Lung compliance, Laplace and surfactant: why alveoli stay open
A film of water lines every alveolus and pulls inward on it. Lung compliance, the law of Laplace and surfactant explain why the lungs do not collapse at the end of each breath.
Explain lung compliance, the law of Laplace in alveoli and how surfactant prevents collapse.
The short version
- Lung compliance is the change in volume per unit change in pressure: the slope of the volume–pressure curve.
- Emphysema raises compliance (elastic fibres lost); pulmonary fibrosis lowers it (collagen replaces elastic tissue).
- By the law of Laplace, P = 2T/r: higher tension needs more pressure, and at the same tension a small alveolus has a higher pressure than a large one.
- Surfactant, made by type II alveolar cells, lowers surface tension, raises compliance and stops alveoli collapsing at the end of expiration.
- Premature infants may lack surfactant, causing neonatal respiratory distress syndrome; a lecithin to sphingomyelin ratio of about 2 or more suggests mature lungs.
Lung compliance and the puzzle of the open alveolus
Your alveoli are lined with a thin film of water, and water pulls on itself. That inward pull should shut the alveoli at the end of every breath.[1][2]
Worse, a small alveolus should empty into a larger neighbour. So why do the lungs stay open? This lesson on lung compliance answers it in three steps: compliance, the law of Laplace in an alveolus, and the surfactant that prevents collapse.
Lung compliance: the slope of the volume–pressure curve
From the first lesson in this series: at rest, the lung's elastic recoil pulls inward, the chest wall pulls outward, and the two balance.[1]
Compliance is how easily something stretches: the change in volume for each unit change in pressure. On a graph of volume against pressure, it is the slope.[3]
the slope of the volume–pressure curve
A steep slope is a floppy, compliant lung. A flat slope is a stiff, low-compliance lung.
Two sources of recoil: elastic tissue and surface tension
The lung's inward pull has two sources: its elastic tissue, and the surface tension of the thin film of fluid lining the alveoli.[1]
Tissue first. In emphysema, elastic fibres are destroyed, recoil is lost, and compliance rises. Those lungs inflate easily but have too little recoil to push the air out. In pulmonary fibrosis, elastic tissue is replaced by collagen, the lung is stiff, and compliance falls.[3]
| Condition | What happens to the tissue | Compliance |
|---|---|---|
| Emphysema | Elastic fibres destroyed, recoil lost | Increased |
| Pulmonary fibrosis | Elastic tissue replaced by collagen | Decreased |
The law of Laplace: small alveoli, high pressure
Now the film of water. At an air–liquid surface, water molecules pull toward each other, and that tries to shrink the surface. For a sphere, the pressure this creates is given by the law of Laplace.[1][2]
P = pressure; T = surface tension; r = radius
Two things follow. The higher the tension, the more pressure is needed to keep an alveolus open. And at the same tension, a small alveolus has a higher pressure than a large one, so it tends to empty into its larger neighbour and collapse.[2]
- Alveolus of radius r at tension T: P = 2T / r
- Halve the radius: P = 2T / (r / 2) = 4T / r
- 4T / r is 2 × (2T / r): the pressure doubles
Without a fix, the lungs would tend to collapse at the end of each breath.[1]
Surfactant: type II cells and DPPC
The fix is surfactant. Type II alveolar cells make it. Its main ingredient is a phospholipid, dipalmitoyl phosphatidylcholine (DPPC), a form of lecithin, which is about two thirds of the phospholipid. It sits at the air–liquid surface and lowers the surface tension.[1][2]
In the exam model, as an alveolus shrinks, the surfactant molecules pack closer, so tension falls more in small alveoli and the pressures even out.[2][6]
In short, surfactant lowers surface tension, raises compliance, and stops alveoli collapsing at the end of expiration.[1][2][4]
Premature babies: neonatal RDS and the L/S ratio
Premature babies may not yet make enough surfactant. The result is neonatal respiratory distress syndrome: stiff, collapsing alveoli, low compliance, and a baby working hard to breathe.[5]
A lecithin to sphingomyelin (L/S) ratio of about 2 or more in amniotic fluid suggests mature lungs; a low ratio means a high risk of distress syndrome. Cut-offs vary between sources, and about 2 or more is the exam convention.[5]
Practice question
Original · USMLE styleA male infant is born at 29 weeks of gestation. At 3 hours of age he has a respiratory rate of 72/min, nasal flaring, intercostal retractions and an audible grunt.
