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.     

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.     

Lidocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation.

STUDY OBJECTIVE: To evaluate the effect of lidocaine inhalation on the circulatory response to direct laryngoscopy and endotracheal intubation. DESIGN: Prospective, randomized study. SETTING: Operating theater at a public hospital. PATIENTS: Eighty patients (ASA physical status I and II ages 25 to 45 years) scheduled for major abdominal surgery. INTERVENTIONS: In the first stage, 40 patients were randomly assigned to receive inhalation of either lidocaine 40 mg or a 0.9% solution of sodium chloride (placebo). In the second stage, the next 20 consecutive patients received inhalation of lidocaine 120 mg, and another 20 consecutive patients received intravenous (IV) lidocaine 1 mg/kg. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure rose significantly in the i.v. lidocaine group (21.2 mmHg; p < 0.05), the saline inhalation group (29.2 mmHg; p < 0.05), and the lidocaine 40 mg inhalation group (22.9 mmHg; p < 0.05), but not in the lidocaine 120 mg inhalation group (10.1 mmHg). The heart rate (HR) response to intubation with lidocaine inhalation was dose dependent. In the saline inhalation group, HR increased by 15.6 beats per minute (bpm) (p < 0.05); in the lidocaine 40 mg inhalation group, HR increased by 9.1 bpm (p < 0.05); and in the lidocaine 120 mg inhalation group, HR increased by only 3.1 bpm. CONCLUSION: Inhalation of lidocaine 120 mg prior to induction of anesthesia is an effective, safe, and convenient method to attenuate the circulatory response to laryngoscopy and endotracheal intubation.     

Anesthesia and hypertension: the effect of clonidine on perioperative hemodynamics and isoflurane requirements

Thirty patients (ASA physical status II-III) with a history of arterial hypertension, whose blood pressure (BP) control varied from normotension to moderate hypertension (diastolic BP less than 110 mmHg), scheduled for elective surgery under general anesthesia, were randomly assigned to two groups. Group 1 was premedicated 90-120 min prior to induction with diazepam 0.15 mg X kg-1 po; group 2, in addition, received clonidine 5 micrograms X kg-1 po. Anesthetic depth was assessed by on-line aperiodic analysis of the electroencephalogram. Following lidocaine 1 mg X kg-1 and fentanyl 2 micrograms X kg-1 (group 1 only), anesthesia was induced with thiopental 3-4 mg X kg-1 and vecuronium 0.1 mg X kg-1 was used to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane in N2O/O2 and supplemented by fentanyl. In group 2, clonidine produced a rapid preoperative control of systolic and diastolic BP from 166 +/- 32/95 +/- 14 to 136 +/- 80 +/- 11 (P less than 0.01), was more effective in blunting the reflex tachycardia associated with laryngoscopy and endotracheal intubation than lidocaine-fentanyl pretreatment. It significantly reduced the intraoperative lability (coefficient of variation) of systolic (P less than 0.01) and diastolic BP and heart rate (HR) (P less than 0.05), and resulted in significantly slower HR during recovery (P less than 0.01). Anesthetic requirements for isoflurane were reduced 40% (P less than 0.01) in group 2; narcotic supplementation was also significantly reduced (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

