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.     

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.     

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.     

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.     

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.     

Thiopentone pretreatment for propofol injection pain in ambulatory patients

This study investigated propofol injection pain in patients undergoing ambulatory anaesthesia. In a randomized, double-blind trial, 90 women were allocated to receive one of three treatments prior to induction of anaesthesia with propofol. Patients in Group C received 2 ml normal saline, Group L, 2 ml, lidocaine 2% (40 mg) and Group T, 2 ml thiopentone 2.5% (50 mg). Venous discomfort was assessed with a visual analogue scale (VAS) 5–15 sec after commencing propofol administration using an infusion pump (rate 1000 μg · kg^?1 · min^?1). Loss of consciousness occurred in 60–90 sec. Visual analogue scores (mean ± SD) during induction were lower in Groups L (3.3 ± 2.5) and T (4.1 ± 2.7) than in Group C (5.6 ± 2.3); P = 0.0031. The incidence of venous discomfort was lower in Group L (76.6%; P < 0.05) than in Group C (100%) but not different from Group T (90%). The VAS scores for recall of pain in the recovery room were correlated with the VAS scores during induction (r = 0.7045; P < 0.0001). Recovery room discharge times were similar: C (75.9 ± 19.4 min); L 73.6 ± 21.6 min); T (77.1 ± 18.9 min). Assessing their overall satisfaction, 89.7% would choose propofol anaesthesia again. We conclude that lidocaine reduces the incidence and severity of propofol injection pain in ambulatory patients whereas thiopentone only reduces its severity.     

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.     

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.     

Propofol anaesthesia in paediatric ambulatory patients: a comparison with thiopentone and halothane

The purpose of this study was to evaluate the haemodynamic changes during induction, as well as the speed and quality of recovery when propofol (vs thiopentone and/or halothane) was used for induction and maintenance of anaesthesia in paediatric outpatients. One hundred unmedicated children, 3–12-yr-old, scheduled for ambulatory surgery were studied. The most common surgical procedures performed were eye muscle surgery (42%), plastic surgery (21%), dental restoration (15%), and urological procedures (15%). The children were randomized to an anaesthetic regimen for induction/maintenance as follows: propofol/propofol infusion; propofol/halothane; thiopentone/halothane; halothane for both induction and maintenance. Succinylcholine 1.5 mg · kg^?1 was used to facilitate tracheal intubation and N₂O/O₂ were used as the carrier gases in each case. All maintenance drugs were titrated according to the clinical response of the patient to prevent movement and/or maintain BP ± 20% of baseline. Two patients (4%) who received propofol expressed discomfort during injection. The mean propofol dose required to prevent movement was 267 ± 83 μg · kg^?1 · min^?1. The overall pattern of haemodynamic changes, as well as awakening (extubation) times were not different among the four groups. Children who received propofol recovered faster (22 vs 29–36 min) (P < 0.05), were discharged home sooner (101 vs 127–144 min) (P < 0.05), and had less postoperative vomiting (4 vs 24–48%) (P < 0.05) than all others. There were no serious complications or adverse postoperative sequelae in any of the patients in the study. It is concluded that induction and maintenance of anaesthesia with propofol is a well-tolerated anaesthetic technique in children, and is associated with faster recovery and discharged as well as less vomiting than when halothane is used.     

RETRACTED ARTICLE: Optimal anti-emetic dose of granisetron for preventing post-operative nausea and vomiting

In order to determine the optimal effective dose of granisetron for preventing postoperative nausea and vomiting, the drug was administered in doses of either 20, 40 or 60 μg sd kg^?1. The efficacy of granisetron was evaluated in a randomized, double-blind comparison with placebo in 100 patients undergoing general anaesthesia for major gynaecological surgery. The patients received a single dose of either granisetron or placebo (saline) iv immediately after recovery from anaesthesia. The effects were assessed during the 24 hr after recovery from anaesthesia by means of a nausea and vomiting score; 0 = no emetic symptoms, 1 = nausea, 2 = vomiting. The treatment groups were similar for patient characteristics, surgical procedures and anaesthetics administered. The mean scores were 0.7, 0.6, 0.2 and 0.2 after administration of placebo, granisetron 20, 40 and 60 μg · kg^?1, respectively. Granisetron 40 μg · kg^?1 was as effective as 60 μg · kg^?1 and both resulted in reduction of the scores compared with placebo and granisetron 20 μg · kg^?1 (P < 0.05). In conclusion, granisetron 40 μg · kg^?1 is considered to be the appropriate dosage for preventing postoperative emesis after anaesthesia.     

