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From *Klinik für Anästhesiologie und Intensivmedizin; and Institut für Medizinische Informatik, Biometrie und Epidemiologie, Universitätsklinikum Essen, Essen, Germany.
Address correspondence and reprint requests to Michael Adamzik, Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Hufelandstr. 55, D-45122 Essen, Germany. Address e-mail to michael.adamzik{at}uni-essen.de.
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Abstract |
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 Top Abstract IntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
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METHODS: Thirty patients with asthma (age 49.1 ± 15.6 yr [mean ± sd]) undergoing intubation after standardized anesthetic induction (etomidate 0.3 mg/kg, fentanyl 5 µg/kg, rocuronium 0.6 mg/kg, 50% nitrous oxide) were studied. Airway resistance was measured immediately after intubation and 5, 10, and 15 min later. Five minutes after intubation, either lidocaine (2 mg/kg IV for 5 min, followed by 3 mg · kg–1 · h–1 for 10 min) or saline was administered.
RESULTS: Airway resistance immediately after intubation averaged 23 ± 12 cm H2O · s · L–1. Airway resistance further increased (+38%) after administration of saline, but decreased (–26%, P < 0.004) to less than the initial values after lidocaine.
CONCLUSIONS: IV lidocaine given after endotracheal intubation mitigates bronchoconstriction in patients with asthma.
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Introduction |
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TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
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The IV administration of the sodium channel blocker lidocaine can attenuate the response to a variety of inhalational challenges in awake volunteers with bronchial hyperreactivity (4–6). Accordingly, lidocaine pretreatment for patients with bronchial hyperreactivity has been recommended before airway irritation (7). In contrast, in patients undergoing propofol/isoflurane anesthesia, IV lidocaine given before induction did not attenuate bronchoconstriction (8). Thus, it is unclear whether lidocaine is effective in attenuating intubation-induced bronchoconstriction.
The effects of IV lidocaine given after intubation on bronchoconstriction have not been studied in anesthetized patients with asthma. We tested the hypothesis that IV lidocaine mitigates bronchoconstriction after intubation in these patients.
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METHODS |
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TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
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All patients had a previous diagnosis of asthma. Thirteen patients were treated with inhaled ß2-adrenergic drugs up to the day of surgery. Five patients took only an antihistaminic as needed, and several were receiving inhaled and/or oral corticosteroids (Table 1). Patients were instructed to take their regular medications up to and including the day of surgery. Twenty patients were smokers. Patients with significant cardiac disease, chronic obstructive pulmonary disease (COPD), emphysema, chronic bronchitis, or those requiring awake fiberoptic intubation were excluded. COPD was defined according to the British Thoracic Society’s definition and the Global Initiative for Chronic Obstructive Lung Disease definition (9,10).
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Twenty-two patients received preoperative spirometry (Table 1) at the request of the attending anesthesiologist. Pulmonary function tests were not a requirement for enrollment.
Measurements
All patients were premedicated with midazolam (0.1 mg/kg p.o.) 30 min before transport to the operating room. After applying standard noninvasive monitoring (electrocardiogram, blood pressure cuff, oximetry), two 18-gauge cannulae were inserted into the right and left antecubital veins to infuse lidocaine or placebo and to withdraw blood, respectively. To assess bronchoconstriction before intubation, auscultation was always performed on either side of the chest at the fourth intercostal space (ICS) in the mid-axillary line, the fifth ICS in the midclavicular line, and the second ICS in the parasternal line before intubation. The presence of wheezing was determined by a simple "yes or no" score by a physician not involved in this study and blind to the protocol.
Anesthesia was induced with etomidate (0.3 mg/kg), fentanyl (5 µg/kg), and rocuronium (0.6 mg/kg), and the trachea was intubated. Patients’ lungs were ventilated mechanically with 50% oxygen in nitrous oxide, a tidal volume of 10 mL/kg, at a rate of 10 breaths/min, without positive end-expiratory pressure. Neuromuscular blockade was regularly assessed (Innervator, Fisher and Payckel, Germany), and showed absence of twitches during supramaximal ulnar nerve stimulation during the study.
To assess the effect of lidocaine versus placebo, we measured exhaled airway resistance, using the passive exhalation method of Comroe et al. (11). Briefly, the respiratory system was inflated with 1500 mL of air by a super syringe via the endotracheal tube, while the expiratory line was occluded by a three-way valve. This volume was held in the lungs for 2–3 s (attaining a steady-state in transthoracic pressure) before rapid rotation of the three-way valve permitted passive exhalation via a heated (37°C) pneumotachograph (Hans Rudolph, model 3830), calibrated using a 2000-mL super-syringe. Volume and flow during passive exhalation via the pneumotachograph were measured with a differential pressure transducer (Validyne MP 45–14). Transthoracic pressure at the tip of the endotracheal tube was measured with a pressure transducer (Validyne MP 45–14). Signals were digitized and stored in a PC running a dedicated respiratory software (Mac Lab, 6.0, respiratory measurement module).
Pressure during sustained thoracic inflation, and flow, pressure, and volume during passive exhalation were analyzed offline. Static total respiratory compliance was calculated by dividing total volume exhaled body temperature and pressure saturated (BTPS) by transthoracic pressure measured immediately before exhalation. During expiration, the point at which expiratory flow was 0.5 L/s was identified and the added volume of gas remaining in the lung at this instant was calculated. Division of this volume by compliance provided the transthoracic pressure required to sustain a flow of 0.5 L/s, from which resistance was derived.
