BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, >8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS: Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P < 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION: Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration.
BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, >8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS:Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P < 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION:Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration.