Background The major sites of obstruction in chronic obstructive pulmonary disease (COPD) are small airways (<2 mm in diameter). We wanted to determine whether there was a relationship between small-airway obstruction and emphysematous destruction in COPD. Methods We used multidetector computed tomography (CT) to compare the number of airways measuring 2.0 to 2.5 mm in 78 patients who had various stages of COPD, as judged by scoring on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) scale, in isolated lungs removed from patients with COPD who underwent lung transplantation, and in donor (control) lungs. MicroCT was used to measure the extent of emphysema (mean linear intercept), the number of terminal bronchioles per milliliter of lung volume, and the minimum diameters and cross-sectional areas of terminal bronchioles. Results On multidetector CT, in samples from patients with COPD, as compared with control samples, the number of airways measuring 2.0 to 2.5 mm in diameter was reduced in...

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Small-Airway Obstruction and Emphysema in Chronic Obstructive Pulmonary Disease

The distribution of tidal volume (VT) and recruitment was investigated by chest computed tomography (CT) in eight sedated-paralyzed patients with the adult respiratory distress syndrome (ARDS). A CT section was obtained in the supine position at 0, 5, 10, 15, and 20 cm H2O positive end-expiratory pressure (PEEP) and at the corresponding inspiratory plateau pressure (21 +/- 1.8, 26 +/- 1.4, 31 +/- 1.8, 38 +/- 2.1, and 46 +/- 3.2 cm H2O [mean +/- SE]), keeping VT constant. Each CT section was divided along its ventral-dorsal height into 10 equally spaced intervals (levels). Vi(insp) and Vi(exp) were defined as the gas volume for level i (i = 1 to 10) at end-inspiration and at end-expiration, respectively. The following variables were computed at each lung level: (1) distribution of CT section tidal volume (VTct), i.e., the fraction of VT that inflates a given lung level; (2) the plateau-induced and PEEP-induced recruitment, i.e., the amount of lung tissue previously collapsed that inflates at plateau pressu...

Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome

In a model of acute lung injury, we showed that positive end-expiratory pressure (PEEP) and tidal volume (VT) are interactive variables that determine the extent of lung recruitment, that recruitment occurs across the entire range of total lung capacity, and that superimposed pressure is a key determinant of lung collapse. Aiming to verify if the same rules apply in a clinical setting, we randomly ventilated five ALI/ARDS patients with 10, 15, 20, 30, 35, and 45 cm H2O plateau pressure and 5, 10, 15, and 20 cm H2O of PEEP. For each PEEP-VT condition, we obtained computed tomography at end inspiration and end expiration. We found that recruitment occurred along the entire volume-pressure curve, independent of lower and upper inflection points, and that estimated threshold opening pressures were normally distributed (mode = 20 cm H2O). Recruitment occurred progressively from nondependent to dependent lung regions. Overstretching was not associated with hyperinflation. Derecruitment did not parallel deflation, and estimated threshold closing pressures were normally distributed (mode = 5 cm H2O). End-inspiratory and end-expiratory collapse were correlated, suggesting a plateau-PEEP interaction. When superimposed gravitational pressure exceeded PEEP, end-expiratory collapse increased. We concluded that the rules governing recruitment and derecruitment equally apply in an oleic acid model and in human ALI/ARDS.

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.164.1.2007011

Recruitment and derecruitment during acute respiratory failure: a clinical study.

We aimed to elucidate the relationships between pleural (Ppl), esophageal (Pes), and superimposed gravitational pressures in acute lung injury, and to understand the mechanisms of recruitment and derecruitment. In six dogs with oleic acid respiratory failure, we measured Pes and Ppl in the uppermost, middle, and most dependent lung regions. Each dog was studied at positive end-expiratory pressure (PEEP) of 5 and 15 cm H2O and three levels of tidal volume (Vt; low, medium, and high). For each PEEP–Vt combination, we obtained a computed tomographic (CT) scan at end-inspiration and end-expiration. The variations of Ppl and Pes pressures were correlated (r = 0.86 ± 0.07, p < 0.0001), as was the vertical gradient of transpulmonary (Pl) and superimposed pressure (r = 0.92, p < 0.0001). Recruitment proceeded continuously along the entire volume–pressure curve. Estimated threshold opening pressures were normally distributed (mode = 20 to 25 cm H2O). The amount of end-expiratory collapse at the same PEEP and Pl wa...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.164.1.2007010

Recruitment and derecruitment during acute respiratory failure: an experimental study.