In vitro diffusion of lidocaine across endotracheal tube cuffs

PURPOSE: Lidocaine diffuses across endotracheal tube cuffs, which may serve as a reservoir for local anesthetic to assist in the prevention of ETT-induced cough while emerging from general anesthesia. However, the rate of diffusion is slow. Two techniques, alkalization and warming, may increase the proportion of uncharged drug available for diffusion. The purpose of this study is to determine the effectiveness of warming alkalization or warming with alkalization on diffusion. METHODS: Four preparations of lidocaine 4% were studied. Group (Gr) L-lidocaine (24 degrees C), Gr WL--warmed lidocaine (38 degrees C), Gr AL--alkalized lidocaine (24 degrees C), Gr WAL--warmed, alkalized lidocaine (38 degrees C). Twenty-four Mallinckrodt 8.0 ID (Mallinckrodt Critical Care Division of Mallinckrodt, Inc., Glens Falls, New York) endotracheal tube cuffs were filled with 6 ml of one of the four preparations. They were then placed in a 20 ml water bath at 38 degrees C and samples were drawn from the water bath at intervals for up to 360 min. The lidocaine concentration in each sample was determined by gas chromatography. RESULTS: The highest lidocaine concentration was reached in Gr WAL (410.98 +/- 8.53 micrograms.ml-1) after 300 min and then decreased to 376.18 +/- 4.59 micrograms.ml-1 after 360 min. In Gr AL the highest concentration (235.05 +/- 2.99 micrograms.ml-1) was reached after 360 min. Lidocaine concentrations in Gr L and WL after 360 min were 3.19 +/- 1.16 micrograms.ml-1 and 4.32 +/- 2.02 micrograms.ml-1 respectively. CONCLUSION: Alkalization with or without warming, but not warming alone, promotes lidocaine diffusion from endotracheal tube cuff.     

The effect of various administration routes of lidocaine on hemodynamics and ECG rhythm during endotracheal intubation

Observations of arterial blood pressure, heart rate and cardiac rhythm during endotracheal intubation and within a five minute period thereafter were made in 80 patients randomly assigned into four groups. The aim was to study the cardiovascular changes following endotracheal intubation using a standard anesthesia technique and to compare the efficacy of lidocaine in controlling cardiovascular changes using different administration techniques. Anesthesia was induced with thiopentone and succinylcholine followed by endotracheal intubation. In group A, the control group, no lidocaine was given. In groups B, C, and D, lidocaine as laryngotracheal spray, transtracheal injection or intravenous injection in a dosage of 1 mg/kg BW was administered prior to endotracheal intubation. In the control group, laryngoscopy and endotracheal intubation caused a significant rise in blood pressure and heart rate with a high percentage (60%) of cardiac dysrhythmias including serious types. In the lidocaine groups, we observed significantly lower values of blood pressure and cardiac dysrhythmias as compared to the control group. Only 20-25% of the cases showed sinus tachycardia. No significant differences were noticed between the lidocaine groups. We conclude from our study that those patients who had received lidocaine prior to endotracheal intubation showed minimal cardiovascular changes. Lidocaine should therefore routinely be used prior to endotracheal intubation.     

Plasma lidocaine concentrations during epidural blockade with isoflurane or halothane anesthesia.

Because isoflurane maintains hepatic blood flow at higher flows than halothane, we proposed that the elimination of lidocaine would be different between these two volatile anesthetics. The plasma lidocaine concentrations were determined in 14 female patients undergoing epidural blockade plus isoflurane anesthesia and compared with those obtained during halothane anesthesia for lower abdominal surgery. General anesthesia was maintained with isoflurane (0.46% +/- 0.04% [mean +/- SE] inspired, n = 7) or halothane (0.48% +/- 0.05% inspired, n = 7) and 67% nitrous oxide in oxygen. All patients received 2% lidocaine solution, 10 mL as a bolus dose and continuous administration at a rate of 10 mL/h, through the epidural catheter. The plasma lidocaine concentrations over 180 min after the epidural injection in patients receiving isoflurane were similar to those in patients receiving halothane. The results suggest that low inspired concentrations of isoflurane do not reduce plasma lidocaine concentrations in patients during epidural blockade, compared with halothane.     

