The tissue elastic and surface tension recoil forces that provide inherent compliance to normal lung tissue were reviewed in Chaps. 4 and 5. For excised lungs, these forces can be examined as if they operated independently of constraints placed on lung expansion by bones and muscles of the thorax. However, the chest wall and airways strongly influence lung distension and the work of breathing (Fig. 6.1). Incorporating these factors into a broad model of ventilation will facilitate understanding of the major categories of lung disorders, the obstructive diseases and restrictive diseases.

The chest wall and diaphragm normally oppose the recoil forces of lung tissue elasticity and surface tension. Thus, the negative P_IP at functional residual capacity (FRC) (see Fig. 4.6) represents the equilibrium when these musculoskeletal elements are bowed inwardly by lung recoil. Since this balance is not intuitive, consider a bilateral pneumothorax when P_IP = P_B (Fig. 6.2). When P_IP increases from −5 to 0 cm H₂O, healthy lungs recoil toward their minimal volume, while the chest walls spring outward and the diaphragm drops toward the abdominal viscera. Indeed, the volume of the open chest when P_IP = P_B is about 80% of a subject’s normal total lung capacity (TLC), implying that musculoskeletal elements will oppose all forces attempting to make the chest either larger or smaller than about 80% of TLC.

Thus, an in situ compliance curve for the entire lung-thorax system is the algebraic sum of the compliance curves for each component. Such a composite compliance curve can be obtained by having a subject perform a relaxation pressure-volume maneuver (Fig. 6.3) using a specialized apparatus for whole-body plethysmography (Chap. 16). While simultaneously monitoring P_IT in the airway and intraesophageal pressure to approximate P_IP, subjects inspire or expire to a series of lung volumes between RV and TLC, and then are locked momentarily at that volume by a valve so they can completely relax their chest wall. Under these conditions, the maneuver begins and the subject’s FRC is empirically defined as that volume when P_IT = P_B = 0 at the mouthpiece. This FRC also is the volume where inwardly directed lung recoil forces are equal and opposite to outwardly directed forces exerted by the chest wall plus diaphragm.

When subjects who are at FRC expire toward RV, their P_IT is less than P_B and a sensation of suction is felt as the thoracic structures are increasingly deviated inward from their preferred resting positions seen with a pneumothorax. Conversely, when the subject inspires to lung volumes above FRC and toward TLC, P_IT exceeds P_B and a sensation of chest compression develops as lung elastic and tension recoil forces increase. Indeed, the subject’s sensation of chest tightness will maximize at lung volumes >80% of TLC (ie, the size of the thoracic space after a pneumothorax) since the chest wall and diaphragm will also then be exerting inwardly directed positive pressures that augment the positive pressure created by lung recoil.

From this explanation, it becomes apparent that if a subject breathes at lung volumes between FRC and about 80% of TLC, each inhalation to inflate the lungs is achieved in part by utilizing potential energy stored in the chest wall and diaphragm as they were pulled inward during the preceding exhalation. By the same argument, every exhalation uses potential energy stored in the inflated lungs to expel the tidal breath, while simultaneously storing potential energy in musculo-skeletal elements being bowed inward. Thus, it is not accurate to consider normal inhalation to be entirely “active” or normal exhalation to be entirely “passive”. Rather, normal breathing is carefully controlled to oscillate around the midrange of available lung volumes so that inhalation consumes less energy than one might think, but exhalation also costs energy.

To this point, models of static lung and chest wall compliance have been used to estimate resistances to ventilation that are generated by surface and tissue recoil of lung tissue, and by thoracic musculoskeletal elements. However, additional resistance to ventilation also occurs in the airways during flow, only to disappear under no-flow conditions such as FRC. Such dynamic airway resistance is nevertheless a powerful determinant of the pattern, energetic cost, and overall efficiency of ventilation. Thus, dynamic airway compliance measurements are made to directly determine in-line resistances due to the airways. Such measurements have shown that most dynamic airway resistance resides in the upper airways (generations 1-7) because their flow rates tend to be high, their end-to-end pressure changes are large, and their aggregate cross-sectional areas are small. By the same argument, the smaller peripheral airways usually contribute less resistance despite having smaller individual diameters, due to their shorter lengths and their exponentially larger cross-sectional areas (Fig. 6.4).