The resistance exerted by the respiratory system to expansion is known as the elastance. Elastance of the respiratory system is the sum of elastance of the lungs and the elastance of the chest wall, which remains relatively constant. Therefore, the resistance against expansion of the system is mainly determined by variations in the lung elastance, which depends on:
- Elastic recoil forces exerted by elastin fibers in the pulmonary interstitium
- Forces due to the surface tension occurring at the air-interstitial fluid interface
What is Surface Tension?
In a liquid medium, molecules are attracted to each other so that, a single molecule will be subjected to attractive forces coming from all directions. When a liquid medium comes into contact with a medium of air, the forces acting from the liquid medium will not be countered by the forces acting from the medium of air. Therefore, the forces acting from the liquid, medium creates a tension at the air-liquid interface. This is known as the surface tension.
The Laplace's Law...
When an air-fluid interface is curved as a bubble, the net force exerted by the surface tension would be acting inwards, creating a collapsing force. To counteract this force, a positive pressure should be exerted from the air medium or a negative pressure should be exerted from the liquid medium. Laplace described that, the transmural pressure required to maintain such a bubble inflated (Pt) is directly proportionate to the surface tension (T) at the interface and is inversely proportionate to the radius (r) of the bubble. Thus, the relationship Pt = 2T/r has been described.
The Laplace's Law in the Alveoli...
According to the law of Laplace, the alveolar surface tension for a particular alveolar radius must be opposed by an appropriate transmural pressure. This is the trasnpulmonary pressure. If the fluid lining the alveoli were purely interstitial fluid, the trasnmural pressure required for even moderate inflation would be enormous. However, the surface tension is considerably lowered by surfactant secreted by the alveolar type II cells.
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What is Surfactant?
Surfactant is a mixture of dipalmatoilphosphatidylcholine (40%), other phospholipids (40%), surfactant associated proteins (5%) and other minor compounds like cholesterol (5%). Surfactant is secreted by the type II alveolar epithelial cells in response to beta adrenergic stimulation and the synthesis is increased by corticosteroids. Being a detergent, surfactant lines the air-fluid interface converting it into an air-surfactant interface. This allows surfactant to serve three functions in the respiratory system:
- Reduction of surface tension
- Maintaining alveolar stability
- Reduction of ultra-filtration (hence, pulmonary oedema)
1. Reduction of Surface Tension
If the alveoli were lined by interstitial fluid (with a surface tension of 70 dyn per cm), at an alveolar radius of 50µm, the trasnmural pressure required to keep the alveoli expanded would be 28 cm H2O. However, surfactant reduces the surface tension by approximately one sixth (12 dyn per cm at FRC). Thus, the trasnmural pressure required to expand the alveoli is reduced to 5 cm H2O.
2. Maintaining Alveolar Stability
The reduction of surface tension by surfactant increases as the thickness of the layer of surfactant increases. The alveoli in the lungs do not have the same radius. Therefore, by the Laplace’s law, the alveoli which have a smaller radius should empty into the alveoli with a larger radius.
But, since the lining of surfactant becomes thicker in smaller alveoli; the reduction in surface tension is greater in smaller alveoli. Thus, the intra-alveolar pressure due to surface tesion becomes equal in both smaller and larger alveoli. This prevents the smaller alveoli from emptying. The honeycomb like arrangement of the alveoli in the lungs also gives the small alveoli an additional stability preventing there collapse.
3. Reduction of Ultra-Filtration
Not only does surfactant lower the overall surface tension and confer alveolar stability, but also assists in preventing pulmonary oedema. The blood that is flowing via the rich alveolar capillary network, like in any other capillary bed in the body, is subjected to the Starling’s forces. That is, the filtration of fluid across the capillary wall into the interstitium depends on the hydrostatic pressure gradient and the osmotic pressure gradient across the capillary wall. In the absence of surfactant, to expand the alveoli, the transpulmonary pressure will have to be increased to -28 cm H2O, and this would lead to a net pressure gradient acting outwards. However, since surfactant reduces the surface tension and thus reduces the required transpulmonary pressure, the net pressure gradient acts inwards maintaining the alveolar interstitium relatively dry.