Surfactant – Function (Guyton & Hall, 4th SA Edition)
Source: Secreted by type II alveolar epithelial cells (~10% of alveolar surface area), which contain lipid inclusions released into the alveolar lining fluid.
Composition: A complex mixture of phospholipids, proteins, and ions. The key active component is dipalmitoyl phosphatidylcholine, along with other surfactant apoproteins and calcium ions.
Mechanism of action: Surfactant is a surface-active agent that lowers the surface tension of the fluid lining the alveoli. Its phospholipid molecules do not dissolve uniformly in the alveolar fluid; instead, part of the molecule dissolves while the rest spreads over the fluid surface, greatly reducing the cohesive attraction between water molecules there.
Quantitative effect on surface tension:
- Pure water: 72 dynes/cm
- Alveolar fluid without surfactant: 50 dynes/cm
- Alveolar fluid with normal surfactant: 5-30 dynes/cm (a 2- to 10-fold reduction)
Functional importance (Law of Laplace):
Pressure tending to collapse an alveolus = 2 x Surface tension / Radius of alveolus
- With normal surfactant, a normal-sized alveolus (radius ~100 µm) generates only about 4 cm H2O collapsing pressure.
- Without surfactant (pure water lining), this pressure rises to about 18 cm H2O, roughly 4.5 times normal.
Thus surfactant:
- Reduces the work of breathing by lowering the elastic (surface tension) resistance of the lungs.
- Prevents alveolar collapse (atelectasis), especially in small alveoli, by proportionally lowering surface tension more as alveolar radius decreases (stabilizing alveoli of different sizes).
- Helps keep alveoli dry by opposing the tendency of surface tension to pull fluid from capillaries into the alveoli, thereby preventing pulmonary edema.
- Guyton and Hall Textbook of Medical Physiology, p. 494-495
Short Note: Respiratory Distress Syndrome (RDS) / Hyaline Membrane Disease
Definition: A condition, most common in premature infants (also seen in infants of diabetic mothers), in which severe respiratory distress develops within hours to days of birth, sometimes causing death from suffocation.
Cause: Type II alveolar epithelial cells do not begin secreting adequate surfactant until the last 1-3 months of gestation. Premature (and occasionally some full-term) infants are therefore born with a deficiency of pulmonary surfactant.
Pathophysiology:
- Lack of surfactant causes surface tension of the alveolar fluid to rise several-fold above normal.
- This produces a strong tendency for alveoli to collapse (atelectasis) and promotes leakage of proteinaceous fluid and plasma from the pulmonary capillaries into the alveoli, causing pulmonary edema.
- At autopsy, alveoli contain large amounts of proteinaceous fluid and desquamated epithelial cells; on microscopy this material resembles a "hyaline membrane," giving the disease its alternate name, hyaline membrane disease.
Clinical consequence: Widespread alveolar collapse and fluid filling severely impair ventilation, leading to hypoxia and, if untreated, death from suffocation. Severity correlates with degree of prematurity - the more premature the infant, the more severe the RDS.
Management (per textbook): Outcomes have improved greatly with surfactant replacement therapy, assisted ventilation, and antenatal corticosteroids (to accelerate fetal lung/surfactant maturation), although hyaline membrane disease remains an important cause of morbidity and mortality in preterm infants.
- Guyton and Hall Textbook of Medical Physiology, p. 546, 1050-1051