Common questions
What is lung compliance?
Lung compliance is the change in volume for each unit change in pressure, the slope of the volume–pressure curve. A steep slope means a compliant lung; a flat slope means a stiff one.
What does the law of Laplace say about alveoli?
For an alveolus, P = 2T/r. Higher tension needs more pressure to keep it open, and at the same tension a smaller alveolus has a higher pressure, so it tends to empty into a larger neighbour. At the same tension, halving the radius doubles the pressure.
How does surfactant prevent alveolar collapse?
Surfactant, made by type II alveolar cells, sits at the air–liquid surface and lowers surface tension. That raises compliance and stops alveoli collapsing at the end of expiration.
Why do premature babies develop neonatal RDS?
They may not yet make enough surfactant, so their alveoli are stiff and collapse, compliance is low and breathing is hard work. An L/S ratio of about 2 or more in amniotic fluid suggests mature lungs.
Transcript
Read the full narration, by chapter713 words
0:00The puzzle: why do alveoli stay open?
Your alveoli are lined with a thin film of water, and water pulls on itself. That inward pull should shut the alveoli at the end of every breath. Worse, a small alveolus should empty into a larger neighbour. So why do your lungs stay open? Today: explain compliance, the law of Laplace in an alveolus, and how surfactant prevents collapse.
0:24Compliance: the slope of the volume-pressure curve
From the first lesson: at rest, the lung's elastic recoil pulls inward, the chest wall pulls outward, and the two balance. Compliance is how easily something stretches: the change in volume for each unit change in pressure. On a graph of volume against pressure, it is the slope. A steep slope is a floppy, compliant lung. A flat slope is a stiff, low-compliance lung.
0:50Two sources of recoil: elastic tissue and surface tension
The lung's inward pull has two sources: its elastic tissue, and the surface tension of the thin film of fluid lining the alveoli. Tissue first. In emphysema, elastic fibres are destroyed, recoil is lost, and compliance rises. Those lungs inflate easily but have too little recoil to push the air out. In pulmonary fibrosis, elastic tissue is replaced by collagen, the lung is stiff, and compliance falls.
1:21The law of Laplace: small alveoli, high pressure
Now the film of water. At an air-liquid surface, water molecules pull toward each other, and that tries to shrink the surface. For a sphere, the pressure this creates is given by the law of Laplace: pressure equals two times surface tension, divided by the radius. Two things follow. The higher the tension, the more pressure is needed to keep an alveolus open. And at the same tension, a small alveolus has a higher pressure than a large one, so it tends to empty into its larger neighbour and collapse. Halve the radius at the same tension, and the pressure doubles. Real alveoli are connected polygons, not separate bubbles, so this is an approximation, but it is the model the exam uses. Without a fix, the lungs would tend to collapse at the end of each breath.
2:13Surfactant: type II cells and DPPC
The fix is surfactant. Type two alveolar cells make it. Its main ingredient is a phospholipid, dipalmitoyl phosphatidylcholine, a form of lecithin, which is about two thirds of the phospholipid. It sits at the air-liquid surface and lowers the surface tension. In the exam model, as an alveolus shrinks, the molecules pack closer, so tension falls more in small alveoli, and the pressures even out. Surfactant lowers surface tension, raises compliance, and stops alveoli collapsing at the end of expiration.
2:49Premature babies: neonatal RDS and the L/S ratio
Premature babies may not yet make enough. The result is neonatal respiratory distress syndrome: stiff, collapsing alveoli, low compliance, and a baby working hard to breathe. A lecithin to sphingomyelin ratio of about two or more in amniotic fluid suggests mature lungs; a low ratio means a high risk of distress syndrome. Contrast them: emphysema lungs are floppy, surfactant-deficient lungs are stiff.