Lidocaine plasma concentrations were determined by high-pressure liquid chromatography (HPLC, Waters 2690, with photo diode array detector, spectrophotometric detection at 200 nm). The lower level of detection was 0.01 µg/mL, and the coefficient of variation was <0.5% (12).
Randomization was performed using computer-generated numbers. Study medications were prepared as a 1% solution (lidocaine or saline) in a 50-mL syringe, with the investigator blinded to content.
Protocol
Blood samples were taken and resistance measurements were performed <1, 5, 10, and 15 min after intubation. After the second resistance measurement 5 min after intubation, either lidocaine (2 mg/kg IV over 5 min, followed by 3 mg · kg–1 · h–1 for 10 min) or saline was administered. Heart rate, arterial blood pressure, and oxygen saturation were recorded at 5-min intervals on the anesthesia record.
Data Analysis
Data are presented as mean ± sd or box plots. The following a priori null hypothesis was tested: Values of airway resistance after intubation do not differ between placebo or lidocaine treatment. To compare between-groups differences of pre–post changes, we used a Mann–Whitney U-Test with Bonferroni–Holm adjustment for multiple tests. Values of variables within groups were compared using the Wilcoxon’s signed rank test. Null hypotheses were rejected, and significant statistical differences were assumed with an a priori 
error P of <0.05.
Sample size estimation was based on data on the effect of albuterol against intubation-induced bronchoconstriction in patients with asthma. The relative difference between groups was assumed to be 40%, with a standard deviation of 50% within the groups (8). We calculated that 15 patients per group would be appropriate to reveal a relevant and statistically significant difference, if present.
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RESULTS |
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TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
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Immediately after intubation, airway resistance averaged 23 ± 12 cm H2O · s · L–1 in all patients. Resistance subsequently increased in nine patients in the saline group, and in four patients in the lidocaine group (Fig. 1). On average, airway resistance increased (+38%) after intubation and administration of saline (from measurement after 1 min to after 15 min), but decreased (–26%, P < 0.004) after intubation and administration of lidocaine (Figs. 2 and 3). Airway resistance after intubation was significantly lower (P < 0.01) after lidocaine administration. One subject in the placebo group had a fourfold increase in airway resistance 15 min after intubation. This patient had a common cold the day after anesthesia, and was probably prodromal the day of surgery. Inclusion of this individual did not alter the statistical significance of the results.
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Heart rate and mean arterial blood pressure were similar in both groups (Fig. 5). There were no cardiovascular side effects after lidocaine administration.
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DISCUSSION |
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TopAbstractIntroductionMETHODSRESULTSDISCUSSIONREFERENCES |
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In awake patients with asthma, bronchodilator treatment must change FEV1 by more than 15% to be considered clinically relevant (13–15). In our study, the difference in airway resistance between treated and nontreated patients averaged approximately 50%, well exceeding this threshold. The magnitude of lidocaine’s effect is not only statistically significant, but also clinically relevant.
Our results differ from those of Weiss and Patwardhan (16), who studied conscious patients with stable asthma and noted only a slight improvement in FEV1 and FVC after administration of IV lidocaine. Loehning et al. (17) found that IV lidocaine did not block the increase in airway resistance elicited by water aerosol in anesthetized healthy patients. However, both studies tested IV lidocaine against either a low baseline airway resistance or evoked only mild bronchoconstriction, and did not assess an effect of profound airway stimulation from endotracheal intubation. Maslow et al. (8) failed to show prophylactic beneficial effects on airway resistance of IV lidocaine in intubated and anesthetized patients with asthma. However, they acknowledged that any effects of lidocaine on bronchomotor tone might have been concealed because of the concomitant administration of propofol and isoflurane, both of which have considerable bronchodilating effects (18,19). We selected etomidate, fentanyl, and nitrous oxide to minimize anesthetic effects on airway resistance (20). Eames et al. (20) demonstrated increased airway resistance after intubation with etomidate. Although etomidate is not the first-choice induction drug for otherwise healthy patients with a history of asthma or COPD, we consider propofol a rather poor choice for elderly patients with cardiovascular disease, in particular those with congestive heart failure, even in the presence of asthma.
Our data are consistent with a previous study from our group (7) in awake volunteers with bronchial hyperreactivity showing that IV lidocaine attenuates bronchial hyperreactivity to the same degree as that of inhaling 1.5 mg salbutamol, with additional effects when both drugs are combined. Our data are also compatible with our previous data showing that IV lidocaine attenuates bronchial hyperreactivity to an acetylcholine inhalation challenge in awake volunteers in a dose-dependent fashion (4). Thus, lidocaine may be suitable for both prophylaxis and treatment of intubation-induced bronchoconstriction.
It is not possible to compare airway resistance before and after intubation. The presence of an endotracheal tube and the different techniques required to measure resistance in awake and intubated/anesthetized patients compromise any direct comparison of preintubation and postintubation airway resistances.
We studied a well-defined group of patients with airway hyperreactivity from asthma and excluded patients with other types of lung disease. Accordingly, we do not know whether our results apply to patients with nonasthmatic bronchial hyperreactivity, e.g., COPD.
In conclusion, this prospective, double-blind, placebo-controlled study in patients with asthma demonstrated that IV lidocaine can mitigate bronchoconstriction when given after anesthetic induction and intubation.
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Footnotes |
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We have disclosed all pertinent involvement with any organization with a financial interest with the subject matter.
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REFERENCES |
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This article has been cited by other articles:
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  B. R. Burches Jr and D. O. Warner Bronchospasm After Intravenous Lidocaine Anesth. Analg., October 1, 2008; 107(4): 1260 - 1262. [Abstract] [Full Text] [PDF]
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