Surfactant Physiology
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Direct answer
Dipalmitoyl phosphatidylcholine, secreted by type II pneumocytes, lines the alveolar air-liquid interface and cuts surface tension from about 50 dynes per centimetre to as low as 5-30 between breaths. Because its molecules crowd more tightly in smaller alveoli, it reduces tension more where radius is least, offsetting Laplace's law (P = 2T/r) and stabilising alveoli of unequal size. Production begins around weeks 24-28 of gestation, matures by weeks 34-35, and is confirmed antenatally by a lecithin-sphingomyelin ratio of 2 or more in amniotic fluid. Deficiency in the premature infant causes neonatal respiratory distress syndrome — stiff, collapsed alveoli, hypoxaemia and hyaline membranes.
What you must remember
- Cell of origin: type II pneumocytes (about 5 per cent of alveolar cells but metabolically the busiest); they also serve as progenitors that reconstitute type I cells after injury.
- Composition: roughly 85-90 per cent lipid (chiefly dipalmitoyl phosphatidylcholine, with phosphatidylglycerol appearing near term) plus the apoproteins SP-A, SP-B, SP-C and SP-D.
- Timeline: surfactant appears at 24-28 weeks, adequate by 34-35 weeks; antenatal betamethasone to the mother accelerates maturation — the basis of giving steroids before 34 weeks of threatened delivery.
- L/S ratio: amniotic fluid lecithin to sphingomyelin of 2 or more (with phosphatidylglycerol present) signals mature lungs.
- Functions: lowers compliance work (surface tension is two-thirds of recoil), stabilises small alveoli, keeps alveoli dry by reducing the suction transuding fluid from capillaries, and SP-A/SP-D contribute innate immunity.
- Neonatal RDS: grinding expiratory effort, grunting (the infant generating auto-PEEP), ground-glass X-ray; treated with exogenous surfactant (poractant or beractant) plus CPAP.
- Infants of diabetic mothers face higher RDS risk because fetal hyperinsulinaemia delays surfactant synthesis — an oft-asked vignette.
- Adult disease: ARDS injures type II cells and inactivates surfactant, contributing to the stiff lungs and low compliance that characterise it.
A typical neonatal case
A 29-week infant born to a mother with poorly controlled gestational diabetes develops grunting, subcostal recession and cyanosis within two hours; the chest X-ray shows a diffuse ground-glass pattern with air bronchograms. The physiology explains every sign. Without surfactant, each expiration collapses small alveoli (Laplace: the smaller the radius, the higher the collapsing pressure), so the next breath must reopen them — expensive elastic work, hence the exhaustion. Grunting is audible auto-PEEP: the infant expires against a partially closed glottis to keep alveolar radius above the collapse threshold. Hypoxaemia follows because collapsed alveoli are perfused but unventilated — shunt. Management follows directly: antenatal corticosteroids if time allowed, CPAP to splint alveoli at a radius where the available surfactant can work, and intratracheal exogenous surfactant to restore the interface. Postnatal steroid is not a rescue for the lung; surfactant is.
Where students slip
Type I versus type II cells get swapped in viva. Type I cells — the flat squamous ones — cover about 95 per cent of the alveolar surface and do gas exchange; type II cells — cuboidal, in corners — make surfactant, turn over in 12-24 hours, and can divide into both types. The second slip is saying surfactant "increases elastic recoil"; it reduces the surface-tension component of recoil, making the lung easier to inflate, while the tissue elastin component is untouched. Third, the diabetes link must be argued correctly: it is fetal insulin from maternal hyperglycaemia that suppresses surfactant production, not the diabetes itself acting on the lung.
Frequently asked questions
Which cell produces pulmonary surfactant?
The type II pneumocyte (granular pneumocyte), which also acts as the alveolar progenitor cell for type I epithelium after injury.
What is the chief component of surfactant?
Dipalmitoyl phosphatidylcholine (lecithin), roughly 85-90 per cent of the film being phospholipid, along with the apoproteins SP-A through SP-D.
At what gestational age is surfactant production adequate?
Functionally adequate by about 34-35 weeks; an amniotic fluid L/S ratio of 2 or more confirms maturity, and antenatal corticosteroids accelerate maturation before that.
How does surfactant stabilise alveoli of different sizes?
Its molecules crowd together more densely in smaller alveoli, lowering surface tension there proportionally more and offsetting the Laplace relation that would otherwise empty small alveoli into large ones.
Why do infants of diabetic mothers have a higher risk of neonatal RDS?
Maternal hyperglycaemia drives fetal hyperinsulinaemia, and insulin antagonises the cortisol-driven maturation of type II cells, delaying surfactant production.