Expiratory flow limitation promotes dynamic hyperinflation during exercise in chronic obstructive pulmonary disease (COPD) patients with a consequent reduction in inspiratory capacity (IC), limiting their exercise tolerance. Therefore, the exercise capacity of patients with tidal expiratory flow limitation (FL) at rest should depend on the magnitude of IC. The presented study was designed to evaluate the role of FL on the relationship between resting IC, other respiratory function variables and exercise performance in COPD patients.Fifty-two patients were included in the study. Negative expiratory pressure (NEP) technique was employed to assess FL. Maximal work rate (WRmax) and oxygen uptake (V'O 2 ,max) were measured during an incremental symptom-limited cycle exercise.Twenty-nine patients were FL at rest. The IC was normal in all non-FL patients, while in most FL subjects it was decreased. Both WRmax and V'O 2 ,max were lower in FL patients (p<0.001, each). A close relationship of WRmax and V'O 2 ,max to IC was found (r=0.73 and 0.75, respectively; p<0.0001, each). In the whole group, stepwise regression analysis selected IC and forced expiratory volume in one second (FEV1)/ forced vital capacity (FVC) (% predicted) as the only significant contributors to exercise tolerance. Subgroup analysis showed that IC was the sole predictor in FL patients, and FEV1/FVC in non-FL patients.Detection of flow limitation provides useful information on the factors that influence exercise capacity in chronic obstructive pulmonary disease patients. Accordingly, in patients with flow limitation, inspiratory capacity appears as the best predictor of exercise tolerance, reflecting the presence of dynamic hyperinflation. Patients with chronic obstructive pulmonary disease (COPD) show widely variable exercise capacities. The relationship between resting lung function and exercise tolerance has been extensively studied in this group of patients [1±5]. In most previous studies, it was found that forced expiratory volume in one second (FEV1) was a poor predictor of exercise capacity [1±3]. Recently, however, it has been shown that indices related to dynamic hyperinflation, such as the inspiratory capacity (IC), are more closely related to exercise tolerance than FEV1 [4,5].Even at rest, patients with COPD often exhibit tidal expiratory flow limitation (FL) [6,7], promoting an increase in end-expiratory lung volume (EELV) due to dynamic hyperinflation with a concomitant decrease in inspiratory capacity and inspiratory reserve volume (IRV) [8,9]. During exercise, normal subjects increase the tidal volume (VT) at the expense of both the IRV and the expiratory reserve volume [8,9]. In contrast, in flowlimited COPD patients, VT increases only at the expense of their reduced IRV and eventually it impinges into the flat portion of the static volume-pressure relationship of the respiratory system [8,9]. Thus, in flow-limited COPD patients the maximal VT (VT,max) achieved during exercise should depend on the magnitude of IC. Since the ...

It has been demonstrated that during pregnancy expiratory reserve volume (ERV) decreases and minute ventilation (VE) increases initially and then stabilizes. In order to determine the role of thoracoabdominal mechanics, control of breathing, and inspiratory muscle function in these alterations, we studied inspiratory pressures, lung volumes, thoracic configuration, and respiratory drive in 18 normal pregnant women at Weeks 13, 21, 30, and 37 of pregnancy. Ten of them were studied 6 months after delivery. Transdiaphragmatic pressure (Pdi) was measured at Week 37 and 3 months after delivery in an additional group of seven women. VE as well as VT/TI increased early during gestation and remained unchanged thereafter. In contrast, mouth occlusion pressure (P0.1) increased progressively during pregnancy, from 1.53 +/- 0.16 (mean +/- SE) to 2.02 +/- 0.18 cm H2O, and fell significantly to 1.1 +/- 0.15 cm H2O after delivery, indicating that effective respiratory impedance increases during pregnancy. Mean P0.1 correlated with progesterone plasma levels (r = 0.918 p less than 0.05). No changes in Plmax, PEmax, and Pdimax, were observed. End-expiratory gastric pressure (Pga) increases significantly during pregnancy: 11.8 +/- 0.8 versus 8.4 +/- 1.12 cm H2O after delivery (p less than 0.012). This increment was correlated with the fall in ERV observed in late pregnancy (r = 0.74 p less than 0.05). Our results demonstrate that during pregnancy ventilatory drive and respiratory impedance increase with the consequent stabilization of VE, but our data do not permit us to differentiate whether the increment in P0.1 is secondary to the increase in impedance or to the rise in progesterone. Respiratory muscle function remains normal despite the alteration of thoracic configuration.