Clonidine decreases intraoperative bleeding in middle ear microsurgery

BACKGROUND: The antihypertensive drug clonidine is a centrally acting alpha2 agonist useful as a premedicant because of its sedative, anxiolytic, and analgesic properties. We examined the effect of clonidine given as an oral preanesthetic medication in producing a bloodless surgical field in patients undergoing middle ear microsurgery. We also evaluated whether the administration of clonidine would alter the reflex cardiovascular response to laryngoscopy and endotracheal intubation, anesthetic requirement, postoperative pain intensity and consumption of analgesics, and pre- and postoperative sedation and anxiety. METHODS: A prospective, randomized, double-blind clinical trial was performed in 40 patients scheduled for elective middle ear surgery under general anesthesia. Twenty-one patients received clonidine (300 microg p.o.) 90 min prior to arrival at the operating theater and 19 received placebo (control group). The hemodynamic endpoint of the anesthetic management was maintenance of hypotension for producing a bloodless surgical field. The desired control of the cardiovascular system was attained with isoflurane (inspired concentration increments of 0.25 vol% up to a maximum of 1.5 vol%)+/-fentanyl (bolus of 1 microg. kg-1)+/-urapidil (bolus of 0.3 mg. kg-1) as needed. Intraoperative bleeding was assessed on a four-point scale from 0=no bleeding to 3=abundant bleeding. RESULTS: There was less bleeding in the clonidine group (mean+/-SEM) than in the control group (0.75+/-0.3 vs 1.1+/-0.4, P<0.05). Patients given clonidine required a mean inspired isoflurane concentration of 0.63+/-0.1 vol% as compared with 1.01+/-0.2 vol% in controls (P<0.05). Fentanyl requirements were also significantly lower (57.10 vs 79.42 microg. kg-1, P<0.05). Four clonidine-treated patients required urapidil to achieve satisfactory hypotension as compared with 11 controls (P<0.05). Clonidine attenuated the associated cardiovascular response following laryngoscopy and intubation, and was more effective than placebo in achieving a satisfactory preoperative sedation and decreasing intensity of postoperative pain. Preoperative anxiety and incidence of adverse events was similar in both groups. CONCLUSION: Premedication with clonidine reduced bleeding in middle ear microsurgery, attenuated hyperdynamic response to tracheal intubation, and reduced isoflurane, fentanyl, and urapidil requirements for controlled hypotension.     

Prevention of atelectasis formation during induction of general anesthesia

General anesthesia promotes atelectasis formation, which is augmented by administration of large oxygen concentrations. We studied the efficacy of positive end-expiratory pressure (PEEP) application during the induction of general anesthesia (fraction of inspired oxygen [FIO(2)] 1.0) to prevent atelectasis. Sixteen adult patients were randomly assigned to one of two groups. Both groups breathed 100% O(2) for 5 min and, after a general anesthesia induction, mechanical ventilation via a face mask with a FIO(2) of 1.0 for another 5 min before endotracheal intubation. Patients in the first group (PEEP group) had continuous positive airway pressure (CPAP) (6 cm H(2)O) and mechanical ventilation via a face mask with a PEEP of 6 cm H(2)O. No CPAP or PEEP was applied in the control group. Atelectasis, determined by computed radiograph tomography, and analysis of blood gases were measured twice: before the beginning of anesthesia and directly after the intubation. There was no difference between groups before the anesthesia induction. After endotracheal intubation, patients in the control group showed an increase of the mean area of atelectasis from 0.8% +/- 0.9% to 4.1% +/- 2.0% (P = 0.0002), whereas the patients of the PEEP group showed no change (0.5% +/- 0.6% versus 0.4% +/- 0.7%). After the intubation with a FIO(2) of 1.0, PaO(2) was significantly higher in the PEEP group than in the control (591 +/- 54 mm Hg versus 457 +/- 99 mm Hg; P = 0.005). Atelectasis formation is prevented by application of PEEP during the anesthesia induction despite the use of large oxygen concentrations, resulting in improved oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during the induction of general anesthesia prevents atelectasis formation. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. Therefore, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management during the anesthesia induction.     

Reduction of the concentration of isoflurane prevents tachycardia and hypertension associated with tracheal intubation

