The laryngeal mask airway (LMA; The Laryngeal Mask Airway Co., Ltd, Nicosia, Cyprus) has been widely used as an alternative to the face mask and oropharyngeal airway, and in some cases, to tracheal intubation, especially for ambulatory anaesthesia. Furthermore, it has been shown that propofol, when used as an induction agent, provides better LMA insertion conditions than thiopental, because it better relaxes the jaw and has a greater depressant effect on airway reflexes [1,2]. Patient response to LMA insertion during propofol induction, however, depends on many factors, such as the method of administration used [e.g. bolus injection, target-controlled infusion (TCI)], dose, speed of injection, and the use of adjuvant drugs such as, midazolam, opioids, lidocaine, muscle relaxants, time elapsed after propofol administration, and propofol plasma and effect-site concentrations at the time of LMA insertion [3–7].
In our previous study, we found that propofol TCI induction at a target plasma concentration (Cpt) of 8 μg ml−1, as compared with 6 μg ml−1, did not improve LMA insertion conditions at the same effect-site concentration, and more careful attention was found to be required for the decreased blood pressure after LMA insertion. In addition, we also found that the incidences of gagging, coughing, and laryngospasm increased when LMAs were inserted at an effect-site concentration of 2.5 μg ml−1 without the aid of a neuromuscular blockade .
Lidocaine has been used both topically and intravenously to reduce cardiovascular responses, coughing, and bucking associated with tracheal intubation, because of its dose-dependent cough-suppressing effect [9–13]. Therefore, we hypothesized that intravenous (i.v.) lidocaine pretreatment would improve LMA insertion conditions during propofol TCI without the aid of a neuromuscular blocker.
The present study was undertaken to determine the effects of 1.5 mg kg−1 i.v. lidocaine pretreatment on LMA insertion at an effect-site concentration of 2.5 μg ml−1 during anaesthesia induction using propofol TCI at a Cpt of 6 μg ml−1 without the aid of a muscle relaxant.
After obtaining approval from the Institutional Review Board, and informed patient consent, 80 patients scheduled for minor surgery requiring the use of an LMA and who met the inclusion criteria were prospectively enrolled in this study. All patients were of American Society of Anesthesiologists (ASA) physical status I or II, between the age of 16 and 54, and weighed between 45 and 100 kg. Patients with difficult airways (Mallampati classification III or IV), a history of gastrointestinal reflux, those regularly taking sedative drugs or antiepileptic medications, those with a history of valvular or ischaemic heart disease, hypertension, renal disease, pregnancy, or known allergies to any anaesthetic drug were excluded.
Patients were premedicated with intramuscular (i.m.) atropine sulfate 0.5 mg, approximate 1 h before the induction of anaesthesia. They were randomly allocated to the lidocaine and control groups using a random number table (0, control group = pretreatment with saline as a placebo; 1, lidocaine group = lidocaine pretreatment). A blood pressure cuff was attached on the contralateral side of the arm into which an 18-gauge cannula had been inserted for the i.v. infusion of normal saline and anaesthetics. In all patients, half of the fluid deficit from fasting was replaced with normal saline over 10–15 min. Patients were connected to a SIEMENS Sirecust 1281 patient monitor (Siemens Medical Electronics, Denver, Colorado, USA) for continuous noninvasive pressure monitoring. After taking baseline measurements of heart rate (HR), systolic blood (SBP), and diastolic arterial blood pressure (DBP), and determining oxygen saturation by pulse oximetry (SpO2), patients were preoxygenated for 3 min before induction. All patients initially received i.v. midazolam 0.04 mg kg−1, and 3 min later anaesthesia was induced by propofol TCI using a Graseby 3500 anaesthesia syringe pump (SIMS Graseby Limited, Hertfordshire, UK) incorporating ‘Diprifusor’. An electronically tagged ‘Diprivan’ prefilled syringe containing 1% propofol (Zeneca Pharmaceuticals, Macclesfield, UK) was used for TCI. All patients in the two groups received 1.5 mg kg−1 lidocaine (lidocaine group) or an equivalent volume of normal saline (control group) 50 s after starting propofol TCI at a Cpt of 6 μg ml−1. LMAs (sizes 4 or 5) were lubricated with water-based gel and inserted using a standard technique when effect-site concentrations reached 2.5 μg ml−1 (as displayed on the infusion pump by pressing the ‘INFO’ soft key) by a single-blinded investigator with 1-year experience of LMA insertion.
The investigator assessed the following conditions during LMA insertion: mouth opening ability (full, partial, nil), intensity of gagging (nil, slight, gross, not assessable due to insertion failure) and coughing (nil, slight, gross, not assessable due to insertion failure), head or limb movement (absent or present), laryngospasm (absent, present, not assessable due to insertion failure), and overall ease of LMA insertion (easy, difficult, not possible). Laryngospasm was defined as the presence of stridor, the absence of a capnograph wave, or any other evidence of upper airway obstruction during assisted or controlled manual ventilation through the inserted LMA lasting for 15 s or more.