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.     

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.     

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.     

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.     

Pharmacodynamic behaviour of rocuronium in the elderly

This study compared the potency and time course of action of rocuronium (ORG 9426) in elderly and young patients during nitrous oxide-opioid anaesthesia. One hundred ASA physical status I– II patients (60, âgéd 65–80 yr, and 40, âgéd 20–45 yr) were studied by measuring the force of contraction of the adductor pollicis in response to train-of-four stimulation of the ulnar nerve. After induction of anaesthesia with thiopentone and maintenance with N₂O/O₂ and fentanyl, rocuronium 120,160, 200, or 240 μg · kg ^?1 was administered to determine dose-response curves. When maximum block had been obtained,further rocuronium to a total of 300 μg · kg ^?1 was given. Additional doses of 100 μg · kg^?1 were administered when the first twitch height (T₁) had recovered to 25% control. At the end of surgery neuromuscular blockade was allowed, whenever possible, to recover spontaneously until T₁ was 90% of control before administration of neostigmine. There was no difference in the potency of rocuronium in the elderly and the younger patients. The ED₅₀ was 196 ±8 (SEE for the mean) in elderly,vs 215 ±17 iμg · kg ^{? 1} in young patients (NS). When individual cumulative dose-response curves were constructed, the ED₅₀ was 203 ± 7(SEM) and 201 ± 10 μg · kg ^{? 1} in the elderly and the young respectively (NS). However, the onset of maximum neuromuscular block was slower in the elderly 3.7 ±1.1 (SD) vs 3.1 ± 0.9 min, P < 0.05). The time to 25% T ₁ recovery was longer in the elderly (11.8 ± 8.1 vs 8.0 ± 6.5 min,P <0.05) as was the recovery index, time from 25 to 75% T₁ recovery (15.5 ± 6.2 vs 11.2 ± 4.9 min, P< 0.05). The duration of neuromuscular block after each maintenance dose was longer in the elderly (P <0.01) and increased gradually with time. It is concluded that rocuronium is an intermediate-acting neuromuscular blocking drug with a similar potency in elderly and young patients, but the onset and recovery of neuromuscular blockade are slower in the elderly.     

Upper airway obstruction during midazolam sedation: modification by nasal CPAP

We examined the depressant effect of midazolam on respiration in 21 healthy women undergoing lower abdominal surgery with spinal anaesthesia. Airway gas flow, airway pressure, and the sound of snoring were recorded together with arterial oxygen saturation (SpO₂. After spinal anaesthesia was established, subjects were deeply sedated with pentazocine 15 mg followed by incremental doses of midazolam 1 mg iv up to 0.1 mg · kg^?1. When SpO₂ decreased to < 90% or snoring and/or apnoea was observed, continuous positive airway pressure applied through the nose (nasal CPAP) was increased until the respiratory deterioration was reversed. While one patient remained free of respiratory events, the other 20 patients were successfully treated with nasal CPAP restoring normal SpO₂ (95.5 ± 1.7%) without snoring. Stepwise reduction of nasal CPAP determined the minimally effective CPAP to prevent snoring to be 5.1 ±2.1 cm H₂O. Further reduction of nasal CPAP induced snoring in 15 patients and obstructive apnoea in five patients with the latter accompanied by a severe reduction of SpO₂ (87.4 ± 6.1%). Patients with apnoea were older than those who snored (P < 0.05). We conclude that upper airway obstruction contributes considerably to decreases in SpO₂ during midazolam sedation for spinal anaesthesia.     

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.     

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.     

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.     

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.