin, and cortisol were assayed at various times before, during and after surgery. Clonidine attenuated the sympathoadrenal response; arterial blood pressure and heart rate increases in association with intubation were lower in clonidine-premedicated patients. Noradrenaline levels were lower throughout and 3 h after surgery in the clonidine group (P less than 0.05). Adrenaline levels were lower in this group 2 min after intubation (P less than 0.05). Growth hormone, vasopressin and cortisol plasma levels were increased at the end of and after surgery, with no differences between the groups. In spite of the effect on sympathoadrenal response, clonidine did not have any significant additive anxiolytic effect. Statistically significant differences were not found as to need for postoperative analgesics.     

Cerebrospinal fluid concentrations of propofol during anaesthesia in humans

The concentration of propofol in and surrounding the human brain during propofol anaesthesia is unknown. We measured simultaneously the concentration of propofol in cerebrospinal fluid (CSF) from an indwelling intraventricular catheter and the concentration in arterial blood in five neurosurgical patients before, during induction (at 2.5 and 5 min) and during a maintenance propofol infusion (at 15 and 30 min). After induction of anaesthesia with propofol 2 mg kg-1, anaesthesia was maintained with an infusion of 8 mg kg-1 h-1 for 15 min and then reduced to 6 mg kg-1 h-1. The plasma concentration of propofol increased rapidly during induction and reached a plateau concentration of mean 2.24 (SD 0.66) micrograms ml-1 after 5 min. The concentration of propofol in CSF showed a slower increase during induction and remained almost constant at 35.5 (19.6) ng ml-1 at 15-30 min after induction. The CSF concentration of propofol that we measured was 1.6% of the plasma concentration and consistent with the high protein binding of the drug in plasma.      

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.     

The influence of alfentanil on the intubating conditions after priming with vecuronium

The ability of alfentanil 15 micrograms kg-1 or 30 micrograms kg-1 to improve intubating conditions was studied in four groups of 25 ASA class 1 patients. Induction of anaesthesia was with thiopentone 5 mg kg-1. Neuromuscular blockade was induced with vecuronium using the priming principle. The priming dose, priming interval and intubating dose were 0.01 mg kg-1, 4 min, and 0.1 mg kg-1, respectively. Intubation was attempted 1 min after the intubating dose. Intubating conditions were judged unacceptable in about 30% of the patients belonging to the control groups. Alfentanil 15 micrograms kg-1, when administered 65 s before intubation, reduced the incidence of coughing and diaphragmatic movement (P less than 0.05) but did not reduce the incidence of overall unacceptable intubating conditions. Alfentanil 30 micrograms kg-1, however, reduced the incidence of vocal cord movement (P less than 0.005) as well as coughing and diaphragmatic movement (P less than 0.002). Alfentanil 30 micrograms kg-1 reduced the incidence of unacceptable intubating conditions from about 30% to 4% (P less than 0.02).