BACKGROUND: High concentration of isoflurane often induces not only tachycardia but also hypertension during induction of anesthesia and causes further hyperdynamic changes after tracheal intubation. METHODS: Forty patients, ASA physical status I, were randomly assigned to receive 4% or 2.5% isoflurane. Anesthesia was induced with thiamylal and vecuronium followed by mask ventilation with 0.5% isoflurane in oxygen. Isoflurane concentration was gradually increased to 4% or 2.5% in 2 min and the trachea was intubated after 3 min. Systolic blood pressure (SBP) and heart rate (HR) were recorded every minute from induction of anesthesia. RESULTS: Mask ventilation with isoflurane induced a significant increase in HR in both groups, but the HR just before intubation was significantly lower in the 2.5% group than in the 4% group. SBP was significantly decreased in the 2.5% group, but a transient increase was seen in the 4% group. Tracheal intubation induced a marked increase in HR in both groups, but the HR was significantly lower in the 2.5% group than in the 4% group (115 +/- 14 and 130 +/- 18 beats x min(-1), respectively; P < 0.01). SBPs just after intubation were 166 +/- 24 and 154 +/- 20 mmHg in the 4% and 2.5% groups, respectively. The difference between the groups was not significant, but the patients in whom the SBP increased more than 180 mmHg were significantly fewer in the 2.5% group than in the 4% group (P < 0.05). CONCLUSIONS: Reduction of the isoflurane concentration from 4% to 2.5% during induction of anesthesia made the circulation stable, and decreased the incidence of excessive tachycardia and hypertension after tracheal intubation.     

Prevention of withdrawal associated with the injection of rocuronium in adults and children

STUDY OBJECTIVE: To determine which technique prevents the withdrawal associated with rocuronium administration in adults and children. DESIGN: Blinded, randomized, prospective trial. SETTING: This study was set at an inpatient anesthesia in a university teaching hospital. PATIENTS: 200 adult patients (aged 19-63 years) and 150 children (aged 2-9 years) undergoing elective surgery requiring endotracheal intubation. INTERVENTIONS: Four groups in adult and 3 groups in children of 50 patients each were investigated. In adult study, control groups with free intravenous (IV) flow (C-F) or the occlusion of IV flow (C-O) received saline as the pretreatment of rocuronium; lidocaine groups with free IV flow (L-F) or the occlusion of IV flow (L-O) received lidocaine as the pretreatment of rocuronium, preceded by thiopental 5 seconds before. In children study, groups P and L received saline and lidocaine as the pretreatment of rocuronium, respectively, and group S received rocuronium mixed with sodium bicarbonate after the pretreatment of placebo preceded by thiopental. MEASUREMENTS AND MAIN RESULTS: The patient's response to rocuronium injection was graded using a 4-point scale. The pH and osmolality of treatment solution were measured. The incidence of no movement after rocuronium was 96% in L-O, 46% in L-F, 26% in C-O, and 18% in C-F in adult and 96% in S, 58% in L, and 8% in P in children. CONCLUSIONS: Withdrawal after rocuronium can be eliminated by the pretreatment of lidocaine during the occlusion of the IV flow in adults and addition of sodium bicarbonate in children.     

Cardiovascular responses caused by the combination of lidocaine and vecuronium in the induction of general anaesthesia

Fentanyl, vecuronium and enflurane may cause bradyarrhythmias during anaesthesia. Lidocaine administered before endotracheal intubation may interact synergistically with these agents. In this randomized and double-blind study, lidocaine 1 mg kg-1 (24 patients) or saline (20 patients) was given, immediately after glycopyrrolate 5 micrograms kg-1, fentanyl 1.5 micrograms ml-1 and thiopentone 3-5 mg kg-1, together with vecuronium 0.1 mg kg-1 as a rapid i.v. injection to healthy (ASA 1) surgical patients. Enflurane 0.8% was included in the inhaled gases 10 min and enflurane 1.6% 25 min after lidocaine administration. The plasma concentrations of lidocaine rose to a mean level of 3.1 micrograms ml-1 (maximum 7.1 micrograms ml-1) which may affect the electrical conduction at various sites in the heart. There were no statistically significant differences in arterial blood pressures or heart rates during anaesthesia between the groups. The incidence of junctional rhythm was 7/24 patients in the lidocaine group and 5/20 patients in the saline group. Three patients in the lidocaine group, and two patients in the control group developed junctional rhythm immediately after intubation. The plasma concentrations of vecuronium were unaffected by lidocaine. The ratio of the unbound lidocaine to plasma protein bound lidocaine was at the expected level and did not differ significantly 2 and 10 min after the injection.     

