Did You Know?
The human lungs are around 100 times more distensible than a balloon.

For any elastic structure, the increase in size or expansion is possible only when there is a difference in the pressure within and around the structure. Pulmonary compliance, which is also referred to as lung compliance, refers to the ability of the lungs to expand. Basically, it is the measure of the change in the volume of the lungs due to the change in pleural pressure or pressure across the lungs.

Increased lung compliance implies that the lungs are able to inflate with air easily. On the other hand, decreased lung compliance implies that the lungs are getting stiffer. Compliance has an inverse relationship to elastance, which is a measure of the tendency of a structure to return to its original form after the removal of a deforming force. Since the lungs and chest wall are both a part of the respiratory system, the elastance of the whole respiratory system is calculated by adding the elastance of the chest wall and the lungs. Elastance in each of the lungs and the chest wall is approximately 5 cmH2O. Therefore, the elastance of the respiratory system is approximately 10 cmH2O.

What is Meant by Pulmonary Compliance?

Lung or pulmonary compliance is a measure of the ease of expansion of the lungs. It is the change in lung volume for each unit change in transpulmonary pressure (difference in pressure between alveolar pressure and pleural pressure) at a given time.

Compliance = Change in Volume ÷ Change in Pleural Pressure

Lung compliance curve
Lung Compliance Curve

Static and Dynamic Compliance

Lung compliance can be classified into two types: static compliance and dynamic compliance. The former represents pulmonary compliance during periods without gas flow, such as during an inspiratory pause. It can be calculated with the formula:

Cstat = VT ÷ Pplat - PEEP

Cstat stands for static compliance. VT stands for tidal volume and Pplat stands for plateau pressure that is measured at the end of inhalation and prior to exhalation using an inspiratory hold maneuver. PEEP stands for positive end expiratory pressure.

During this maneuver, airflow is discontinued for half a second, which eliminates the effects of airway resistance. Pplat is never more than PIP and is typically 3-5 cmH2O lower than PIP (Peak inspiratory pressure or the maximum pressure during inspiration, when airway resistance is not elevated).

On the other hand, dynamic compliance represents pulmonary compliance during periods of gas flow, such as during active inspiration. It can be affected by changes in airway resistance, chest wall compliance, and lung compliance. Dynamic compliance is always less than or equal to static lung compliance. It is calculated using the following equation:

Cdyn = VT ÷ PIP - PEEP

Cdyn stands for dynamic compliance; VT for tidal volume; PIP for Peak inspiratory pressure, and PEEP for Positive End Expiratory Pressure.

Factors Affecting Lung Compliance

Lung compliance and elasticity are two closely-related subjects. While the former is the measure of distensibility or the elastic properties of the lungs, the latter refers to the tendency of the lungs to resist distension and recoil or return to the normal size after distension.

Elastic tension increases during inspiration and decreases due to recoil during expiration. Lung compliance is inversely proportional to elastic resistance. The elastic forces that are responsible for lung compliance include:

Elastin and collagen fibers of the lung tissue

Elastic forces of the fluid or the surfactant secreted by the type II epithelial cells

Type II epithelial cells are cells that line the inner walls of the alveoli and the lung passages. The construction of the lung is such that inflation of an alveolus tends to increase the inflation of the one adjacent to it (interdependence). These tissue factors account for about one-third of the compliance behavior of the lung. On the other hand, the fluid air surface tension elastic forces in the alveoli contribute to two-third of the lung capacity.

Each alveolus is an air-water interface. Surface tension is a result of unequal attraction between gas molecules and liquid molecules. Water molecules are more likely to attract each other than getting attracted to air molecules. Thus, there is a tendency to decrease the surface area of the air water interface (to 'contract'). In an alveolus, this means that surface tension tends to promote deflation (collapse). If there was no surface tension elastic forces, the water molecules would attract each other, forcing air from the alveoli to bronchi and causing the alveoli to collapse.

Pulmonary surfactant that is synthesized by the type II alveolar cells reduces the surface tension, helping prevent the alveoli from collapsing. The surfactant is composed of phospholipids, protein, and calcium ions. Surfactant's main component is a phospholipid called dipalmitoyl phosphatidylcholine, which is stored in lamellar bodies in Type II pneumocytes and released by exocytosis to the alveolar surface.

The polar head allows them to interact with water molecules and reduce the surface tension. The phospholipids get interspersed in water. The phospholipids dissolve unequally in the fluid lining the alveoli, thereby reducing the surface tension. The surfactant stabilizes the alveolar size, increases compliance, and keeps the lungs dry.

Intra-alveolar pressure = 2T ÷ R

T stands for tension and R stands for the radius of the alveolus.

Law of Laplace and alveoli
Effect of the Law of Laplace on the Alveoli

Smaller alveoli have a larger intraluminal pressure. As gas flows from a region of high pressure to low pressure, it flows from the small to large alveolus, which can cause the small alveolus to collapse. However, the decrease in alveolar volume decreases surface area, which concentrates the surfactant molecules. This reduces the surface tension. When the surface tension decreases due to the surfactant, the pressure becomes lower in the small alveolus. As a result, gas flows from the large alveolus to the smaller one. This prevents it from collapsing.

Effect of Emphysema and Fibrosis on Lung Compliance

Effect of diseases on the Lung Compliance Curve
Effect of Diseases on the Lung Compliance Curve

A high degree of compliance indicates a loss of elastic recoil of the lungs, which can occur due to old age or medical conditions such as emphysema. Decreased compliance means that a greater change in pressure is needed for a given change in volume. This could occur due to atelectasis (failure of alveoli to expand), edema (fluid retention), fibrosis (formation of excess fibrotic tissue), pneumonia (inflammation of lungs), or absence of surfactant. Dyspnea (shortness of breath) on exertion is the main symptom of diminished lung compliance.

In case of pulmonary fibrosis, the elastic properties of the lungs get affected due to the replacement of elastin by collagen. Collagen is not as elastic as elastin, which affects the ability to lungs to stretch or expand. This leads to reduced compliance. On the other hand, emphysema is characterized by damage to the elastic tissue of the alveolar sacs in the lungs due to enzymes secreted by leukocytes (white blood cells). Smokers are at a high risk for emphysema. The secretion of enzymes occurs due to exposure to irritants from cigarette smoke. Emphysema leads to poor elastic recoil, which in turn leads to high lung compliance. People affected by emphysema find it harder to exhale or expel air out of the lungs. As a result, they experience shortness of breath. At times, the alveolar sacs could become filled with fluid due to edema, which in turn might be observed in case of pneumonia or left-sided heart failure. This will also result in reduced lung compliance.

On a concluding note, lung compliance can get affected due to certain medical conditions. Changes in elastance or surface tension forces in the lungs can have an adverse effect on pulmonary compliance, which in turn can lead to breathing problems.