Effects of Small-Particle Aerosols of Local Anaesthetic on Dyspnoea in Patients with Respiratory Disease

Abstract
The hypothesis that dyspnea could be mediated by unmyelinated vagal sensory nerve endings (type J receptors) situated at alveolar level in the lung was tested. A modified jet nebulizer was used to generate an aerosol of local anesthetic in particles small enough to allow alveolar deposition. Lignocaine (2 and 5%) produced aerosols with an arithmetic mean diameter (.+-. SD) of 1.5 .+-. 0.3 and 1.2 .+-. 0.6 .mu.m, respectively, the mass median diameters being 1.7 (geometric SD = 1.2) and 2.5 (geometric SD = 1.7) .mu.m, respectively. In experimental animal models a vagally mediated tachypnea may be induced acutely by pulmonary microembolism. This response is known to be mediated by unmyelinated pulmonary afferent nerves in the vagus. Local anesthetic agents administered as small particles, but not as large particles, obtunded this response, which suggests that the aerosol was capable of penetration to alveolar level. A clinical study was designed to compare the effects of lignocaine with placebo both given as small-particle aerosols. Six patients, including 2 with diffuse alveolar pathology and 4 with chronic airflow obstruction, were studied. Respiratory frequency was determined before and after the aerosol, and exercise tolerance and breathlessness were measured with a 6 min walking test and visual analog scales. After lignocaine there was no clinical evidence of anesthesia of the upper airways but bronchoconstriction occurred. While no overall effect of lignocaine on dyspnea was apparent, individual patients showed some evidence of benefit. Although other factors deserve consideration, the lack of a dramatic effect on dyspnea suggests that dyspnea in such patients is not mediated principally by J receptors.