When LMA insertion was not possible, further attempts to insert were made after effect-site concentration increased by 0.5 μg ml−1. Total numbers of attempts were recorded. However, insertion conditions were compared only for first attempts. When an LMA could not be inserted at the fifth attempt, or functional failure without fibre-optic visualization of cords occurred (fibre-optic score: 0) , or when cough or laryngospasm after insertion was so severe that ventilation was deemed impossible, the inserted LMA was removed and reinserted with/without the aid of muscle relaxant. All patients, including those in whom LMA insertion was not possible at the first attempt, were categorized as LMA insertion failures. SBP, DBP, and HR measurements were taken at seven time points, before and 3 min after i.v. midazolam, at loss of consciousness and eyelash reflex, at an effect-site concentration of 2.5 μg ml−1, and immediately 1 and 3 min after LMA insertion.
Statistical analyses were performed only when LMA insertion was successful at the first attempt.
The unpaired t-test was used to compare the lidocaine and control groups with respect to age, weight, and haemodynamic variables, whereas the Chi-squared test (with Fisher's exact probability test when appropriate) was used to compare sex, ASA physical status, smoking habit, and LMA insertion conditions. Repeated measures analysis of variance (ANOVA) was used to compare haemodynamic variables within groups. Data are expressed as patient numbers (percentages) or as means ± standard deviation (SD). P values of less than 0.05 were considered statistically significant.
No significant difference was observed between the lidocaine and control groups in terms of age, weight, sex ratio, ASA physical status, or smoking habit (Table 1).
Gagging (25 vs. 55%), coughing (5 vs. 22.5%), and laryngospasm (2.5 vs. 17.5%) were significantly lower in the lidocaine group (Table 2, P < 0.05), but no significant differences were observed between the two groups in terms of degree of mouth opening, head or limb movements, ease of insertion (Table 2), incidences of hiccups or apnoea, or LMA insertion success rates (Table 3). The failure rates of LMA insertion at an effect-site concentration of 2.5 μg ml−1 were 15% (six patients) in the control group and 2.5% (one patient) in the lidocaine group. LMA insertion was not possible at an effect-site concentration of 2.5 μg ml−1 in four patients in the control group as a result of no jaw opening (two patients) or biting (two patients). For three of these four patients, LMA insertion was possible at an effect-site concentration of 3.0 μg ml−1 and in the other at 3.5 μg ml−1. In another two patients in the control group, the inserted LMA was removed and intubation was achieved with the aid of a muscle relaxant because of severe coughing followed by laryngospasm or severe coughing with large amounts of oral secretion. LMA insertion was not possible in one patient in the lidocaine group at an effect-site concentration of 2.5 μg ml−1 due to biting, but was possible by reinsertion at an effect-site concentration of 3.0 μg ml−1. None of the seven patients in whom LMA insertion failed at an effect-site concentration of 2.5 μg ml−1 showed desaturation to less than 90%, and their postoperative courses were uneventful. All seven were interviewed in the recovery room and no patient had any recall of the incident.
On restricting the study to patients in whom LMA insertion was successful at the first attempt, we were able to compare the haemodynamic responses of 34 patients (85%) in the control group with 39 patients (97.5%) in the lidocaine group. The changes in SBP, DBP, and HR from the values before i.v. midazolam are presented as percentages. SBP and DBP decreased and HR increased significantly throughout the study period, but no significant inter-group differences were observed. In both groups, SBP, DBP and HR significantly increased immediately after LMA insertion compared with those before insertion (Fig. 1).
In this study, i.v. lidocaine (1.5 mg kg−1) 50 s after starting propofol TCI at a Cpt of 6 μg ml−1 improved LMA insertion conditions at an effect-site concentration of 2.5 μg ml−1 by reducing coughing, gagging, and the incidence of laryngospasm without aggravating haemodynamic responses, which may have been due to the suppression of laryngeal reflexes or a greater anaesthetic depth.
The fact that i.v. lidocaine reduces cardiovascular responses and cough reflex associated with tracheal intubation is well known. However, published results on this topic vary widely as a result of different dosages and timings of lidocaine administration and the types of induction agent used. Yukioka and colleagues  showed that i.v. lidocaine at least 1 mg kg−1 suppresses cough reflex dose dependently during tracheal intubation and that cough reflex is suppressed completely at a dose of 2 mg kg−1. However, a large dose of i.v. lidocaine (2 mg kg−1) has been shown to cause systemic side effects such as a peri-oral tingling sensation . Therefore we chose to administer 1.5 mg kg−1 in this study. The many studies performed to determine the optimal timing of lidocaine administration have produced disparate results. Yukioka and colleagues  reported that coughing was suppressed completely and decreased significantly 1 min and 3–5 min after administering i.v. lidocaine 2 mg kg−1, respectively. In studies that utilized i.v. lidocaine 1.5 mg kg−1, optimal timings of administration on the basis of the attenuation of haemodynamic responses by intubation were determined to be 1 min , 2–3 min , or 3 min  prior to intubation. In our previous study , it took an average of 140 s to reach an effect-site concentration of 2.5 μg ml−1 during propofol TCI using a Cpt of 6 μg ml−1. Therefore, in the present study, we administered lidocaine 50 s after starting TCI in order to allow 90 s before LMA insertion.
