Loss Of Lung Recoil Research Articles

Anatomy, pathology, and physiology of the tracheobronchial tree: Emphasis on the distal airways

This article covers the airway tree with respect to anatomy, pathology, and physiology. The anatomic portion discusses various primate groups so as to help investigators understand similarities and differences between animal models. An emphasis is on distal airway findings. The pathology section focuses on the inflammatory responses that occur in proximal and distal airways. The physiologic review brings together the anatomic and pathologic components to the functional state and proposes ways to evaluate the small airways in patients with asthma.

Chronic Obstructive Pulmonary Disease

Fifty years ago, chronic obstructive pulmonary disease (COPD) was the ideal disease for physiologically oriented clinicians to study, for a number of reasons. First, it was becoming recognized as a major health problem. Second, it could only be diagnosed reliably by physiological testing; x-rays did not work. Third, it was associated with a lot of interesting pathophysiology, including cor pulmonale, alterations in the control of ventilation, and perhaps most interesting of all, abnormalities that were primarily related to the distributions of ventilation and/or perfusion as opposed to global inadequacy of either of them.

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

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.

Effect of bronchomotor tone on static mechanical properties of lung and ventilation distribution.

To study the relationship between bronchomotor tone, static mechanical properties of the lung, and ventilation distribution, we measured the pressure-volume (P-V) curve of the lung and several ventilatory indexes before and after intravenous atropine in eight normal subjects. The indexes of ventilation distribution were derived from multiple breath N2 washouts by a recently developed analysis (7,8). The latter not only provides a sensitive measure of overall ventilation inhomogeneity but distinguishes between the convection-dependent inhomogeneity (CDI) among larger lung units and that due to the interaction of convection and diffusion (DCDI) within the lung periphery. Atropine decreased lung elastic recoil but distensibility, as defined by the exponent (K) in the monoexponential analysis of the P-V data, was unchanged. The overall ventilation inhomogeneity increased by 37% after atropine (P less than 0.02) due to an increase in the CDI component. More importantly, there was a significant correlation between the loss of lung recoil (but not K) and each of the indexes of CDI among the subjects. There was no correlation between the changes in lung recoil and in DCDI. Our findings indicate that normal bronchomotor tone contributes to the elastic recoil of the lung. Furthermore, the tone is distributed in a way that enhances the uniformity of ventilation distribution among diffusion-independent lung units. Presumably this is achieved by minimizing interacinar intrinsic inequalities in static mechanical properties.

Physiologic Correlates of Airway Collapse in Chronic Airflow Obstruction

Forty percent of 89 patients with chronic airflow obstruction (CAO) demonstrated maximum expiration flow-volume (MEFV) patterns consistent with sudden collapse or marked narrowing of large central airways. In contrast, 43 percent of the CAO patients demonstrated a curvilinear (C) pattern; the remainder (17 percent) were intermediate. Volume displacement plethysmography indicated that the airway collapse (AC) pattern was influenced by, but was not solely, a gas compression artifact. Airway collapse patients had more obstruction and hyperinflation than C patients and also had decreased diffusing capacity, absence of density dependence, reduced lung recoil, and no effort dependence of airflow. Bronchodilator administration in AC patients typically produced large reduction of residual volume and increase of vital capacity, with a smaller increase of airflow. These data suggest that AC patients have significant, partially reversible peripheral airways obstruction plus emphysema. Possible determinants of AC include reduced central airway support, increased peripheral resistance, loss of lung recoil, and increased pleural pressures during forced expiration. The MEFV contour appears to evolve from normal to curvilinear to the AC pattern as the severity of airflow obstruction worsens.

Sex and age differences in intrathoracic airways mechanics in normal man

Expiratory pressure-volume curves and maximal expiratory flow-volume curves were obtained in 74 healthy subjects (49 males 25 females) aged between 20 and 64. Maximal expiratory flowstatic recoil (MEFSR) curves were then constructed. Aging was associated with loss of lung recoil and reduction in maximal expiratory flow measured between 80 and 50% total lung capacity (TLC), in both males and females, with the slope of the MEFSR curve becoming steeper. In subjects less than 40 yr old the conductance of the upstream segment increased from 80 to 50% TLC, whereas in older subjects it decreased. We also studied the effects of alveolar gas compression artifacts on MEFSR curves in 12 additional subjects and 10 patients with chronic obstructive lung disease; consistent changes were found, but the subsequent shift of the MEFSR curve toward the left was only mild. These changes are interpreted as reflecting the net effects of an increase in the unstressed dimensions of the airways together with a decrease in intraparenchymal airways diameter, probably due to loss of parenchymal airways diameter, probably due to loss of parenchymal support. It was also concluded that the analysis of the MEFSR curve did not allow a quantitative estimate of the chantes in airways compressibility with aging.

Wedge Pressure Measurement in Obstructive Pulmonary Disease

Mean pulmonary capillary wedge absolute pressures relative to atmosphere were compared with effective wedge pressures in 19 patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine whether a mean wedge or effective wedge pressure provided the most useful diagnostic information when intrathoracic pressure changes were great. The effective wedge pressure was determined by subtraction of the esophageal pressure from the measured wedge pressure. In 16 of 19 patients the actual or estimated difference between the mean wedge and effective wedge pressure ranged within ±3 mm Hg. In three patients, however, all with intrathoracic pressure changes of greater than 20 mm Hg, the mean wedge elevated (range=+6 to +17 mm Hg) in relation to the effective wedge pressure. In patients with chronic obstructive pulmonary disease with loss of lung recoil and airways obstruction, a simple mean of the wedge pressure can be elevated secondary to positive intrathorack pressures which are generated during expiration and influence the recorded absolute wedge pressure. However, in most patients, the use of the electrical mean appears to be a useful method to compensate for respiratory fluctuations in wedge pressure.

Contributions of loss of lung recoil and of enhanced airways collapsibility to the airflow obstruction of chronic bronchitis and emphysema.

We investigated the contributions of intrinsic disease of the airways, loss of lung recoil and enhanced airway collapsibility to the airflow obstruction of 17 patients with chronic bronchitis and emphysema. Airways conductance at low flow (G(aw)), maximum expiratory flow (V(E, MAX)) and static lung recoil pressure [P(st) (l)] were measured at different lung volumes, and conductance-static recoil pressure and maximum flow-static recoil pressure curves constructed. Low values of DeltaG(aw)/DeltaP(st) (l) and DeltaV(E), max/DeltaP(st) (l) were attributed to intrinsic airways disease. Airway collapsibility was assessed by comparing G(aw) with upstream conductance on forced expiration and by the intercept of the maximum flow-static recoil curve on the static recoil pressure axis (P(tm)'). All patients had reduced G(aw) at all volumes but in seven DeltaG(aw)/DeltaP(st) (l) was normal. On forced expiration, maximum flow in all patients was reduced more than could be accounted for by loss of lung recoil. DeltaV(E, MAX)/DeltaP(st) (l) was reduced in the patients in whom DeltaG(aw)/P(st) (l) was low. In contrast DeltaV(E, MAX)/DeltaP(st) (l) was normal in three and only slightly reduced in another three of the seven patients with normal DeltaG(aw)/DeltaP(st) (l). In these patients G(aw) greatly exceeded upstream conductance and P(tm)' was increased.We conclude that loss of lung recoil could account for the reduction in resting airways dimensions in 7 of the 17 patients. Enhanced airway collapsibility commonly contributed to reduction in maximum flow. In three patients the airflow obstruction could be entirely accounted for by loss of lung recoil and enhanced airway collapsibility.