Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: A comparison of propofol and isoflurane

The purpose of this study was to compare two anaesthetic protocols for haemodynamic instability (heart rate (HR) or mean arterial pressure (MAP) <80 or > 120% of ward baseline values) measured at one-minute intervals during carotid endarterectomy (CEA). One group received propofol/alfentanil (Group Prop; n = 14) and the other isoflurane I alfentanil (Group Iso; n = 13). Periods of haemodynamic instability were correlated to episodes of myocardial ischaemia as assessed by Holler monitoring (begun the evening before surgery and ceasing the morning of the first postoperative day). In Group Prop, anaesthesia was induced with alfentanil 30 μg · kg^?1 rv, propofol up to 1.5 mg · kg^?1 and vecuronium 0.15 mg · kg^?1, and maintained with infusions of propofol at 3–12 mg · kg^?1· hr^?1 and alfentanil at 30 μg · kg^?1 · hr^?1. In Group Iso, anaesthesia was induced with alfentanil and vecuronium as above, thiopentone up to 4 mg · kg^?1 and maintained with isoflurane and alfentanil infusion. Phenylephrine was infused to support MAP at 110 ± 10% of ward values during cross-clamp of the internal carotid artery (ICA) in both groups. Emergence hypertension and/or tachycardia was treated with labetalol, diazoxide or propranolol. Myocardial ischaemia was defined as ST-segment depression of >-1 mm (60 msec past the J-point) persisting for >-one minute. For the entire anaesthetic course (induction to post-emergence), there was no difference between groups for either duration or magnitude outside the <80 or >120% range for HR or MAP. However, when the period of emergence from anaesthesia (reversal of neuromuscular blockade to post-extubation) was assessed, more patients were hypertensive (P = 0.004) and required vasodilator therapy in Group Iso (10/ 13 vs 5/14; P = 0.038 Fisher’s Exact Test). The mean dose of labetalol was greater in Group Iso (P = 0.035). No patient demonstrated myocardial ischaemia during ICA cross-clamp. On emergence, 6/13 patients in Group Iso demonstrated myocardial ischaemia compared with 1/14 in Group Prop (P = 0.029). Therefore, supporting the blood pressure with phenylephrine, during the period of ICA cross-clamping, appears to be safe as we did not observe any myocardial ischaemia at this time. During emergence from anaesthesia, haemodynamic instability was associated with myocardial ischaemia. Under these specific experimental conditions, with emergence, hypertension and myocardial ischaemia were more prevalent with more frequent pharmacological interventions in patients receiving isoflurane.     

Atropine-induced heart rate changes: a comparison between midazolam-fentanyl-propofol-N2O and midazolam-fentanyl-thiopentone-enflurane-N2O anaesthesia

Atropine-induced heart rate (HR) changes were studied in 19 patients (ASA physical status I) during anaesthesia maintained predominantly with propofol-N₂O or thiopentone-enflurane-N₂O. Ten patients (Group A) received midazolam (0.07 mg · kg^?1), fentanyl (1 μg · kg^?1), propofol (2 mg · kg^?1) and succinylcholine (1 mg · kg^?1). Following tracheal intubation, anaesthesia was maintained with propofol (6 mg · kg^?1 · hr^?1), N₂O (67 per cent) and O₂ (33 per cent). In nine patients (Group B) thiopentone (4 mg · kg^?1) was substituted for propofol and anaesthesia maintained with N₂O (67 per cent) O₂ (33 per cent), and enflurane (0.5 per cent inspired concentration). The study was non-randomised because Group B patients were only included if HR before administration of atropine < 90 beats · min^?1. IPPV was performed in all patients using a Manley ventilator (minute vol. 85 ml · kg^?1; tidal vol. 7 ml · kg^?1). Ten minutes after tracheal intubation, incremental doses of atropine (equivalent cumulative doses: 1.8, 3.6, 7.2, 14.4, 28.8 μg · kg^?1) were administered at two-minute intervals and HR responses calculated during the last 45 sec of each intervening period. No differences were observed between the groups following 1.8 and 3.6 μg · kg^?1 atropine, but propofol-N₂O anaesthesia was associated with reduced responses (P < 0.01) following 7.2, 14.4 and 28.8 μg · kg^?1 atropine. These results suggest that there is a predominance of parasympathetic influences during propofol-N₂O anaesthesia compared with thiopentone-enflurane-N₂O anaesthesia.     

