6.1: Compression of Airways During Expiration

The interaction of intrapleural and airway pressures is relatively simple during inspiration; intrapleural pressure becomes more negative, and the airways are pulled open as lung volume increases. This chapter will focus on the interaction of these forces during expiration and the potential for intrapleural pressure to cause airway compression.

Although this phenomenon is present in the healthy lung, we will see how it is exacerbated in certain disease states and how this exacerbation can be detected by common pulmonary function tests.

First, let us look at the forces involved during a normal, passive expiration.

For simplicity, the schematic in figure 6.1 shows one airway and an alveolus within the thoracic cavity. At the onset of passive expiration (driven by the recoil of the expanded lung), the intrapleural pressure is negative (about −8 cm H₂O). As it remains negative, intrapleural pressure helps keep the airways open.

The elastic forces of the alveolus wall exert an inward force of about +10 cm H₂O. This results in a net force of +2 cm H₂O in the alveolus, and a gradient between this positive pressure is established between the alveolus and the atmosphere outside the lung. That means that along the airway toward the mouth there is a gradient of progressively decreasing pressure to zero (shown in maroon).

Figure 6.1: Intrapleural and airway pressures during normal/passive expiration.

Importantly in this example of passive expiration the airway pressure is greater than the pleural pressure along the whole length of the airway toward the mouth. Along with the radial traction provided by the surrounding parenchymal tissue, this favorable transmural pressure gradient helps keep the airway open during expiration.

Now let us look at what happens if expiration is forceful, or active, rather than passively relying on lung recoil.

In a forced expiration (see figure 6.2) the intrapleural pressure can become positive (as much as 120 cm H₂O), but in this example we will say it is 25 cm H₂O. This positive pressure in the pleural cavity comes from the chest wall and diaphragm now "pushing" the pleural membranes together and compressing the lung.

Figure 6.2: Intrapleural and airway pressures during forced expiration.

Again, we have the elastic forces of the alveolus generating an inward force (still +10 cm H₂O), and when summed with the now positive intrapleural forces, we end up with an alveolar pressure of +35 cm H₂O.

Again, a pressure gradient between the alveolus and the atmosphere is established (again shown in maroon), but this time there is a fundamental difference caused by the larger intrapleural pressure.

At some point along the airway, as airway pressure is decreasing, the intrapleural pressure exceeds airway pressure (in this example it is 25 cm H₂O). At this "choke" point (arrows pointing toward airway in figure 6.2), the airway can become compressed or even collapse.

This effect is somewhat reduced by the radial traction of the parenchyma, but airway compression occurs even in the healthy normal lung, and the greater the effort of expiration (i.e., the more positive the intrapleural pressure), the greater degree airways compress and compression occurs closer to the alveoli (i.e., further up the pressure gradient in the airway).

If airways are already narrowed, as in obstructive lung diseases such as asthma, or parenchymal traction is lost, such as in emphysema, dynamic airway compression occurs to a greater extent. In these obstructive diseases the increased airway resistance results in the patient having to forcefully expire to overcome the increased resistance of the narrowed airways. This promotes airway compression and leads to air being trapped behind the choke point, causing hyperinflation (breathing at an elevated lung volume).

This airway compression or any other increase in airway resistance can be demonstrated by a common pulmonary function test, the flow-volume loop.