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Am. J. Respir. Crit. Care Med., Volume 160, Number 3, September 1999, 808-816

Chest Wall Hyperinflation during Acute Bronchoconstriction in Asthma

MASSIMO GORINI, IACOPO IANDELLI, GIANNI MISURI, FRANCESCO BERTOLI, MARIO FILIPPELLI, MARCO MANCINI, ROBERTO DURANTI, FRANCESCO GIGLIOTTI, and GIORGIO SCANO

Fondazione Pro Juventute Don C Gnocchi ONLUS, Firenze, Terapia Intensiva Polmonare e Fisiopatologia Toracica, Ospedale di Careggi, Clinica Medica III, Università di Firenze, Firenze, Italy

The mechanics of the chest wall was studied in seven asthmatic patients before and during histamine-induced bronchoconstriction (B). The volume of the chest wall (VCW) was calculated by three-dimensional tracking of 89 chest wall markers. Pleural (Ppl) and gastric (Pga) pressures were simultaneously recorded. VCW was modeled as the sum of the volumes of the pulmonary-apposed rib cage (VRC,p), diaphragm-apposed rib cage (VRC,a), and abdomen (VAB). During B, hyperinflation was due to the increase in end-expiratory volume of the rib cage (0.63 ± 0.09 L, p < 0.01), whereas change in VAB was inconsistent (0.09 ± 0.07 L, NS) because of phasic recruitment of abdominal muscles during expiration. Changes in end-expiratory VRC,p and VRC,a were along the rib cage relaxation configuration, indicating that both compartments shared proportionally the hyperinflation. VRC,p-Ppl plot during B was displaced leftward of the relaxation curve, suggesting persistent activity of rib cage inspiratory muscles throughout expiration. Changes in end-expiratory VCW during B did not relate to changes in FEV1 or time and volume components of the breathing cycle. We concluded that during B in asthmatic patients: (1) rib cage accounts largely for the volume of hyperinflation, whereas abdominal muscle recruitment during expiration limits the increase in VAB; (2) hyperinflation is influenced by sustained postinspiratory activity of the inspiratory muscles; (3) this pattern of respiratory muscle recruitment seems to minimize volume distortion of the rib cage at end-expiration and to preserve diaphragm length despite hyperinflation.




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Copyright © 1999 American Thoracic Society