Oral clonidine premedication reduces vomiting in children after strabismus surgery

This is a prospective randomized double-blind trial conducted to determine whether preoperative orally administered clonidine causes or potentiates postoperative vomiting in 140 children (3–12 yr) undergoing strabismus surgery. They were all inpatients and classified randomly into four groups (n = 35 each); placebo (control), diazepam 0.4 mg · kg^?1, clonidine 2 μg · kg^?1, and clonidine 4 μg · kg^?1. These agents were administered 93–112 min (mean: 100 min) before the anticipated time of induction of anaesthesia. All children received inhalational anaesthesia with halothane and nitrous oxide in oxygen.’ Muscle relaxation in all patients was obtained with vecuronium and residual neuromuscular blockade was antagonized with neostigmine and atropine before tracheal extubation. Diclofenac suppository was prescribed to prevent postoperative pain. No opioids or postoperative antiemetics were administered. All children remained in hospital for two days postoperatively. The incidence and frequency of vomiting were compared in the groups with Kruskall-Wallis Rank test. Clonidine 4 μg · kg^?1 caused a lower incidence and frequency of vomiting than did placebo and diazepam (incidence and frequency: 11% and 1,37% and 3, and 34% and 2 in clonidine 4 μg · kg^?1, placebo, and diazepam, respectively; P < 0.05 for clonidine 4 μg · kg^?1 vs placebo and diazepam). However, lowdose clonidine was ineffective. These data suggest that preanaesthetic medication with clonidine 4 μg · kg^?1 may be useful for preventing emesis following strabismus surgery. This property of clonidine indicates that it may be superior to other sedative premedicants such as diazepam and midazolam.     

Plasma concentrations after high-dose (45 mg · kg−1) rectal acetaminophen in children

Although the recommended dose of rectal acetaminophen (25–30 mg · kg^?1) is twice that for oral administration (10–15 mg · kg^?1), the literature justifies the use of a higher dose when acetaminophen is administered via the rectal route. We measured’ venous plasma acetaminophen concentrations resulting from 45 mg · kg^?1 of rectal acetaminophen in ten ASA 1, 15 kg paediatric patients undergoing minor surgery with a standardized anaesthetic. After induction of anaesthesia, a single 650 mg suppository (Abenol®, SmithKline Beecham Pharma Inc.) was administered rectally. Plasma was sampled at t = 0, 15, 30, 45, 60, 90, 120, 180, 240 min in the first five patients and at t = 0, 30, 60, 90, 120, 180, 240, 300, 420 min in the subsequent five. Acetaminophen plasma concentrations were determined’ using a TDxFLx® fluorescence polarization immunoassay (Abbott Laboratories, Toronto, Ontario). The maximum plasma concentration was 88 ± 39 μmol · L^?1 (13 ± 6 μg · ml^?1) and the time of peak plasma concentration was 198 ± 70 min (mean ± SD). At 420 min, the mean plasma concentration was 46 ± 18 μmol · L^?1 (7.0 ± 0.9 μg · ml^?1). No plasma concentrations associated with toxicity (> 800 μmol · L^?1) were identified. A 45 mg · kg^?1 rectal dose of acetaminophen resulted in peak plasma concentrations comparable with those resulting from 10–15 mg · kg^?1 of oral acetaminophen at three hours after suppository insertion. It is concluded that the delayed and erratic absorption of acetaminophen after rectal administration leads to unpredictable plasma concentrations. Rectal acetaminophen will not be consistently effective for providing rapid onset of analgesia in children.     

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.     

Left ventricular regional wall motion and haemodynamic changes following bolus administration of pipecuronium or pancuronium to adult patients undergoing coronary artery bypass grafting

