3.2: Lung Compliance
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Lung compliance is a description of how easy the lung is to inflate, more specifically, how much volume will change for a given pressure differential. Figure 3.3 shows a typical and normal lung compliance curve. The lower line shows how volume changes as intrapleural pressure becomes more negative (as the chest wall and diaphragm expand the thorax). The upper curve is the compliance of the lung during expiration, and it is clearly different; this is an example of hysteresis, meaning that the relationship depends on direction, and we will see why this exists later.
Figure 3.3: Lung compliance curve.
Lung Compliance During Inspiration
You will notice at low lung volumes the slope of the compliance curve (figure 3.3) is shallower, meaning that it takes a relatively large pressure change to cause an increase in volume. This tells us at low lung volumes the lung is less distensible, or has low compliance.
If we start to breathe at a higher lung volume, the slope of the curve is steeper, meaning that for a similar change in pressure there is a greater change in volume (i.e., the lung is more compliant).
If we start breathing at a higher lung volume still, closer to total lung capacity, we see the slope of the compliance curve flatten out again, showing that at the lung volumes the compliance of the lung is low.
As you might imagine, the normal range for breathing is in the middle range where the slope is steep and the lung compliant. This corresponds to an intrapleural pressure range of −5 to −10 cm H2O, which you should know is the normal range of intrapleural pressures during tidal breathing. This means we normally breathe at a lung volume at which the lung is most compliant and therefore takes less work to inflate.
Too low a lung volume and compliance falls and work of breathing increases, likewise during breathing at high lung volumes, another contributing reason for why tidal volume plateaus during exercise.
So now let us look at why compliance is low at high and low lung volumes, starting with the cause of low lung compliance at low volumes.
Low compliance at low volumes—Surface tension: The reason why the lung takes more pressure to inflate at low volumes is surface tension. As mentioned in chapter 1 the alveoli have a thin layer of fluid lining their inner surface. As we saw in the pleural space, this causes surface tension. Unlike the surface tension in the pleural space, in the alveoli surface tension is a disadvantage.
Surface tension is generated as water molecules cluster together to reduce their exposure to the gas in the alveolar space. As they gather together they drag the alveolar wall with them, producing a force that tends to pull the alveolar walls inward. The alveolar pressure opposes this force and should prevent the alveolus from collapsing (figure 3.4).
The relationship between these two opposing forces is described by Laplace’s law that states the outward (alveolar) pressure needed to oppose the inwardly directed tension is proportionate to the tension (obviously), but also inversely related to the radius of the alveolus (i.e., the smaller the radius, the greater the inwardly acting force). (A lecturette on Laplace’s law is available.)
Figure 3.4: Opposing forces of alveolar pressure and surface tension.
This explains why compliance is low at low lung volumes. At low lung volumes the alveoli are smaller and thus have a smaller radius. Laplace’s law states that with a low radius the pressure needed to overcome the inward force will be greater, explaining why a larger alveolar (outward) pressure is needed to inflate the alveolus from a low starting volume.
As lung volume increases, and thus alveolar radius increases, the pressure needed to overcome the inward acting force becomes less and the compliance of the lung increases. This explains why compliance is improved at the normal operating range of lung volumes.
This also explains the hysteresis of the compliance curve. During expiration as alveoli are becoming progressively smaller, the inwardly acting force generated by surface tension becomes progressively greater. This phenomenon consequently assists expiration and contributes to expiration being a passive process.
Low compliance at high lung volumes—Elastic limit: At high lung volumes the alveolar radius has increased further, suggesting that compliance should be further improved as the effect of surface tension will be much less. But surface tension is not the only factor involved, and the compliance curve flattens here, meaning a greater pressure is needed to achieve a volume change at high lung volumes. The low compliance at high lung volumes is caused by another phenomenon altogether. At high lung volumes expansion of the lung becomes limited by the elastic limit of the lung, a little like trying to further stretched an already stretch elastic band—it is harder to do.
Figure 3.5: Summary of lung volumes and compliance. At low volumes alveoli are small and subject to greater surface tension forces that generate an inwardly acting force that requires greater alveolar pressure to achieve inflation. At higher lung volumes surface tension is less effective at generating an inward force, so less pressure is required to cause inflation (the lung is more compliant). At very high lung volumes surface tension poses even less of a problem, but the elastic limits of the lung are being reached, and increases in volume require alveolar pressures to overcome elastic recoil.
So with surface tension causing problems at low lung volumes and tissue elastic limit causing problems at high lung volumes, the compliance curve is steepest (i.e., most favorable) in the middle, as mentioned before, which is the operating volume of the lung. These principles are summarized in figure 3.5.
Improving lung compliance with surfactant: So after that information on how surface tension is a problem for the lung, we now have to look at how it could be so much worse if the lung did not protect itself.
Despite it having an effect, particularly at low lung volumes, the lung actually reduces the effect of alveolar surface tension by releasing "surfactant," a molecule that disrupts surface tension. In brief, the surfactant molecule (dipalmitoyl phosphatidylcholine) has a similar structure to the phospholipids that make up cell membranes with a hydrophobic end and a hydrophilic end, allowing it to surround water and repel it at the same time, thus breaking up the interaction between water molecules. So as surfactant significantly reduces surface tension, it thereby increases lung compliance and the risk of alveolar collapse. It also helps keep the air space dry, as excessive surface tension tends to draw water into the space from the capillaries and interstitial spaces.
Surfactant is released onto the alveolar inner surface by Type II alveolar cells (recall Type I cells are those making up the alveolar wall). Type II cells produce surfactant at a high rate and thus demand a constant and generous blood flow; therefore any condition that disrupts this blood supply will cause surfactant concentrations to decline and therefore put the alveolus at risk of collapse as surface tension is allowed to increase.
A good illustration of the effect of surfactant is respiratory distress syndrome of the newborn. The underdeveloped lungs of infants born prematurely (at about twenty-eight weeks), cannot produce sufficient surfactant. Alveoli rapidly collapse (known as atelectasis), and pulmonary edema develops because of the excessive surface tension in the alveolar walls.
References, Resources, and Further Reading
Text
Levitsky, Michael G. "Chapter 2: Mechanics of Breathing." In Pulmonary Physiology, 9th ed. New York: McGraw Hill Education, 2018.
West, John B. "Chapter 7: Mechanics of Breathing—How the Lung Is Supported and Moved." In Respiratory Physiology: The Essentials, 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins, 2012.
Widdicombe, John G., and Andrew S. Davis. "Chapter 2." In Respiratory Physiology. Baltimore: University Park Press, 1983.
Figures
Figure 3.1: Lung volumes detected by spirometry. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/3.1_20220125/mode/1up
Figure 3.2: Changes in breathing tidal volume and respiratory rate with increasing levels of exercise. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/3.2_20220125/mode/1up
Figure 3.3: Lung compliance curve. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/3.3_20220125/mode/1up
Figure 3.4: Opposing forces of alveolar pressure and surface tension. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/3.4_20220125/mode/1up
Figure 3.5: Summary of lung volumes and compliance. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/3.5_20220125/mode/1up