INSPIRATORY MUSCLE MECHANICS OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE DURING INCREMENTAL EXERCISE

Citation
S. Yan et al., INSPIRATORY MUSCLE MECHANICS OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE DURING INCREMENTAL EXERCISE, American journal of respiratory and critical care medicine, 156(3), 1997, pp. 807-813
Citations number
36
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
156
Issue
3
Year of publication
1997
Pages
807 - 813
Database
ISI
SICI code
1073-449X(1997)156:3<807:IMMOPW>2.0.ZU;2-C
Abstract
Inspiratory muscles are weak and contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). Differential inspiratory pressure contributions from the diaphragm and inspiratory rib cage mu scles (RCMs) during exercise in patients with COPD patients are insuff iciently described. We measured, in 16 patients with COPD, the global inspiratory muscle pressure (Delta Pmus) and transdiaphragmatic pressu re (Delta Pdi) during an incremental bicycle exercise to exhaustion. T he pressures needed to overcome the elastic load were further partitio ned into portions for overcoming the PEEPi-imposed inspiratory thresho ld load (before the beginning of inspiratory flow) and for inflating t he respiratory system (between the beginning and end of inspiratory fl ow). The Delta Pdi/Delta Pmus ratio was used to quantify the pressure contribution from RCMs relative to that from the diaphragm for a given inspiratory effort. We observed that in patients with COPD during exe rcise (1) there is a progressive increase in total inspiratory pressur e contribution from RCMs relative to that of the diaphragm, and the ma gnitude of this increase appears to depend on the RCMs reserves during resting breathing; (2) most of the diaphragmatic pressure contributio n occurs before the beginning of inspiratory flow, to overcome the PEE Pi-imposed inspiratory threshold load; (3) RCMs pressure contribution predominates during the period of inspiratory flow once PEEPi is neutr alized, not only for overcoming the elastic load caused by increased t idal volume, but also for compensating for the diaphragmatic pressure contribution during this interval that was gradually lost with increas ing exercise work load.