The objective of this study was to compare the haemodynamic and myocardial effects of pipecuronium and pancuronium in patients undergoing coronary artery bypass grafting (CABG) during benzodiazepine/sufentanil anaesthesia. Twenty-seven ASA III–IV patients received lorazepam (1–3 mg) po and midazolam (<0.1 mg · kg^?1) iv before induction of anaesthesia with sufentanil (3–8 μg · kg^?1). Vecuronium (0.1 mg · kg^?1) was administered to facilitate tracheal intubation. According to random allocation, each patient received either pipecuronium (150 μg · kg^?1) or pancuronium (120 μg · kg^?1) after stemotomy but before heparinization. Mean arterial pressure, central venous pressure (CVP), pulmonary artery pressure (PAP), ST segment position and ECG (leads HI, V₅, AVF) were monitored continuously throughout the procedure. Thermodilution determinations of CO in triplicate were made immediately before, and at two and five minutes after muscle relaxant administration. Multiplane transoesophageal echocardiography (TEE, midpapillary short axis views of the left ventricle) images were continuously recorded from ten minutes before until ten minutes after muscle relaxant administration and graded by two experienced echocardiographic readers. Heart rate, MAP and CO increased after administration of pancuronium (by 13.6 beats · min^?1, 10.8 mmHg and 1.0 L · min^?1 respectively) but not after pipecuronium (P < 0.05). Evidence of myocardial ischaemia was not detected in any patients using ECG ST segment analysis or TEE assessment of left ventricular wall motion. We conclude that pancuronium caused increases in HR, MAP and CO but that neither pancuronium nor pipecuronium caused myocardial ischaemia.     

Attenuation of the catecholamine response to tracheal intubation with oral clonidine in children

We conducted a prospective, randomized, double-blind, controlled clinical trial to examine (1) whether plasma catecholamine (CA) concentrations increased in response to tracheal intubation in children, and (2) the effects of clonidine on the CA responses. Sixty children (ASA physical status I) aged 7– 13 yr were allocated to one of three groups (n = 20 for each group): diazepam 0.4 mg · kg^{? 1} (active control), clonidine 2 μg · kg^{? 1}, or clonidine 4 μg · kg^{? 1} po. These agents were administered 105 min before induction of anaesthesia followed by oral atropine 0.03 mg · kg^{? 1} given 60 min before anaesthesia which was induced with thiamylal 5 mg · kg^{? 1} and tracheal intubation was facilitated with vecuronium 0.2 mg · kg^{? 1}. Laryngoscopy, lasting 30 sec, was attempted two minutes after administration of the induction agents. Serial values for blood pressure, heart rate, and venous plasma CA concentrations were compared among the three groups and with the respective preinduction measurements. Children receiving diazepam or clonidine 2 μg · kg^{? 1} showed remarkable increases in systolic and diastolic blood pressures, heart rate, and plasma CA concentrations in response to tracheal intubation (P < 0.05). The increases were similar for the two regimens. These haemodynamic and CA changes were smaller in children receiving clonidine 4 μg · kg^{? 1} (P < 0.05). The haemodynamic responses were positively correlated with the CA responses. These findings indicate that tracheal intubation following rapid sequence induction of anaesthesia in children provokes a reflex increase in sympathetic activity characterized by increased plasma CA concentrations, and that attenuation of the cardiovascular changes with a high oral dose of clonidine may be due to suppression of the increase in sympathetic activity evoked by the intubation.     

Oral clonidine premedication attenuates the haemodynamic effects associated with ketamine anaesthetic induction in humans

Induction of anaesthesia is often associated with undesirable variations in blood pressure and heart rate. Clonidine has been demonstrated to attenuate many of these undesirable effects when used as a premedicant. Other alpha₂ adrenergic agonists have been used to ameliorate the cardiostimulatory effects of ketamine in animals but there are few data on the use of this combination in humans. The effect of oral clonidine premedication, 5 μg · kg^?1 on the haemodynamic changes induced by iv ketamine was studied in 42 patient volunteers. Ninety minutes before surgery, patients randomly received clonidine (C), diazepam (D), or a placebo (P) in a double-blinded fashion. Anaesthesia was induced with a ketamine infusion of I mg · kg^?1· min^?1 until loss of consciousness. Heart rate and phasic blood pressure were measured noninvasively prior to induction, before and up to seven minutes after tracheal intubation. There were no differences in demographics or baseline vital signs among the three groups. With ketamine administration, increases in heart rate and blood pressure were less in those patients given C preoperatively than in those who received either D or P. The peak increase in mean blood pressure was 39% (C) versus 70% (D) and 55% (P) (P < 0.01). Heart rate increased by a maximum of 20% (C) versus 41% (D) and 46% (P) (P < 0.01). We conclude that oral clonidine attenuates the hyperdynamic effects of anaesthetic induction with iv ketamine.     

