title: Lung sounds during allergen-induced asthmatic responses in patients with asthma.
abstract: We postulated that the distinct pathophysiologic mechanisms of airway narrowing during the early (EAR) and the late (LAR) asthmatic responses to inhaled allergens are reflected by the generation or transmission of lung sounds in asthma. Therefore, we measured FEV1 and recorded lung sounds in eight mildly asthmatic subjects before a standardized allergen challenge (PRE), during the EAR, during the recovery phase at 2 h (MID), during the LAR at 7 h, and after inhalation of a bronchodilator (POST). The recordings were made during flow- and volume-standardized quiet breathing, and during maximal forced breathing maneuvers. Airflow-dependent power spectra were analyzed for lung sound intensity (LSI), quartile power points (Q25, Q50, Q75), and extent of wheezing (W). These sound characteristics were compared among the various stages of the challenge in the presence (EAR, LAR) and absence (PRE, MID, POST) of acute airway obstruction using ANOVA. LSI, Q25 - Q75, and W were all elevated during airway obstruction. When matched for percent fall in FEV1, during the EAR and the LAR (mean +/- SD: 26.7 +/- 4.0, and 28.9 +/- 5.7, respectively; p = 0.385), the increase in Q25, and Q50 with airflow during quiet expiration, as well as the extent of wheezing, were higher during the LAR than during the EAR (p < or = 0.042 and p < or = 0.012, respectively). At similar levels of FEV1 (p > or = 0.156), LSI on expiration was higher at POST than at PRE or MID (p < or = 0.067), whereas Q25 (p < or = 0.047) and Q50 (p < or = 0.064) were lower at POST than at PRE. During forced expiration W was higher at MID and POST than at PRE (p < or = 0.014). We conclude that LSI, frequency content, and the extent of wheezing vary during the subsequent stages of allergen-induced bronchoconstriction in asthma despite matched values of FEV1. This suggests that airflow-standardized phonopneumography is a sensitive method for detecting differences in the pathophysiology of airway narrowing in asthma.
authors.affiliation: Department of Pulmonology, University Hospital, Leiden, The Netherlands.
authors.forename: H J
authors.initials: HJ
authors.lastname: Schreur
authors.forename: Z
authors.initials: Z
authors.lastname: Diamant
authors.forename: J
authors.initials: J
authors.lastname: Vanderschoot
authors.forename: A H
authors.initials: AH
authors.lastname: Zwinderman
authors.forename: J H
authors.initials: JH
authors.lastname: Dijkman
authors.forename: P J
authors.initials: PJ
authors.lastname: Sterk
mesh_terms: D000162:Acoustics; D000208:Acute Disease; D000328:Adult; D000402:Airway Obstruction / Q000503:physiopathology; D000485:Allergens; D000704:Analysis of Variance; D001249:Asthma / Q000503:physiopathology*; D001985:Bronchial Provocation Tests; D016084:Bronchoconstriction / Q000502:physiology; D001993:Bronchodilator Agents; D005541:Forced Expiratory Volume; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008448:Maximal Expiratory Flow Rate; D012123:Pulmonary Ventilation / Q000502:physiology; D012135:Respiratory Sounds / Q000503:physiopathology*
chemical_list: D000485:Allergens; D001993:Bronchodilator Agents