Lung compliance Factors affecting lung compliance

You really need to understand the difference between resistance and compliance.


Lung compliance is simply the relationship between how much pressure is required to produce a degree of volume change of the lungs. It is affected by the elastic properties of the lung, which are reduced in emphysema, where lung compliance is high. Lung compliance can be reduced in diseases such as idiopathic pulmonary fibrosis, where the elastic fibres of the lung (elastin) are replaced by stiffer collagen. Patients with decreased lung compliance need to work harder in order to breathe.

Lung compliance

Imagine if we took the whole lungs out of the body and connected them to a set of bellows so that we could inflate them. If we simultaneously measure the pressure required to inflate the lungs, and the change in volume as they were inflated, we could plot the compliance curve (see Figure 1).

lung compliance
Figure 1: If a lung was inflated outside the body using bellows while pressure and volume were recorded then the relationship between these could be established (the numbers are arbitrary). The gradient of this line (in the middle portion where it is fairly linear) is lung compliance. The curve flattens out at the top as the lungs reach maximum capacity. Compliance can be altered in disease states and affects the mechanics of breathing. Lungs with low compliance are harder to inflate.

This curve is close to linear along its middle portion, but flattens out at higher volumes as the lungs become maximally inflated. The gradient of the line represents lung compliance, so:


Factors affecting lung compliance

Two main factors determine lung compliance. The first is the connective tissue of the lung, which is rich in the protein elastin, which as its name implies is inherently stretchy. This elastic property of the lung allows the lungs to recoil of their own accord during passive expiration (although elastin is only partly responsible – see below). There are two textbook examples of changes in the elasticity of the lung. Firstly, in fibrotic diseases such as idiopathic pulmonary fibrosis elastin is replaced by collagen, which is not as elastic. This makes the lungs harder to inflate (since it won’t stretch as easily) and hence have reduced compliance. By contrast, in emphysema - where the elastin is degraded - the lungs have increased compliance and are very easy to inflate, but have reduced capacity to recoil. A patient with a lung such as this may have to force their expiration in order to get the air out of their lungs.

The second major influence on compliance is easy to forget about because it is only affected in quite specific circumstances (pre-term labour): pulmonary surfactant. If pulmonary surfactant is absent or production is reduced, then the surface tension in the fluid lining the alveoli is so high that they are virtually impossible to inflate at all. As a consequence, lung compliance is decreased enormously.

In disease states where some of the alveoli become filled with fluid, compliance will also decrease. Oedema due to inflammation of the alveoli – sometimes seen in pneumonia – will cause such a decrease but there can be non-inflammatory causes of alveolar oedema as well. For example, in left-sided heart failure, the heart cannot adequately pump the blood from the pulmonary vein to the body. As a result, back pressure accumulates in the lung and water is forced by this hydrostatic pressure into the alveoli. In both cases, compliance is reduced because fluid-filled alveoli cannot be inflated.

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