3:19Your turn: a preterm infant with fast breathing
Your turn. A male infant is born at 29 weeks. At 3 hours of life he has a respiratory rate of 72 a minute, nasal flaring, intercostal retractions and an audible grunt. Which of the following best describes his alveoli and lungs? Each option gives alveolar surface tension, lung compliance, and the tendency to collapse at the end of expiration. A, decreased, increased, decreased. B, decreased, decreased, increased. C, increased, increased, increased. D, normal, decreased, normal. E, increased, decreased, increased. Pause here and decide.
4:06The answer, option by option
A is out: that is the pattern of lungs with plenty of surfactant, a low tension and a compliant lung that stays open. B is out: lowering surface tension reduces collapse, it would not increase it. C is out: a high-compliance lung is the emphysema pattern, and a surfactant-deficient lung is stiff. D is out: a normal surface tension cannot explain surfactant deficiency, and it would not cause collapse. So the answer is E. Without enough surfactant the tension is high, compliance is low, and the alveoli collapse at the end of expiration.
4:46Pocket-card recap
Three things to keep. One: compliance is the slope of the volume-pressure curve. Emphysema is high, fibrosis is low. Two: by Laplace, pressure equals two times tension over radius, so small alveoli tend to empty into large ones. Three: surfactant, made by type two cells, lowers surface tension so small alveoli stay open.
5:13Next lesson: V/Q mismatch
Next lesson: ventilation and perfusion mismatch, and how shunt differs from dead space.
Sources
Numbers in the text, e.g. [1], point here- OpenStax Anatomy and Physiology 2e, 22.3 The Process of Breathing. openstax.org/books/anatomy-and-physiology-2e/pages/22-3-the-process-of-breathing
- Deranged Physiology. Properties, production and regulation of lung surfactant. derangedphysiology.com/main/node/4880
- Respiratory mechanics review, compliance as dV/dP and its change in fibrosis and emphysema. PMC. pmc.ncbi.nlm.nih.gov/articles/PMC8360707/
- Surfactant, surface tension and compliance review. PMC. pmc.ncbi.nlm.nih.gov/articles/PMC13391948/
- Neonatal RDS biomarkers review. PMC. pmc.ncbi.nlm.nih.gov/articles/PMC12062013/
- Surfactant and alveolar surface tension. PMC. pmc.ncbi.nlm.nih.gov/articles/PMC9808719/
- Alveolar surface tension measurements. PMC. pmc.ncbi.nlm.nih.gov/articles/PMC10070844/
- Lung compliance. Wikipedia (secondary source, used for cross-checking only).
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined): lungs, emphysematous alveoli, newborn, fetus in utero. Alveoli cutaway: NIAID NIH BioArt Source (public domain), adapted. Original diagrams drawn in code: compliance curves, Laplace diagram, surfactant and type II cell schematic, L/S bars, pocket card. L/S bars are schematic. L/S cut-offs vary between sources; about 2 or more is the exam convention, and the alveolar tension model is the classic textbook one. No AI-generated teaching images.
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-RESP-003.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01Lung volumes and capacities, explained5:26
- EP 02Obstructive vs restrictive lung disease: FEV1/FVC and loops5:23
- EP 03Lung compliance, Laplace and surfactant: why alveoli stay open5:23
- EP 04V/Q mismatch: shunt, dead space and the oxygen test5:18
- EP 05A-a gradient: the alveolar gas equation and the causes of hypoxaemia5:39
- EP 06Oxygen-hemoglobin dissociation curve: P50, shifts and content5:19
- EP 07CO₂ transport: bicarbonate, the chloride shift, Bohr vs Haldane5:29
- EP 08Central vs peripheral chemoreceptors and oxygen-induced hypercapnia5:27
- EP 09Hypoxic pulmonary vasoconstriction and cor pulmonale5:41
- EP 10CO, cyanide and methaemoglobin: why SpO₂ and PaO₂ fool you5:34