RESPIRATORY · FOUNDATIONS

Pulmonary Surfactant

What surfactant is, what it's made of, how it's produced and how it actually works - and the deficiency that underlies respiratory distress syndrome.

THE BIG PICTURE

Why surfactant matters

Pulmonary surfactant is a complex mixture of lipids and proteins produced by type II pneumocytes. Its primary role is to reduce alveolar surface tension.

Prevents alveolar collapse at end-expiration
Improves lung compliance
Reduces the work of breathing
Promotes uniform lung inflation
Helps maintain functional residual capacity
Reduces pulmonary oedema

Why it's centralSurfactant deficiency is the primary cause of neonatal respiratory distress syndrome (RDS).

WHAT IT'S MADE OF

Composition

Surfactant is approximately 90% lipid and 10% protein.

Component	Approx %	Function
DPPC Dipalmitoyl phosphatidylcholine	~50%	Principal surface-tension-lowering component
Unsaturated phosphatidylcholine	~20%	Improves surfactant spreading
Phosphatidylglycerol (PG)	~8%	Enhances surfactant stability
Neutral lipids	~8%	Structural support
Surfactant proteins	~8%	Surfactant function and immunity
Other phospholipids	small	Additional stability

RememberDPPC is the most physiologically important surfactant phospholipid - it does most of the surface-tension lowering.

THE FOUR PROTEINS

Surfactant proteins

Protein	Main function
SP-A	Host defence and surfactant regulation
SP-B	Essential for surfactant function
SP-C	Essential for surfactant function
SP-D	Host defence and inflammation regulation

Hydrophilic (SP-A & SP-D)

The collectins - mainly innate immunity rather than mechanics.

SP-A - the most abundant surfactant protein; supports innate immunity, facilitates tubular myelin formation and regulates surfactant recycling.

SP-D - structurally similar to SP-A; antiviral and antibacterial; modulates inflammation.

Hydrophobic (SP-B & SP-C)

The proteins that make surfactant actually work.

SP-B - the most clinically important; critical for surfactant activity and phospholipid adsorption; required for normal lung function.

SP-C - works with SP-B and enhances surfactant spreading.

Neonatal pearlSP-B and SP-C are responsible for surfactant function. SP-A and SP-D are primarily involved in host defence.

PRODUCTION & STORAGE

Made, stored, then assembled

Produced by

Type II pneumocytes - the main source.
Clara (club) cells contribute to SP-A and SP-B production.

Stored & assembled

Surfactant is stored in lamellar bodies, secreted into the alveolus, then organised into tubular myelin before forming the surface film.

Lamellar bodies→Tubular myelin→Surface film

WHAT CHANGES THE TIMELINE

What speeds it up - and slows it down

The pace of surfactant maturation is modified by fetal stress and by hormones - which is why some at-term babies are surfactant-deficient and some preterm babies are not.

Accelerate maturation

Fetal stress states: chronic placental insufficiency, IUGR, maternal hypertension, pre-eclampsia, PROM, chorioamnionitis.

Hormonal: corticosteroids, thyroid hormones, prolactin, oestrogens, beta-agonists.

Clinical pearlAntenatal corticosteroids are the most clinically important accelerator of surfactant production.

Delay maturation

Maternal: diabetes mellitus, Rh isoimmunisation with hydrops.

Fetal: male sex, prematurity, second-born twin.

Hormonal: insulin, androgens.

Clinical pearlMaternal diabetes is classically associated with delayed surfactant maturation.

SECRETION

What triggers release

Surfactant secretion (release of stored surfactant) increases with:

Lung distensionFetal breathing movementsBeta-agonistsProstaglandinsPurines

THE PHYSICS

How surfactant works - Laplace's law

P = 2T / r

P = pressure needed to keep the alveolus open · T = surface tension · r = alveolar radius

Without surfactant

Surface tension is constant, so by Laplace's law smaller alveoli generate higher pressure than larger ones. Air therefore moves small alveolus → large alveolus.

The small alveolus collapses and the large one overdistends - this is the physiology of RDS.

With surfactant

As an alveolus gets smaller, the surfactant molecules become more concentrated, so surface tension falls further.

This offsets the pressure rise predicted by Laplace's law and stabilises alveoli of different sizes, keeping them all open.

WHEN THE GENES FAIL

Genetic surfactant dysfunction - ABCA3

ABCA3 deficiency is the most common known genetic cause of surfactant dysfunction. It is autosomal recessive and reflects a defect in lipid transport into the lamellar bodies - so there is reduced DPPC, reduced phosphatidylglycerol and abnormal lamellar bodies.

🔴 Severe phenotype

Typically a term infant
Severe respiratory distress shortly after birth
Progressive respiratory failure

🟠 Chronic phenotype

Childhood interstitial lung disease
Faltering growth
Clubbing
Chronic respiratory symptoms

REPLACEMENT

Exogenous surfactant

When the lung can't make enough, surfactant can be replaced. Preparations differ by source and by which surfactant proteins they contain - and that matters for efficacy.

Preparation	Source	Proteins present
Curosurf Poractant alfa	Porcine lung	SP-B, SP-C
Survanta Beractant	Bovine lung	Low SP-B, SP-C
Exosurf	Synthetic	None
ALEC	Synthetic	None
Surfaxin	Synthetic	SP-B analogue

Current practiceCurosurf is the most commonly used preparation in Australia. Natural surfactants outperform the older protein-free synthetic preparations, and the presence of SP-B and SP-C is important for efficacy (beractant is notably low in SP-B; poractant contains more). For how it's delivered (INSURE, LISA/MIST), see support & ventilation.

Where surfactant shows up across the respiratory topics:

Respiratory distress syndrome Lung development & physiology Support & ventilation Meconium aspiration ← All respiratory topics