Different priming techniques,including mivacurium,accelerate the onset of rocuronium

Different priming sequences of equipotent doses of rocuronium and mivacurium on the onset of maximum neuromuscular block and intubating conditions were compared with those obtained after succinylcholine. During thiopentone-fentanylnitrous oxide anaesthesia, 70 patients were randomly assigned into seven groups. Group I received mivacurium 0.15 mg · kg^?1 as a single bolus dose. Group II received a priming dose of mivacurium 0.015 mg · kg^?1 followed three minutes later by mivacurium 0.135 mg · kg^?1. Group III received rocuronium 0.6 mg · kg^?1 as a single bolus dose, and Group IV received an initial dose of rocuronium 0.06 mg · kg^?1 followed by rocuronium 0.54 mg · kg^?1. Group V received a priming dose of mivacurium 0.015 mg · kg^?1 followed by rocuronium 0.54 mg · kg^?1. Group VI received an initial dose of rocuronium 0.06 mg · kg^?1 followed by mivacurium 0.135 mg · kg^?1. Group VII received succinykholine 1.0 mg · kg^?1. Groups I, III, and VII received a placebo injection before the administration of the neuromuscular blocking drug. Additional thiopentone 2 mg · kg^?1 iv was given 30 sec before intubation. Onset times (mean (95% confidence interval)) after priming a rocuronium block with either rocuronium (73 (57–90) sec) or mivacurium (58 (47–69) sec) were similar to those after succinykholine (54 (40–68) sec), and were shorter (P < 0.01) than that observed in other groups. Intubating conditions were not different between the groups. The duration of neuromuscular block was shortest with succinykholine. It is concluded that priming a rocuronium block with either mivacurium or rocuronium resulted in a neuromuscular block comparable to that of succinykholine in both the onset of action and intubating conditions.     

Propofol for pulsed dye laser treatments in paediatric outpatients

Pulsed dye laser is a new treatment for port-wine stains, congenital lesions in the cutaneous vascular plexus. We report our anaesthetic experience with paediatric outpatients treated in the dermatology clinic. From April to November 1993, 48 ASA 1 children were anaesthetised for a total of 105 consecutive laser treatments. The youngest was eight months old, the oldest was 12 yrs old and most of the sessions (43%) were done for children aged from two to four years. Each received acetaminophen (10 mg · kg^?1 po) before treatment. A propofol infusion was chosen for anaesthesia to achieve early discharge and to reduce the incidence of postoperative emesis. The infusion was adjusted to maintain blood pressure within 20% of baseline and to keep the child immobile. The dose was progressively reduced during the procedure from 400 μg · kg^?1 · min^?1 to 100 μg · kg^?1 · min^?1. Fentanyl (2 μg · kg^?1 iv) was added for analgesia. Respiration was spontaneous through a nasopharyngeal airway (air in oxygen 40%). Anaesthesia proceeded uneventfully in all cases and lasted for 15–30 min (63% of treatments), 30–45 min (28%) or 45–60 min (9%) according to the size of the lesion. The mean stay in the recovery room was 25.1 min and none of the patients experienced emesis. Our experience shows that general anaesthesia with propofol supplemented with fentanyl offers a rapid onset and awakening, a painless treatment and an immobile child. It is a safe solution to alleviate pain from repeated painful procedures even in small children under two years of age.     

Regional anaesthesia for hernia repair in children: local vs caudal anaesthesia

The purpose of this study was to compare the effect of local anaesthesia (LA) with that of caudal anaesthesia (CA) on postoperative care of children undergoing inguinal hernia repair. This was a randomized, single-blind investigation of 202 children aged 1–13 yr. Anaesthesia was induced with N₂O/O₂ and halothane or propofol and maintained with N₂O/O₂/halothane. Local anaesthesia included ilioinguinal and iliohypogastric nerve block plus subcutaneous injection by the surgeon of up to 0.3 ml · kg^?1 bupivacaine 0.25% with 5 μg · kg^?1 adrenaline. The dose for caudal anaesthesia was 1 ml · kg^?1 up to 20 ml bupivacaine 0.2% with 5 μg · kg^?1 adrenaline. Postoperative pain was assessed with mCHEOPS in the anaesthesia recovery room, with postoperative usage of opioid and acetaminophen in the hospital, and with parental assessment of pain with a VAS. Vomiting, time to first ambulation and first urination were recorded. The postoperative pain scores and opioid usage were similar; however, the LA-group required more acetaminophen in the Day Care Surgical Unit. The incidence of vomiting and the times to first ambulation and first urination were similar. The LA-patients had a shorter recovery room stay (40 ± 9 vs 45 ± 15 min, P < 0.02). The postoperative stay was prolonged in the CA group (176 ± 32 vs 165 ± 26 min, P = 0.02). We conclude that LA and CA have similar effects on postoperative care with only slight differences.     

