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Anesth Analg 2006;102:156-159 © 2006 International Anesthesia Research Society doi: 10.1213/01.ANE.0000184040.85956.98
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Abstract |
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We investigated the effect of IV lidocaine on the hemodynamic and bispectral index responses to induction of general anesthesia and endotracheal intubation. Forty patients (ASA I) were randomly allocated into 2 groups of 20 to receive normal saline or lidocaine 1.5 mg/kg IV 30 s after induction. Ninety seconds later, endotracheal intubation was performed. Systolic blood pressure, heart rate, and bispectral index were measured at baseline, 1 min after induction, at preintubation, and every minute until 5 min after endotracheal intubation. Bispectral index at 1 min after induction and preintubation in the lidocaine group were significantly lower compared with the control group (P < 0.05). Systolic blood pressure increased significantly at 1 and 2 min after intubation in the control group compared with the baseline value (P < 0.05) but did not increase significantly in the lidocaine group. Heart rate increased at 1 to 3 min in both groups (P < 0.05), but there was no significant difference between the two groups. One patient in the control group had recall of the procedure. We conclude that the administration of IV lidocaine (1.5 mg/kg) does not suppress the hypnotic response to endotracheal intubation.
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Introduction |
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The bispectral index (BIS) is an electroencephalogram (EEG)-derived parameter that has been optimized to correlate with level of sedation and loss of consciousness (1). Previous studies have shown that tracheal intubation is associated with increases in BIS as well as heart rate (HR) and arterial blood pressure (2–4). Therefore, intubation is likely to affect both the hypnotic and antinociceptive components of anesthesia. Instrumentation of the pharynx and tracheal intubation may result in tachycardia, hypertension, and increased plasma catecholamine concentrations that may evoke life-threatening conditions among susceptible individuals, especially those with cardiovascular disease (5,6). Various pharmacological attempts have been made to blunt such responses, including local anesthetics (7),
- and ß-blocking drugs (8), vasodilators (9), and opioids (10). Menigaux et al. (11) suggested that esmolol not only attenuated hemodynamic and somatic responses to laryngoscopy and endotracheal intubation but also prevented BIS arousal reactions in patients anesthetized with propofol. Lidocaine hydrochloride, an aminoethylamide local anesthetic and class IB antidysrhythmic drug, is acceptable for attenuation of the cardiovascular response to intubation and also diminishes cough reflexes, dysrhythmias, and increases in intracranial and intraocular pressure (12). Senturk et al. (13) reported IM local anesthetics decreased both the induction and maintenance doses of propofol.
Previous studies assessing the effectiveness of lidocaine in blunting the hemodynamic alterations induced by laryngoscopy and endotracheal intubation did not investigate the hypnotic response to endotracheal intubation. There is a possibility that lidocaine administration may alter anesthetic depth in response to induction and intubation. We therefore designed a randomized, double-blind, placebo-controlled study to investigate the effect of lidocaine on hemodynamic and BIS responses to induction of general anesthesia and endotracheal intubation.
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Methods |
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The study population comprised patients scheduled for elective orthopedic or gynecologic surgery who were aged 18–60 yr and classified as ASA physical status I. Patients with known neurological, cardiac, or metabolic disease, including those taking cardiovascular medication, were excluded. The Human Studies Subcommittee approved the study and all patients gave written informed consent. The patients were randomly allocated into 2 groups of 20, to receive normal saline (control group) or lidocaine 1.5 mg/kg (lidocaine group).