Administration of bleomycin into the lungs of experimental animals has been utilized as a model to understand human pulmonary fibrosis. Most of the studies, however, have focused on early stages of the lung reaction. We hypothesized that chronic stages of the model may not mimic idiopathic pulmonary fibrosis, since in preliminary studies, lung volume and compliance were not decreased. Eight male Sprague-Dawley rats receiving intratracheal bleomycin (0.5 U/100 g body weight) underwent measurement of FRC, inspiratory capacity, and lung compliance 120 d later. Lung histologic changes were evaluated using light microscopy. Eight rats without intervention served as controls. Results show that our model, in early stages, has histologic changes no different from those previously described elsewhere. In chronic stages, however, the model does not behave as a restrictive syndrome: FRC is normal or increased, whereas lung compliance is normal. Focal peribronchiolar inflammation and fibrosis associated with paracicatricial emphysematous changes are the main histologic features of long-term lung remodeling after bleomycin. We conclude that while the chronic stages of the model may be informative in understanding mechanisms of fibrosis, care should be taken not to extrapolate to human idiopathic pulmonary fibrosis. We speculate that the model might resemble a particular subgroup of human interstitial lung disease, namely, those involving peribronchiolar structures.

Effects of noninvasive ventilation on lung hyperinflation in stable hypercapnic COPD. O. Díaz, P. Bégin, B. Torrealba, E. Jover, C. Lisboa. #ERS Journals Ltd 2002. ABSTRACT: Two previous uncontrolled studies have suggested that noninvasive mechanical ventilation (NIMV) in patients with hypercapnic chronic obstructive pulmonary disease (COPD) improves arterial blood gas tensions by decreasing lung hyperinflation with the consequent reduction in inspiratory loads and changes in ventilatory pattern. The aim of this randomised placebo-controlled study was to determine whether these mechanisms play a pivotal role in the effects of NIMV on arterial blood gases.Thirty-six stable hypercapnic COPD patients were randomly allocated to NIMV or sham NIMV. A 2-week run-in period was followed by a 3-week study period, during which ventilation was applied 3 h?day -1 , 5 days a week. Arterial blood gases, spirometry, lung volumes, and respiratory mechanics were measured before and after application of NIMV.Patients submitted to NIMV showed changes (mean (95% confidence interval)) in daytime arterial carbon dioxide tension (Pa,CO 2 ) and arterial oxygen tension of -1.12 (-1.52--0.73) kPa (-8.4 (-11.4--5.5) mmHg) and 1.14 (0.70-1.50) kPa (8.6 (5.3-11.9) mmHg), respectively. Total lung capacity, functional residual capacity (FRC) and residual volume were found to be reduced by 10 (7-13), 25 (18-31), and 36 (27-45)% of their predicted value, respectively, whereas forced expiratory volume in one second and forced vital capacity increased by 4 (1.5-6.9) and 9 (5-13)% pred, respectively. Tidal volume (VT) increased by 181 (110-252) mL. All of the above changes were significant compared with sham NIMV. Changes in Pa,CO 2 were significantly related to changes in dynamic intrinsic positive end-expiratory pressure, inspiratory lung impedance, VT and FRC.It was concluded that the beneficial effects of noninvasive mechanical ventilation could be explained by a reduction in lung hyperinflation and inspiratory loads.