Lansoprazole reduces preoperative gastric fluid acidity and volume in children

The purpose of this study was to explore the efficacy of lansoprazole, a proton pump inhibitor, in reducing the acidity and volume of gastric aspirate in children immediately following the induction of anaesthesia. One hundred healthy in-patients aged 3–11 yr undergoing elective surgery were randomly allocated to four groups (n = 25 each): lansoprazole-lansoprazole, placebo-placebo, placebo-lansoprazole, and lansoprazole-placebo. For each treatment regimen, the first medication was administered at 9:00 pm on the night before surgery and the second at 5:30 am on the morning of the day of surgery (three hours preoperatively). The dose of lansoprazole was 30 mg (approximately 1.4 mg · kg^?1 mean). Children were offered 10 ml · kg^?1 apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. Lansoprazole increased gastric fluid pH and decreased gastric fluid volume regardless of whether it was administered before or after placebo. Two consecutive doses of lansoprazole was the most effective means of increasing the pH and reducing the volume of gastric aspirate; in this group, there were no subjects with gastric aspirate volume >0.4 ml · kg^?1 and pH <2.5. Oral lansoprazole, at least 30 mg, given on the night before surgery or on the morning of surgery will improve the gastric environment at the time of induction of paediatric anaesthesia. The most effective regimen was two doses (at bedtime and on the morning) of lansoprazole.     

Oral ondansetron decreases vomiting after tonsillectomy in children

Vomiting is a common, unpleasant aftermath of tonsillectomy in children. Intraoperative intravenous ondansetron (OND) reduces vomiting after this operation. Our doubleblind, placebocontrolled, randomized investigation studied the effect of the oral form of OND on vomiting after outpatient tonsillectomy in children. We studied 233 healthy children age 2–14 yr undergoing elective tonsillectomy. Subjects were given placebo (PLAC) or OND 0.1 mg · kg^?1 rounded off to the nearest 2 mg one hr before surgery. Anaesthesia was induced with either propofol or halothane/N₂O. Vecuronium 0.1 mg · kg^?1 was administered at the discretion of the anaesthetist. Anaesthesia was maintained with halothane/N₂O, 50 μg · kg^?1 midazolam iv and 1–1.5 mg · kg^?1 codeine im. At the end of surgery, residual neuromuscular blockade was reversed with neostigmine and atropine. All episodes of inhospital emesis were recorded by nursing staff. Rescue antiemetics in the hospital were 1 mg · kg^?1 dimenhydrinate ivfor vomiting × 2 and 50 μg · kg^?1 droperidol iv for vomiting × 4. Parents kept a diary of emesis after discharge. Postoperative pain was treated with morphine, codeine and/or acetaminophen. The two groups were similar with respect to demographic data, induction technique and anaesthesia time. Oral OND (n = 109) reduced postoperative emesis from 54% to 39%, P < 0.05. This effect was most dramatic inhospital, where 10% of the OND-patients and 30% of the PLAC-group vomited, P < 0.05. The OND-subjects required fewer rescue antiemetics, 7% vs 17%, P < 0.05. In conclusion, oral ondansetron decreased the incidence of vomiting after outpatient tonsillectomy in children.     

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.     

Midazolam coinduction does not delay discharge after very brief propofol anaesthesia

Previous reports have demonstrated synergism of midazolam and propofol for induction of anaesthesia in humans. We tested the hypothesis that in the presence of alfentanil, the combination of midazolam with propofol for a very brief operative procedure would not affect the recovery phase. During pre-oxygenation, 64 outpatients scheduled for dilatation and curettage received placebo, or low-dose midazolam (0.03 mg · kg^?1), or high-dose midazolam (0.06 mg · kg^?1) iv, in a randomized double-blind manner. They then received alfentanil 10 μg · kg^?1 iv, followed by titrated doses of propofol iv for induction and maintenance of anaesthesia. Ventilation with 70% N₂O in O₂ by mask was controlled to achieve a PETCO₂ 30–40 mmHg. Outcome measures were: propofol dose (induction and maintenance), time until eye-opening to command, and time to discharge-readiness. Propofol induction dose was decreased by increasing doses of midazolam (P = 0.00005). Midazolam delayed time to eye-opening (P = 0.02) but not time to discharge-readiness. This study had an 80% power to detect a 39 min difference in time to discharge-readiness. We conclude that midazolam propofol co-induction in the presence of alfentanil delays eye-opening, but does not delay discharge after anaesthesia.     