We have examined the effect of airway wall thickening, loss of lung recoil, and airway smooth muscle shortening on the increase in airway resistance using a model of the human tracheobronchial tree. The values for airway wall thickening were determined morphometrically on the postmortem or surgically resected lungs of normal subjects, patients with moderate chronic obstructive pulmonary disease, and patients with severe asthma. Loss of recoil was simulated by deflating airways along their pressure-area curves by 1 to 3 cm H2O. Values of smooth muscle shortening between 20 and 40% were used in the model to generate sigmoidal-shaped "dose-response" curves. The analysis shows that moderate amounts of airway wall thickening, which have little effect on baseline resistance, can profoundly affect the airway narrowing caused by smooth muscle shortening--especially if the wall thickening is localized in peripheral airways. The combination of a loss of recoil and airway wall thickening are more than additive in their effect on simulated airway responsiveness. We conclude that airway wall thickening and a loss of lung recoil can partially explain the airway hyperresponsiveness observed in patients with chronic obstructive lung disease and asthma.

A model of airway narrowing in asthma and in chronic obstructive pulmonary disease.

Flow patterns in models of the human bronchial airways.

The prediction of pressure drop and variation of resistance within the human bronchial airways.

Energy losses and pressure drop in models of human airways.

Bulk elastic properties of excised lungs and the effect of a transpulmonary pressure gradient.

The airways of the lung form a rapidly diverging system of branched tubes, and any discussion of their mechanics requires an understanding of the effects of the bifurcations on the flow downstream of them. Experiments have been carried out in models containing up to two generations of symmetrical junctions with fixed branching angle and diameter ratio, typical of the human lung. Flow visualization studies and velocity measurements in the daughter tubes of the first junction verified that secondary motions are set up, with peak axial velocities just outside the boundary layer on the inner wall of the junction, and that they decay slowly downstream. Axial velocity profiles were measured downstream of all junctions at a range of Reynolds numbers for which the flow was laminar.In each case these velocity profiles were used to estimate the viscous dissipation in the daughter tubes, so that the mean pressure drop associated with each junction and its daughter tubes could be inferred. The dependence of the dissipation on the dimensional variables is expected to be the same as in the early part of a simple entrance region, because most of the dissipation will occur in the boundary layers. This is supported by the experimental results, and the ratio Z of the dissipation in a tube downstream of a bifurcation to the dissipation which would exist in the same tube if Poiseuille flow were present is given by
 \[
 Z = (C/4\surd{2})(Re\,d/L)^{\frac{1}{2}},
 \]
 where L and d are the length and diameter of the tube, Re is the Reynolds number in it, and the constant C (equal to one for simple entry flow) is equal to 1·85 (the average value from our experiments). In general, C is expected to depend on the branching angles and diameter ratios of the junctions used. No experiments were performed in which the flow was turbulent, but it is argued that turbulence will not greatly affect the above results at Reynolds numbers less than and of the order of 10000. Many more experiments are required to consolidate this approach, but predictions based upon it agree well with the limited number of physiological experiments available.

M.F. Sudlow

Papers

Flow patterns in models of the human bronchial airways.

The prediction of pressure drop and variation of resistance within the human bronchial airways.

Energy losses and pressure drop in models of human airways.

Bulk elastic properties of excised lungs and the effect of a transpulmonary pressure gradient.

Flow and pressure drop in systems of repeatedly branching tubes