Haemodynamic and catecholamine responses to calcitonin gene-related peptide during volatile anaesthesia

PURPOSE: Calcitonin gene-related peptide (CGRP) produces vasodilatation, hypotension, and tachycardia. Tachycardia induced by CGRP may be due to sympathetic activation. Volatile anaesthetics attenuate activation of arterial baroreflexes. We examined the haemodynamic and endocrine effects of CGRP infusion (4 micrograms.kg-1) during anaesthesia with either enflurane or isoflurane in dogs. METHODS: Measurements of haemodynamic variables and hormone assays for plasma catecholamines were made before, during, and after CGRP infusion. Anaesthesia consisted of induction with 25 mg.kg-1 pentobarbital, followed by either enflurane (n = 7) or isoflurane (n = 7) to achieve a 1.0 end-tidal minimum alveolar concentration in oxygen 100%. RESULTS: Mean arterial pressure and systemic vascular resistance decreased (P < 0.01) and the reductions in both variables were similar during CGRP infusion in both groups. Cardiac index (CI) was increased (P < 0.01) in the enflurane group throughout the study while CI increased (P < 0.01) only during infusion in the isoflurane group. Heart rate (HR) remained unchanged (from 135 +/- 6 bpm to 134 +/- 7 bpm) in the enflurane group but tended to increase (from 162 +/- 9 bpm to 171 +/- 9 bpm) in the isoflurane group during infusion. Intergroup differences in HR were found (P < 0.05). Plasma epinephrine concentrations increased (from 42.4 +/- 12.7 pg.ml-1 to 115.3 +/- 41.8 pg.ml-1, P < 0.01) during infusion in the isoflurane group. However, these increases were suppressed (from 46.6 +/- 23.2 pg.ml-1 to 64.7 +/- 32.4 pg.ml-1) to a greater extent in the enflurane group. CONCLUSION: The haemodynamic responses, except for HR, of CGRP infusion are similar during enflurane and isoflurane anaesthesia. Suppression of tachycardia induced by CGRP is greater with enflurane than with isoflurane. The differences in HR may be due to the roles of catecholamine responses resulting from the anaesthetic-induced sympathetic suppression.     

The effects of intracuff lidocaine on endotracheal-tube-induced emergence phenomena after general anesthesia

Coughing during emergence from general anesthesia is a common clinical problem. We sought to determine whether inflating the endotracheal tube cuff with lidocaine would create a reservoir of local anesthetic, which might diffuse across the cuff membrane to anesthetize the mucosa, thus attenuating stimulation during extubation of the trachea. A total of 63 patients undergoing elective surgery were enrolled in a prospective, randomized, double-blinded study. After intubation of the trachea with an endotracheal tube, the cuff of the tube was inflated with either lidocaine 4%, saline, or air. After extubation, a blinded observer noted heart rate, blood pressure, oxygen saturation, end-tidal isoflurane concentration, and the incidence of coughing. Data were analyzed by using analysis of variance, Student's t-test, and the chi(2) test for multiple variables. The groups were demographically comparable. There was no difference in hemodynamic or oxygen saturation data between either group. The incidence of coughing was decreased in the lidocaine group for the time period of 4-8 min postextubation (P < 0.05). We conclude that inflation of the cuff of the endotracheal tube can reduce the incidence of coughing in the initial postextubation period, a finding that may benefit certain patient groups in which this is particularly desirable. IMPLICATIONS: Tracheal intubation with an endotracheal tube is often necessary during anesthesia. After intubation, inflating a cuff around the endotracheal tube maintains a seal. This can result in coughing during emergence from anesthesia. Our study shows that inflating the cuff of an endotracheal tube with lidocaine rather than air can reduce the incidence of postextubation coughing.     