Patients were premedicated with an IM injection of 0.2 mg glycopyrrolate 1 h before the operation. No premedication sedative was administered before surgery. On arrival in the operating room, electrocardiograph (ECG) monitoring, pulse oximetry, and noninvasive arterial blood pressure monitoring were established and baseline values were obtained. A standard BIS monitor strip (BIS Sensor®; Aspect Medical Systems, Newton, MA) was placed on the forehead before induction of anesthesia. Anesthesia was then induced with IV thiopental 5 mg/kg, fentanyl 1.5 µg/kg, and rocuronium 0.6 mg/kg. Either normal saline (6 mL) or lidocaine 1.5 mg/kg (in 6 mL saline) was administered 30 s after induction in a double-blind fashion. Direct laryngoscopy was performed 2 min after administration of rocuronium. Systolic blood pressure (SBP; mm Hg), HR (bpm), and BIS were recorded again 1 min after rocuronium administration, immediately before endotracheal intubation (preintubation), and at every minute after endotracheal intubation during the study period using an anesthesia monitor (Eagle 3000; Marquette Medical Systems, Milwaukee, WI). The EEG recording was continuous using an Aspect A2000 BISTM EEG monitor (Aspect Medical Systems) that also computed the BIS (version 3.3). Durations of laryngoscopy were recorded. Each intubation was performed by an experienced anesthesiologist and was accomplished within 20 s. After tracheal intubation, patients' lungs were ventilated with a tidal volume of 10 mL/kg and respiratory rate of 12 breaths/min. Anesthesia was maintained with a 1.0% inspired concentration of sevoflurane and 50% nitrous oxide in oxygen for 5 min. All patients were interviewed in the recovery room regarding awareness during the study period.
A power analysis was performed on the basis of d (µ – µ'/
) = 0.8 (where µ – µ' = difference in mean and = sd), = 0.05, and ß = 0.2 (power of 80%), which determined that a sample size of 20 patients per group was adequate to detect a significant difference in BIS. Data were analyzed using the SPSS version 11.0 for Windows statistical package (SPSS Inc., Chicago, IL). Student's t-test was used for continuous data. The 
2 test was used to compare gender differences between the two groups. All variables were compared with baseline, 1 min after induction, and preintubation values by one-way analysis with repeated measurements and significant results were analyzed using Tukey's post hoc test. P values < 0.05 were considered significant; values are presented as mean ± sd.
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Results |
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The two groups were similar with regard to age, sex, height, weight, and duration of laryngoscopy (Table 1). Figure 1 presents BIS, SBP, and HR changes after induction of general anesthesia and endotracheal intubation in both groups. After administration of lidocaine, BIS at 1 min after induction and preintubation in the lidocaine group were significantly lower compared with the control group (P < 0.05). The means of BIS values at preintubation and 1, 2, 3, 4, and 5 min after intubation in the control group (66.8, 70.7, 72.2, 72.1, 70.6, and 68.5, respectively) and at 1 to 5 min after intubation in the lidocaine group (68.1, 71.0, 70.0, 68.6, and 68.2, respectively) were higher than 60. Both SBP and HR changed significantly with time (P < 0.0001) but were not significantly affected by the test drug. SBP increased significantly at 1 and 2 min after intubation in the control group compared with baseline (P < 0.05) but did not increase significantly in the lidocaine group. HR increased at 1, 2, and 3 min in both groups compared with baseline, but there was no significant difference between the two groups. No signs of local anesthetic toxicity or side effects were observed in any patients. Abnormal ECG and Spo2 <98% were not observed throughout the study period. One patient in the control group had recall of the procedure.
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P < 0.05 versus its 1 min after induction value; 
P < 0.05 versus its preintubation value, #P < 0.05 versus the control group.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The results of this study demonstrate that BIS at 1 minute after induction and preintubation in the lidocaine group were lower compared with the control group. Lidocaine suppressed SBP increases at 1 and 2 min after intubation but did not prevent HR increases at 1, 2, and 3 min.
Several investigations have been conducted to evaluate the hemodynamic response of lidocaine during anesthesia induction and intubation. Yorukoglu et al. (14) reported that the combination of lidocaine 1.5 mg/kg and rocuronium 0.6 mg/kg along with propofol effectively blocked increases in HR after intubation. Kindler et al. (15) and Durrani et al. (16) reported that IV lidocaine 1.5 mg/kg did not reliably prevent the increase of HR associated with laryngoscopy and intubation.
