A mathematical model of maximal expiratory flow was developed. Coupled equations describing the pressure losses in the flow and the pressure-area behavior of the airway were integrated along the airway from the periphery to the flow-limiting site. Equations describing pressure losses in the flow were adapted from studied of bronchial casts. The bronchial anatomy utilized was that described by Weibel. Bronchial mechanical properties were obtained from measurements in excised human lungs for the central airways and by extrapolations of these data for the peripheral airways. The maximal flow for air and helium predicted by the model agrees with that of five lungs from which mechanical properties were obtained. The model predictions agree with published values of density and viscosity dependence of maximal flow. At high and midlung volumes, maximal flow is determined primarily by the wave-speed mechanism. At low lung volumes, maximal flow is primarily determined by the coupling of viscous pressure losses and airway mechanical properties.
The elastic constants of dog lungs were determined at various degrees of inflation. In one set of experiments, the lobes were subjected to deformations that approximated the conditions of uniaxial loading. These data, together with the bulk modulus data obtained from the local slope of the pressure-volume curve, were used to determine the two elastic moduli that are needed to describe small nonuniform deformations about an initial state of uniform inflation. The bulk modulus was approximately 4 times the inflation pressure, and Young's modulus was approximately 1.5 times the inflation pressure. In a second set of experiments, lobes were subjected to indentation tests using cylindric punches 1-3 cm in diameter. The value for Young's modulus obtained from these data was slightly higher, approximately twice the inflation pressure. These experiments indicate that the lung is much more easily deformable in shear than in dilatation and that the Poisson ratio for the lung is high, approximately 0.43.
To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.
The mechanics of the pleural space has long been controversial. We summarize recent research pertaining to pleural mechanics within the following conceptual framework, which is still not universally accepted. Pleural pressure, the force acting to inflate the lung within the thorax, is generated by the opposing elastic recoils of the lung and chest wall and the forces generated by respiratory muscles. The spatial variation of pleural pressure is a result of complex force interactions among the lung and other structures that make up the thorax. Gravity contributes one of the forces that act on these structures, and regional lung expansion and pleural pressure distribution change with changes in body orientation. Forces are transmitted directly between the chest wall and the lung through a very thin but continuous pleural liquid space. The pressure in pleural liquid equals the pressure acting to expand the lung. Pleural liquid is not in hydrostatic equilibrium, and viscous flow of pleural liquid is driven by the combined effect of the gravitational force acting on the liquid and the pressure distribution imposed by the surrounding structures. The dynamics of pleural liquid are considered an integral part of a continual microvascular filtration into the pleural space. Similar concepts apply to the pulmonary interstitium. Regional differences in lung volume expansion also result in regional differences in interstitial pressure within the lung parenchyma and thus affect regional lung fluid filtration.
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