Successful LMA insertion requires an adequate depth of anaesthesia. Casati and colleagues  found that the mean Cpt of propofol required to place an LMA was 4.3 μg ml−1, and that to successfully place an LMA in 95% of patients an increase of Cpt to 6 μg ml−1 was required. However, Kodaka and colleagues  showed that 50% and 95% of patients did not respond to LMA insertion when propofol plasma concentrations were 3.24 μg ml−1 and 4.07 μg ml−1, respectively. We attribute this discrepancy to the different methods used. Casati and colleagues  started with TCI at a Cpt of 2.0 μg ml−1 and then raised Cpt in increments of 0.5 μg ml−1. Kodaka and colleagues  started at a Cpt of 4.0 μg ml−1 and waited for plasma and effect-site concentrations to equilibrate, and used modification of Dixon's up-and-down method. However, we started with TCI at a Cpt of 6 μg ml−1 and inserted LMAs at an effect-site concentration of 2.5 μg ml−1. During LMA insertion, effect-site concentration increased continuously and reached about 3.1 μg ml−1 immediately after insertion, as was found during our previous study . Taylor and Kenny  reported that LMA insertion success rates increased at higher target propofol concentrations. However, in our previous study, we found that increasing the Cpt of propofol to 8 μg ml−1 from 6 μg ml−1 did not improve LMA insertion conditions at the same effect-site concentration, and that greater care was required for the decreased blood pressure after LMA insertion. Moreover, because LMA insertion conditions during propofol TCI may be dependent only on effect-site concentration at the time of insertion and not dependent on Cpt, insertion at an effect-site concentration more than 2.5 μg ml−1 might be easier.
In this study, the success rate of LMA insertion was high (85% in the control group and 97.5% in the lidocaine group) at a relatively low effect-site concentration. We attribute this in part to premedication with i.v. midazolam 0.04 mg kg−1 3 min before starting TCI, because propofol and midazolam act synergistically [19,20]. Moreover, in addition to the cough-suppressing effects of lidocaine, it may be that increased anaesthetic depth also contributed to the high insertion success rate in the lidocaine group in the present study. Several studies have reported the effect of lidocaine on decreasing minimum alveolar concentration of inhaled anaesthetics [21–23]. Lidocaine blood levels of 3–6 μg ml−1 are known to potentiate the effects of nitrous oxide anaesthesia on reducing the minimum alveolar concentration of halothane in humans . Furthermore, cough reflex was found to be completely suppressed when lidocaine plasma concentrations exceeded 3 μg ml−1. Bedford and colleagues  observed a mean lidocaine level in blood of 3.2 μg ml−1 1.5 min after administering 1.5 mg kg−1 i.v. In view of previously published data, we believe that in the present study lidocaine plasma concentrations at the time of LMA insertion may well have been higher than 3 μg ml−1, but unfortunately they were not measured.
Laryngeal mask airway insertion is possible with or without the use of neuromuscular blocking agents, although several studies [7,25] have shown that small doses of muscle relaxants improve LMA insertion conditions. LMA itself is very useful and widely used, especially for outpatient surgery anaesthesia which requires the patient to ventilate spontaneously. In the present study, to mimic this clinical situation we inserted LMAs without the aid of muscle relaxants.
We found that SBP and DBP decreased significantly, whereas HR increased significantly during the study period. We found that SBP and DBP decreased maximally at an effect-site concentration of 2.5 μg ml−1 in both groups by 17.6–22.3% (Fig. 1). Although reported degrees of hypotension vary between studies, hypotension after the induction of anaesthesia with propofol has been well documented . Furthermore, several studies [26,27] have shown BP and HR increase significantly after LMA insertion. Similarly, we noted significant increases in SBP, DBP, and HR immediately after LMA insertion in both groups, but no significant inter-group differences were observed, which suggests that i.v. lidocaine fails to attenuate but does not aggravate cardiovascular response to LMA insertion. Several previous studies have reported that i.v. lidocaine does not attenuate cardiovascular response to laryngoscopy and tracheal intubation [28,29]. However, unlike that observed for laryngoscopy and intubation, we observed that SBP and DBP after LMA insertion remained lower than they were prior to midazolam premedication. It has been established that the use of an LMA obviates the need for laryngoscopy and intubation of the trachea, which cause undesirable increases in BP and HR in patients with a pre-existing myocardial or cerebrovascular insufficiency.
We conclude that i.v. lidocaine 1.5 mg kg−1 injected 50 s after starting propofol TCI with a Cpt of 6 μg ml−1 (90 s before LMA insertion) improves LMA insertion conditions at an effect-site concentration of 2.5 μg ml−1 without aggravating haemodynamic responses.
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