Interpleural administration of 1.0% and 1.5% lidocaine with epinephrine for pain relief after thoracotomy

Pain relief following thoracotomy and arterial concentration profiles after interpleural administration of lidocaine were studied in 23 adult patients. They were allocated to three groups and given interpleural injection of 20 ml each of 1.0% (group 1, N = 9, non-pneumonectomy patients), 1.5% (group 2, N = 10, non-pneumonectomy patients), and 1.5% (group 3, N = 4, pneumonectomy patients) lidocaine with epinephrine (5 micrograms.ml-1). Complete pain relief was obtained within 20 min after injection in all patients. The mean duration of analgesia was 2.8 hr, 3.1 hr, and 5.1 hr in group 1, 2, and 3, respectively. The maximum plasma concentrations of lidocaine (Cmax) were 1.7 +/- 1.0 (mean +/- SD) microgram.ml-1, 2.2 +/- 0.6 micrograms.ml-1, and 0.7 +/- 0.2 micrograms.ml-1 in group 1, 2, and 3, respectively. The mean duration of analgesia was significantly longer in group 3 than in group 2 (P less than 0.01). Cmax was significantly lower in group 3 than in group 2 (P less than 0.01). In conclusion, we consider interpleural injection of lidocaine with epinephrine to be an effective method of providing postoperative analgesia after thoracotomy. Our data also suggest that the duration of analgesia may increase and the plasma levels of lidocaine may remain quite low in total pneumonectomy patients, because local anesthetic solution is not absorbed through the visceral pleura but absorbed only through the parietal pleura alone in these patients.     

Effects of Intravenous Lidocaine on Isoflurane Concentration,Physiological Parameters,Metabolic Parameters and Stress‐related Hormones in Horses Undergoing Surgery

Physiological parameters, metabolic parameters and stress‐related hormones are evaluated in horses anaesthetized with isoflurane in oxygen combined with lidocaine intravenously. Two groups of horses anaesthetized with isoflurane (six horses in each group) were studied: a lidocaine group (IL), which received intravenous lidocaine and a control group (C), which received intravenous saline. Horses in both groups were pre‐medicated with detomidine (IV), and anaesthesia was induced with midazolam‐ketamine (IV). The lidocaine group received intravenous lidocaine as a loading dose of 2.5 mg kg⁻¹ at 15 min after induction of anaesthesia directly followed by a maintenance dosage of 50 μ kg⁻¹ min⁻¹, while the control group received saline (IV) following the same regime. End‐tidal isoflurane and standard physiological parameters were measured. Blood was sampled for measurement of lidocaine, stress hormones and metabolic parameters. The end‐tidal isoflurane concentration in the lidocaine group was 0.96 ± 0.06% versus 1.28 ± 0.06% (mean ± SD) in the control group, a significant (P < 0.05) reduction of 25%. No significant differences were found regarding stress‐related hormones, metabolic and physiological parameters. This study suggests that the use of lidocaine to decrease the concentration of isoflurane to obtain a sufficient surgical anaesthesia has no subsequent effects on physiological and metabolic parameters or stress‐related hormones.     

Cerebral arterial blood flow velocity during induction of general anesthesia: rapid intravenous induction versus awake intubation.

Changes in middle cerebral arterial flow velocity (MCAV) during rapid intravenous induction and awake intubation using transcranial Doppler sonography were investigated. The study involved 20 patients without disorders of the central nervous or cardiovascular systems who were scheduled for maxillofacial surgery. In the intravenous induction group, anesthesia was induced with sodium thiopental, and orotracheal or nasotracheal intubation was facilitated with succinylcholine chloride or alcuronium chloride. In the awake intubation group, orotracheal or nasotracheal intubation was performed under intravenous sedation with diazepam and topical anesthesia with 4% lidocaine. Arterial blood pressures, heart rate, and MCAV were monitored at specific intervals. During intravenous induction, blood pressures decreased after the administration of thiopental and muscle relaxants and increased during endotracheal intubation. MCAV was remarkably slowed after the administration of thiopental and during mask ventilation. During awake intubation, blood pressures were increased by endotracheal intubation. MCAV was decreased from the administration of diazepam to the transtracheal injection of lidocaine, but returned to the control value from endotracheal spray to endotracheal intubation. These results suggest that smooth awake intubation may be the safest method of induction for patients with cerebrovascular disorders.     