EEG is a continuous, noninvasive method that has been used as a measure of anesthetic drug action on the central nervous system (CNS) (17). The addition of induction drugs (18) or inhaled anesthetics (19) is frequently used before tracheal intubation to blunt hemodynamic responses but this may deepen both the hypnotic and antinociceptive components of anesthesia. BIS is an empirically derived multifocal EEG measurement and a dimensionless number between 0 and 100 that correlates with hypnosis. Several studies have suggested that sympatholytic drugs may be effective alterations to opioid analgesics. Nakayama et al. (20) reported that fentanyl modified hemodynamic changes during induction of anesthesia with propofol without affecting BIS responses.
The mechanisms by which IV lidocaine suppresses airway reflexes are unknown. However, rapid equilibration of local anesthetics between blood and brain suggest that a depressant effect on the CNS may contribute to this action (21). Lidocaine produces a central sedative analgesic effect when introduced into the bloodstream in appropriate doses. In our study, BIS at 1 min after induction and at preintubation in the lidocaine group were lower compared with the control group. This finding was observed under no nociceptive stimulation (i.e., before intubation). There were no differences between the two groups after intubation. In contrast, Menigaux et al. (11) concluded that addition of esmolol to general anesthesia with propofol did not affect BIS before intubation but attenuated BIS responses after intubation.
Slavov et al. (22) suggested that SBP changes after induction of anesthesia were more sensitive than BIS in predicting movement in response to laryngoscopy and intubation. This may be explained as the action sites of hemodynamic and hypnotic responses to intubation. A reflex response to tracheal intubation is mediated at the subcortical level and thus may be unrelated to the BIS value, instead reflecting cerebral cortical activity (3). However, peripheral noxious stimuli reach the brain through the ascending reticular activating systems of the brainstem and may cause EEG activation (3). Therefore, the direct anesthetic effect of lidocaine may be inadequate to reduce the hypnotic response to intubation.
The limitation of this study was that the mean values of BIS after the intubations in both groups were higher than 60 and the mean value of BIS at preintubation in the control group was also higher than 60. No values were higher than 80, a value that is associated with awareness (23). However, one patient in the control group had recall during the study period. Schneider et al. (24) suggested that BIS does not reliably predict awareness in relation to intubation, but we observed a recall in the control group. A larger sample size study is needed to assess recall incidence between the two groups. Because BIS between 40 and 60 is recommended to guide the administration of hypnotic and sedative drugs during general anesthesia, the anesthetic depth in this study seems to be insufficient for the stimulus of intubation.
In conclusion, we found that lidocaine attenuated hemodynamic responses to laryngoscopy and endotracheal intubation and decreased BIS after induction but did not prevent BIS increases in response to laryngoscopy and endotracheal intubation. These results suggest that IV lidocaine to blunt the hemodynamic alterations induced by laryngoscopy and endotracheal intubation does not suppress the hypnotic response to endotracheal intubation.
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Footnotes |
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Supported, in part, by a research grant from Korea University, Seoul, Korea.
Presented, in part, at Euroanesthesia, Vienna, Austria, May 28–31, 2005.
Accepted for publication May 19, 2005.
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References |
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- Glass PS, Bloom M, Kearse L et al. Bispectral analysis measures sedation and memory effects of propofol, midazolam, isoflurane, and alfentanil in healthy volunteers. Anesthesiology 1997;86:836–47.[Web of Science][Medline]
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[Abstract/Free Full Text] - Mi WD, Sakai T, Takahashi S, Matsuki A. Haemodynamic and electroencephalograph responses to intubation during induction with propofol or propofol/fentanyl. Can J Anaesth 1998;45:19–22.[Web of Science][Medline]
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[Abstract/Free Full Text] - Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987;59:295–9.
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