Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android. Learn more here!


“Arterialization” of venous blood requires matching of the distribution of air and blood within the lung, thereby ensuring effective gas exchange across the alveolar–capillary membrane*. Arterialization comprises a series of interrelated processes that begin with the mechanical performance of the ventilatory apparatus—that is, the lungs and the chest wall, including the rib cage, diaphragm, and abdominal wall. Ventilation is critical for replenishing fresh air to the lungs for gas exchange. Although the function of each component of the lung and of the chest bellows can be deranged by injury or disease, the design of the ventilatory apparatus provides for considerable reserve. As a result, mechanical derangements are usually quite severe by the time clinical symptoms appear or arterial blood-gas levels become abnormal.

In many clinical instances, characterization of the mechanical abnormality provides insight into disease pathogenesis and affords a quantitative measure of severity. This is true in a variety of settings, including management of ventilator-dependent patients in the intensive care unit.1

During breathing, the lungs and chest wall operate in unison. The lungs fill the chest cavity so that the visceral pleurae are in contact with the parietal pleurae of the chest wall. The two pleural surfaces are separated by only a thin liquid film, which interconnects the lungs and chest wall.

At the end of a normal exhalation, when the respiratory muscles are at rest, the ventilatory apparatus is in a state of mechanical equilibrium. The pressure along the entire tracheobronchial tree from the airway opening to the alveoli is equal to atmospheric pressure (“zero gauge pressure”). The tendency of the lung is to deflate, however, and lung elastic recoil is directed inwardly toward the center of the chest cavity (i.e., centripetally). This is counterbalanced by the elastic recoil of the chest wall, which is directed outwardly (i.e., centrifugally) to favor an increase in volume. These opposing forces generate a subatmospheric pleural pressure of about −5 cmH2O (Fig. 10-1A). The tendency for the lung to recoil inward and for the chest wall to recoil outward is illustrated by the observation that when the chest is opened at autopsy, the lungs collapse to a nearly airless state, and the thorax expands.

Figure 10-1

Respiratory pressures during a breathing cycle. A. End expiration. B. During inspiration. C. End inspiration. Ppl, pleural pressure; PA, pressure in the alveoli; Pao, pressure at the airway opening.

Although conventionally pleural pressure is considered a single, mean value that reflects mechanical events within the entire ventilatory apparatus, this is clearly an oversimplification on several accounts: (1) pleural pressure is not directly determinable because normally there is only a potential space between the visceral and parietal pleura; (2) on conceptual grounds, distinctions exist between surface and liquid ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.