Alveolar surface tension and surfactant

Definitions & Key takeaways

Alveolar surface tension is the tension that results from the forces acting on the liquid surfaces of the alveoli. The primary force acting on the liquid surface is due to the cohesive forces between neighboring water molecules.

These forces are called "hydrogen bonds" and they are responsible for water's unique properties, such as its ability to form droplets ( rain, dew, etc.). Surface tension tends to collapse the alveoli, but this is countered by a kind of "coating" that covers the alveolar surface called surfactant. Surfactant reduces the surface tension of water, keeping the alveoli open so that we can breathe easily.

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Introduction0:00–0:43

The alveoli are the tiny air sacs in the lungs where gas exchange happens. And their walls are lined by a thin film of water, which creates a force at their surface called surface tension.
Surface tension tends to collapse the pulmonary alveoli, and, as you can imagine, this could turn into a big problem - not being able to breathe in.
Luckily, alveolar cells have found a way to counteract surface tension by producing surfactant, which is a phospholipoprotein that reduces the surface tension, keeping the alveoli open so that we can breathe properly.
That being said, take a deep breath, because we’re about to delve into the physics of surface tension. The water molecules, known as H2O to their friends, stay close together because of hydrogen bonds that form between the negatively charged oxygen ion of one molecule and the positively charged hydrogen ion of another molecule.

Water chemistry0:43–1:34

Within the bulk of water, the molecules are equally pulled in every direction by neighboring molecules, so the resulting net force is zero.
However, when you add air into the mix, the whole system becomes unbalanced, because at the water-air interface, water molecules are not surrounded by other water molecules.
This creates too many cohesive forces between water molecules at the surface, that pull the water molecules at the surface closer together, making the surface of the water shrink to the minimum surface area possible.
Now, the interior of the alveoli is also spherical, so the net force of surface tension is directed to the center of the alveoli, which tends to collapse the alveolar walls towards the center.

Laplace law1:34–3:02

The magnitude of this force is predicted by Laplace law, which states that the pressure collapsing the alveolus is directly proportional to the surface tension generated by molecules of fluid lining the alveolus, and inversely proportional to the radius of the alveoli.
So the smaller the alveoli, the larger the collapsing pressure.Now, when we breathe out, alveolar size decreases, because the air that was inflating it is now expelled from the lungs.
This means that the alveolar radius reduces, which increases the collapsing pressure according to Laplace. It also means that for inspiration to occur – which is literally trying to inflate the alveoli, it will take too much force to first overcome this collapsing pressure, meaning the entire inspiration process will be quite difficult.
Difficulty in inflating individual lung alveoli results in reduced lung compliance, which is the ability of the lung to stretch and inflate as a whole.
Luckily enough, this doesn’t happen in normal individuals, because human alveoli synthesize a lipoprotein compound called pulmonary surfactant.
The surfactant lines the alveolar walls over the water film, and then reduces the surface tension and thus the collapsing pressure.Diving deep into this, let’s zoom in and look at a cross-section of the wall of the pulmonary alveoli.

Alveoli3:02–3:52

It largely consists of type I pneumocytes, which are flat squamous epithelial cells. These cells are very thin and widespread making up to 97 % of the whole alveolar surface, which ensures an efficient diffusion needed in gas exchange between the alveoli and blood within a surrounding capillary network.Next to type I pneumocytes lies type II pneumocytes, which are cuboidal cells that contain lamellar bodies - the organelles that secrete pulmonary surfactant.
In humans, lamellar bodies start producing surfactant at 24 to 28 weeks of gestational age, and usually by the week of 35, alveoli have enough surfactant to keep them from collapsing.Now, let's have a look at the pulmonary surfactant itself.

Pulmonary surfactants3:52–5:01

It is a phospholipoprotein complex, consisting mainly of Dipalmitoyl phosphatidylcholine or just DPPC, and some proteins such as surfactant proteins – A and D.
Mainly, the role of surfactant is played by DPPC. It is an amphipathic compound because its structure consists of a hydrophilic phosphate and an amine group, attached to two hydrophobic 16-carbon saturated chains.
The hydrophilic end adheres to the surface of the water film that lines the alveolar wall, while the hydrophobic tails float in the air towards the center of alveoli.
These hydrophobic tails have very few intermolecular forces, so they don't really attract one another. This considerably reduces the alveolar surface tension all over the surface of the alveoli.
The protein component of the surfactant plays an immune role, such as helping with opsonization, which is when they tag any bacteria invading the alveoli to be destroyed by macrophages.Lowering the surface tension brings in a number of benefits.

Surface tension5:01–6:21

First, it improves compliance because it makes it easy for the alveoli to expand during inflation. During inspiration, alveoli inflate and become larger in size.
At this time, the surfactant becomes more scattered out over the surface of the water film, making its amount relatively decreased as it becomes less dense on the water surface, which then reduces its action.
This fairly increases surface tension, which slows down the rate of alveolar expansion, increasing the tendency to recoil instead.
On the other hand, when alveoli deflate during expiration, meaning the alveoli are decreasing in size, the surfactant starts to be clustered together, getting denser over the water film, thus increasing its ability to counteract the surface tension.
With very little surface tension, the alveolar wall becomes more elastic and compliant, making it easy to inflate during inspiration.
Both these two mechanisms work together to regulate the size of the alveoli all over the lungs, making all alveoli in the lungs inflate and deflate almost at the same rate, as one that inflates more rapidly will undergo a rapid increase in surface tension, thus slowing its rate of expansion.
For a quick-deflating alveolus, the surface tension quickly reduces, thus slowing its recoil speed. Sometimes there’s a deficiency of pulmonary surfactant, like in extremely premature newborns that are born before there is enough production of it.

Associated disorders6:21–7:17

These newborns typically present with neonatal respiratory distress syndrome characterized by difficulty in breathing, seen as chest wall recessions and fast breathing rate, usually above 60 breaths per minute.
This happens because breathing in takes too much effort to inflate the surfactant-depleted alveoli because they are less elastic...
or more technically less compliant. After difficulty in breathing, follows signs of poor tissue oxygenation - what's called hypoxia.
Babies can develop a fast heart rate, and cyanosis, which is blue discoloration of the skin, and can even die. Caring for such newborns involves ventilation support with supplemental oxygen, and delivering exogenous surfactant, which is mainly derived from the lungs of other animals.Alright, as a quick recap… pulmonary alveoli are lined with a thin film of water, which creates a surface tension that tends to collapse them.

Review7:17–7:54

According to Laplace law, the collapsing pressure is directly proportional to the surface tension, and inversely proportional to the radius of the alveolus.
To counteract this surface tension, type II pneumocytes produce surfactant, an amphipathic substance that helps to lower the surface tension and thus; increase the alveoli compliance and also regulate the size of individual alveoli.
A deficiency in pulmonary surfactant results in reduced alveolar compliance, seen as respiratory distress.