Inhaled albuterol, but not intravenous lidocaine, protects against intubation-induced bronchoconstriction in asthma

Background: The ability of intravenous lidocaine to prevent intubation-indu ced bronchospasm is unclear. The authors performed a prospective, randomize d, double-blind, placebo-controlled trial to test the ability of intravenou s lidocaine and inhaled albuterol to attenuate airway reactivity after trac heal intubation in asthmatic patients undergoing general anesthesia. Methods: Sixty patients were randomized to receive either 1.5 mg/kg intrave nous lidocaine or saline, 3 min before tracheal intubation, An additional 5 0 patients were randomized to receive 4 puffs of inhaled albuterol or place bo 15-20 min before tracheal intubation, Anesthesia was induced with propof ol. Immediately after intubation and at 5-min intervals, transpulmonary pre ssure and airflow were recorded, and lower pulmonary resistance (R-L) was c alculated. Isoflurane was administered after the initial two measurements t o assess reversibility of bronchoconstriction. A bronchoconstrictor respons e to intubation was defined as R-L greater than or equal to 5 cm H2O.1(-1). s(-1) in the first two measurements after intubation and R-L subsequently d ecreasing by 50% or more after isoflurane, Results: The lidocaine and placebo groups were not different in the peak R- L before administration of isoflurane (8.2 cm H2O . l(-1) . s(-1) vs. 7.6 c m H2O . l(-1) . s(-1)) or frequency of airway response to intubation (lidoc aine 6 of 30 vs. placebo 5 of 27), Iu. contrast, the albuterol group had lo wer peak R-L (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 intubati on in asthmatic patients, whereas intravenous lidocaine did not.