Omeprazole reduces preoperative gastric fluid acidity and volume in children

To explore the effects of oral omeprazole on preoperative gastric fluid pH and volume in children, 104 healthy in-patients aged 4–9 yr were randomly allocated to four groups (n = 26). Subjects in the Omeprazole-Omeprazole Group received two doses of omeprazole (20 mg per dose), those in the Placebo-Placebo Group, two doses of placebo, those in the Placebo-Omeprazole and Omeprazole-Placebo Groups, one dose each of the two preparations by mouth. For each treatment regimen, the first medication was administered at 9:00 p.m. on the night before surgery and the second at 5:30 a.m. on the morning of the day of surgery (three hours preoperatively). Children undergoing elective surgery were offered 10 nil · kg^?1 of apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. The administration of omeprazole at bedtime before surgery increased gastric pH (3.3 ± 1.3 vs 2.0 ± 0.6, P < 0.05) in comparison with placebo, as did two doses of omeprazole (pH = 4.8 ± 1.6, P < 0.05). A single dose of omeprazole administration on the morning of the day of surgery failed to increase gastric pH. There was a reduction in the number of children with a pH < 2.5 and a volume > 0.4 ml · kg^?1 in the Omeprazole-Omeprazole and Omeprazole-Placebo Groups compared with the Placebo-Placebo or Placebo-Omeprazole Groups. Oral omeprazole 20 mg administered on the night prior to surgery will improve the gastric environment at the time of induction of anaesthesia, thus reducing the potential risk of pneumonitis, should the aspiration of gastric contents occur following the induction of anaesthesia. These data also suggest that this drug, when administered in a single dose of approximately 1.0 mg · kg^?1 three hours before surgery, is ineffective in increasing gastric fluid pH to > 2.4.     

Clonidine does not affect lidocaine seizure threshold in rats

We investigated the effect of clonidine on intravenous (iv) lidocaine-induced haemodynamic changes and convulsions in awake rats. Wistar rats (200–250 g) were divided into three groups of eight and were pretreated with iv clonidine or normal saline 15 min before lidocaine infusion. Group 1 received normal saline; Group 2, 1 μg · kg^?1 clonidine; and Group 3, 10 μg · kg^?1 clonidine. After surgical preparation and recovery from anaesthesia, all groups received a continuous iv infusion of lidocaine (15 mg · ml^?1) at a rate of 4 mg · kg^?1 · min^?1 until generalized convulsions occurred. Oxygenation was well maintained in all groups. Pretreatment with clonidine changed neither cumulative convulsant doses (Group 1: 41.8 ± 2.2, Group 2: 43.8 ± 2.6, Group 3: 42.3 ± 2.0 mg · kg^?1, respectively) nor plasma concentrations of lidocaine at the onset of convulsions (Group 1: 10.5 ± 0.3, Group 2: 10.8 ± 0.3, Group 3: 10.6 ± 0.3 μg · ml^?1, respectively). The mean arterial blood pressures in Groups 2 and 3 were decreased after clonidine pretreatment (Group 2: 93 ± 1, P < 0.01, Group 3: 90 ± 1%, P < 0.01, respectively) and they gradually increased during lidocaine infusion. The heart rates decreased after clonidine pretreatment (Group 2: 94 ± 2, P < 0.05, Group 3: 86 ± 2%, P < 0.01, respectively) and the combination of clonidine and lidocaine potentiated the bradycardic effect of lidocaine at a subconvulsant dose. Our results indicate that clonidine has neither anticonvulsant nor proconvulsant effects on lidocaineinduced convulsions. However, the interactions of clonidine and lidocaine on blood pressure and heart rate should be investigated further.     

Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials

Intraoperative monitoring of somatosensoryevoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexusevoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 ± 6 (SD) yr, weight 68 ± 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg· kg^{? 1} and fentanyl 3 μg· kg^{? 1} and was followed by succinylcholine 1 mg· kg^{? 1}. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 μg · kg^{? 1}· hr^{? 1}, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide ± 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anaesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 ± 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 ± 4% vs 48 ± 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isofluranenitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxideisoflurane anaesthesia but less than the predicted additive effect.     