The influence of different volatile inhaled anesthetics on the plasma protein binding of lidocaine

The author investigated the interactions of protein binding of lidocaine by inhaled anesthetics (halothane, enflurane, isoflurane and sevoflurane in vitro and in vivo. In the in vitro study, no significant changes of protein binding ratio were observed between the controls and any concentrations of the inhaled anesthetics even under high concentration (10 MAC). However, the percent of protein binding was inversely related to the total plasma lidocaine concentration. At lidocaine concentrations of 2, 5 and 9 micrograms.ml-1, the binding ratios were 66.37 +/- 5.36 (%), 55.58 +/- 4.38(%) and 51.66 +/- 4.12(%) respectively. By regression analysis (in vivo), the following relationship was obtained. Y = -0.66X +/- 57.4 (Y: % of protein binding fraction, X: lidocaine concentration). In terms of lidocaine protein binding, there seems to be no hazard in using lidocaine with any inhaled anesthetics.     

Timing of injection and plasma concentration of lidocaine before endotracheal intubation

The optimal time of intravenous lidocaine for attenuation of pressor responses to laryngoscopy and endotracheal intubation was evaluated in fifty adult patients and the correlation between plasma lidocaine level and its clinical effects were also studied.The plasma lidocaine levels were highest 0.5min after administration of lidocaine 1.5mg·kg^–1 intravenously. However, endotracheal intubation 0.5min after lidocaine administration caused significant increase in mean arterial pressure (MAP) and heart rate (HR). Mean arterial pressure and HR increased with endotracheal intubation following 1, 2 and 3min after lidocaine administration, but the magnitude of increase was not statistically significant. There were no significant differences in MAP changes among these three groups. It was concluded that the plasma lidocaine levels did not correlate with its suppressive effect on circulatory responses due to laryngoscopy and endotracheal intubation. Laryngoscopy and endotracheal intubation should be carried out at least 1min after intravenous lidocaine administration.(Okuda M, Ohi Y, Kurata M et al.: Timing of injection and plasma concentration of lidocaine before endotracheal intubation. J Anesth 4: 150–154, 1990)     

Desflurane and Isoflurane Increase Lumbar Cerebrospinal Fluid Pressure in Normocapnic Patients Undergoing Transsphenoidal Hypophysectomy

Background: Rapid emergence from anesthesia makes desflurane an attractive choice as an anesthetic for patients having neurosurgery. However, the data on the effect of desflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that isoflurane and desflurane increase intracranial pressure compared with propofol.

Methods: Anesthesia was induced with intravenous fentanyl and propofol in 30 patients having transsphenoidal hypophysectomy with no evidence of mass effect, and it was maintained with 70% nitrous oxide in oxygen and a continuous 100 micro gram [centered dot] kg sup -1 [centered dot] min sup -1 infusion of propofol. Patients were assigned to three groups randomized to receive only continued propofol infusion (n = 10), desflurane (n = 10), or isoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the desflurane and isoflurane groups received, in random order, two concentrations (0.5 minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of desflurane or isoflurane for 10 min each. Lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations were monitored continuously.

Results: Lumbar CSF pressure increased significantly in all patients receiving desflurane or isoflurane. Lumbar CSF pressure increased by 5 +/- 3 mmHg at 1-MAC concentrations of desflurane and by 4 +/- 2 mmHg at 1-MAC concentrations of isoflurane. Cerebral perfusion pressure decreased by 12 +/- 10 mmHg at 1-MAC concentrations of desflurane and by 15 +/- 10 mmHg at 1-MAC concentrations of isoflurane. Heart rate increased by 7 +/- 9 bpm with 0.5 MAC desflurane and by 8 +/- 7 bpm with 1.0 MAC desflurane, and by 5 +/- 11 bpm with 1.0 MAC isoflurane. Systolic blood pressure decreased in all but the patients receiving 1.0 MAC desflurane. To maintain blood pressure within predetermined limits, phenylephrine was administered to six of ten patients in the isoflurane group (range, 25 to 600 micro gram), two of ten patients in the desflurane group (range, 200 to 500 micro gram), and in no patients in the propofol group. Lumbar CSF pressure, heart rate, and systolic blood pressure did not change in the propofol group.