March 8, 2001

Inhaled Albuterol, but Not Intravenous Lidocaine, Protects Against Intubation-Induced Bronchoconstriction in Asthma
Maslow A, Regan M, Israel E, Darvish A, Mehrez M, Boughton R, Loring S.
Anesthesiology 2000: 93: 1198-1204.

Commentary by Beverly Philip, M.D.

[see abstract below]

Asthmatic patients undergoing general anesthesia with tracheal intubation have increased risk for intubation-induced bronchospasm. A variety of drugs have been tried perioperatively to affect airway response to intubation. For intravenous lidocaine, the literature suggests that it may produces bronchodilation, but most of the studies were not conducted during general anesthesia with tracheal intubation. Therefore, these authors prospectively studied the effects of intravenous lidocaine in asthmatic patients undergoing general anesthesia. When preliminary results failed to show a protective effect, they extended the study using the same patient population and study protocol to include a test of inhaled albuterol, a drug known to be an effective bronchodilator with asthmatic patients.

One hundred ten patients scheduled for elective surgery that required general anesthesia and tracheal intubation were recruited over an eight-year period. All patients had a diagnosis of asthma by their primary care physician for at least one year, and all had been treated for reactive airway disease with inhaler therapy in the month before surgery. Patients with significant cardiac disease or those requiring awake or fiberoptic intubation were excluded. Patients were instructed not to take any of their regular asthma medicines on the day of surgery.

Part 1 of the study tested the efficacy of intravenous lidocaine as a randomized double-blind trial compared to placebo. Part 2 tested the efficacy of inhaled albuterol in the same study protocol also compared to placebo. To assess effectiveness, the authors measured lower pulmonary resistance, R_L. Because of the relatively high and variable resistance due to the upper airway, measurements before and after intubation could not be compared. Therefore, measurements of lower pulmonary resistance were performed after intubation only. Two measurements were taken at approximately 5 min intervals. The bronchodilator anesthetic isoflurane was begun and then three additional resistance measurements taken. Patients with high pulmonary resistance (R_L > 5 cmH₂O· l^-1•s^-1) after intubation and before administration of isoflurane, whose resistance subsequently decreased by 50% or more while breathing isoflurane, were deemed to have "responded" to intubation with bronchoconstriction.

Transpulmonary pressure was measured with a differential transducer connected between an esophageal balloon catheter and a tracheal catheter positioned at the tip of the endotracheal tube. Airflow was measured with a pneumotachometer and pressure transducer.

In part 1, intravenous lidocaine 1.5 mg/kg or saline was given as a bolus 2.5-3 minutes before planned intubation. In part 2, albuterol or placebo was administered in four puffs from a metered dose inhaler, 15-20 minutes before planned intubation. All patients were premedicated with midazolam 1-2 mg and given 100% oxygen to breathe. Anesthesia was induced with propofol 2 mg/kg, fentanyl 3 �g/kg, and vecuronium 0.1 mg/kg and was maintained with a propofol infusion 100-200 �g/kg/min and 50% nitrous oxide in oxygen. Intubation was performed after laryngoscopy using 7.5 mm tube for men and 7.0 mm for women, and the esophageal and tracheal catheters were then positioned. After the initial two resistance measurements, isoflurane inhalation (2% inspired concentration) was begun and the propofol infusion was discontinued.

Results

There was one patient among the 110 subjects who demonstrated sufficiently severe bronchoconstriction to require termination of the protocol and prompt treatment; this patient was in the intravenous lidocaine group. There were no significant differences between the groups in preoperative patient or pulmonary characteristics.

Part 1: Lidocaine-Placebo

There was no difference in hemodynamic values after intubation, suggesting the groups were anesthetized to similar depth. Comparing lidocaine and placebo, there were no significant differences in lower pulmonary resistance (R_L) after intubation or after isoflurane. There were also no significant differences in the number of responders to tracheal intubation between the two groups.

Part 2: Albuterol-Placebo

There was no difference in hemodynamic responses to intubation between the groups. The R_L after intubation and after isoflurane was lower than in the albuterol treated group compared to placebo. There were also significantly fewer ‘responders’ (high postintubation resistance that lowered with isoflurane treatment) in the albuterol group compared to placebo.

Effects of Isoflurane

There was statistically significant reduction in R_L after the administration of isoflurane in all study groups. This corroborates the known bronchodilation effect of this drug.

Conclusion

These results show that intravenous lidocaine, 1.5 mg/kg, given within 3 minutes before intubation, was not effective in preventing postintubation bronchospasm in asthmatic patients undergoing propofol-induced general anesthesia with tracheal intubation. However, inhaled albuterol was effective. The authors further note they did not demonstrate any association between bronchial response to intubation and preoperative FEV₁ or change in FEV₁ after bronchodilation. These data suggest that preoperative FEV₁ may not be useful in predicting which patients may exhibit bronchoconstriction in response to intubation.

ABSTRACT

Inhaled Albuterol, but Not Intravenous Lidocaine, Protects Against Intubation-Induced Bronchoconstriction in Asthma

AUTHORS:
Maslow A, Regan M, Israel E, Darvish A, Mehrez M, Boughton R, Loring S

SOURCE:
Anesthesiology 2000: 93: 1198-1204.

ABSTRACT:
BACKGROUND: The ability of intravenous lidocaine to prevent intubation-induced bronchospasm is unclear. The authors performed a prospective, randomized, double-blind, placebo-controlled trial to test the ability of intravenous lidocaine and inhaled albuterol to attenuate airway reactivity after tracheal intubation in asthmatic patients undergoing general anesthesia.

METHODS: Sixty patients were randomized to receive either 1.5 mg/kg intravenous lidocaine or saline, 3 min before tracheal intubation. An additional 50 patients were randomized to receive 4 puffs of inhaled albuterol or placebo 15-20 min before tracheal intubation. Anesthesia was induced with propofol. Immediately after intubation and at 5-min intervals, transpulmonary pressure and airflow were recorded, and lower pulmonary resistance (RL) was calculated. Isoflurane was administered after the initial two measurements to assess reversibility of bronchoconstriction. A bronchoconstrictor response to intubation was defined as RL greater than or equal to 5 cm H2O. l-1. s-1 in the first two measurements after intubation and RL subsequently decreasing by 50% or more after isoflurane. RESULTS: The lidocaine and placebo groups were not different in the peak RL before administration of isoflurane (8.2 cm H2O. l-1. s-1 vs. 7.6 cm H2O. l-1. s-1) or frequency of airway response to intubation (lidocaine 6 of 30 vs. placebo 5 of 27). In contrast, the albuterol group had lower peak RL (5.3 cm H2O. l-1. s-1 vs. 8.9 cm H2O. l-1. s-1; P < 0.05) and a lower frequency of airway response (1 of 25 vs. 8 of 23; P < 0.05) than the placebo group.

CONCLUSIONS: Inhaled albuterol blunted airway response to tracheal intubation in asthmatic patients, whereas intravenous lidocaine did not.