Morphine does not affect the awakening concentration of sevoflurane

This study was designed to determine whether morphine 0.1 mg·kg^?1 iv given intraoperatively altered the end-tidal concentration of sevoflurane which is associated with eye opening to verbal command. We studied 24 healthy ASA physical status I patients to determine whether morphine, or placebo administered about 60 min before the end of surgery affected recovery from sevoflurane/oxygen anaesthesia. During anaesthesia no other anaesthetics or drugs were given. After surgery, end-tidal sevoflurane concentration was reduced gradually at the rate of less than 0.01% · min^?1. The end-tidal concentration at the time patients could respond to verbal command was recorded as MACawake. The MACawake was 0.58 ± 0.12% (mean ±SD) for the control group to whom placebo had been administered, and 0.57 ± 0.11% for morphine group to whom morphine had been administered. In both groups, the MACawake decreased with age, and the ratio to age-adjusted sevoflurane MAC was 0.31 ± 0.04 (mean ± SD) for the control group and 0.30 ± 0.04 for the morphine group. The ratio had no correlation with age. It is concluded that the awakening concentration of sevoflurane during recovery from anaesthesia is not affected by analgesic doses of morphine 0.1 mg · kg^?1 iv administered intraoperatively.     

Optimizing sedation following major vascular surgery: a double-blind study of midazolam administered by continuous infusion

A randomized, double-blind study was undertaken to determine the dose requirements, recovery characteristics, and pharmacokinetic variables of midazolam given by continuous infusion for sedation in patients following abdominal aortic surgery. Thirty subjects, 50–75 yr, scheduled to undergo aortic reconstructive surgery, entered the study. Following a nitrous oxide-isoflurane-opioid anaesthetic technique, patients were randomly allocated to receive one of three loading doses (0.03, 0.06 or 0.1 mg · kg^?1) and initial infusion rates (0.5, 1.0 or 1.5 μg · kg^?1 · min^?1) of midazolam, corresponding to groups low (L), moderate (M) and high (H). The infusion of midazolam was adjusted to maintain sedation levels of “3, 4 or 5,“ which permitted eye opening in response to either verbal command or a light shoulder tap, using a seven-point scale ranging from “0” (awake, agitated) to “6” (asleep, non-responsive). Additionally, morphine was given in increments of 2.0 mg iv prn for analgesia. On the morning after surgery, midazolam was discontinued, and the tracheas were extubated when patients were awake. Blood samples were taken during, and at increasing intervals for 48 hr following discontinuation of the infusion, and analyzed by gas chromatography. The desired level of sedation was maintained during more than 94% of the infusion period in all three groups, with a maximum of three dose adjustments per patient, for treatment which lasted 16.3 ± 0.6 hr. There was, however, an increase in both the infusion rates and mean plasma concentrations from Group L to Group H (P < 0.05), which corresponded to an inverse relationship of morphine requirements during the period of sedation (P < 0.05, Group H vs Group L). Optimal midazolam infusion rates and resulting plasma concentrations at the times the infusions were discontinued (in parentheses) were as follows — Group L: 0.60 ± 0.18 μg · kg^?1 min^?1 (76 ± 32 ng · mL^?1), Group M: 0.90 ± 0.52 μg · kg^?1 · min^?1 (133 ± 71 ng · mL^?1), and Group H: 1.34 ± 0.69 μg · kg^?1 · min^?1 (206 ± 106 ng · mL^?1). Times to awakening were longer in Group H: 3.1 ± 3.4 hr, than in Group L: 1.1 ± 0.8 h, P < 0.05. Pharmacokinetic variables were found to be dose- independent over the range of infusion rates. Mean values were t_1/2β = 4.4 ± 1.5 hr, CL = 5.94 ± 1.69 mL · min^?1 · kg^?1, Vd = 3.13 ± 1.07 L · kg^?1. It is concluded that midazolam, infused between 0.6–0.9 μg · kg^?1 · min^?1, provides a stable level of sedation, when administered in conjunction with intermittent iv morphine following AAS. This sedation technique, which costs $1.65 ± 0.73 hr^?1 ($Can), is associated with rapid recovery and minimal side effects.