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Describe how changes in intrapleural, alveolar pressure and hence airflow are generated by the respiratory muscles

We know already that in order for there to be flow of a fluid (just as blood around the body through the heart), there needs to be a pressure difference between two different regions: which will then allow the fluid to move from the area of high concentration to that of a lower concentration. But pressure is not the only thing that influences the movement of a fluid: so does resistance; the higher the resistance the lower the flow of fluid.

Therefore, what the lungs need to do in order to get air in and out (so gaseous exchange can be carried out between it and the small blood vessels in the alveoli) is to ensure that it can effectively change both the pressure and the resistance in it.

An easy way to change pressure is through changing volume: the smaller the volume of a fluid the larger the pressure it exerts on its container, and the opposite. What changes this volume will be muscles.

It is important to understand the spaces that are concerned and discussed when discussing the lungs and the pressure, and the tendencies of these spaces and their boundaries.

  1. We have the chest itself: the intercostal muscles allow movement up or down of the chest wall.

  2. We have the lungs: there is a tendency for the lungs to collapse and take up the smallest space possible (because of the surface tension due to the liquid in them)

  3. There is the interpleural space – a mostly potential space in-between the parietal and the visceral pleura, containing the pleural fluid

Some important concepts need to be laid down at this point:

  1. We always refer to the pressure of the air outside the body (and in the trachea for example) as being 0 – this is done in order to make it easier to talk about pressures in the chest relative to this 0 pressure

  2. If we want air to move intothe lungs, we need the pressure in the lungs to be lower than 0 – negative (so it can move from higher to lower pressure)

  3. If we want the air to move outof the lungs, we need the pressure in the lungs to be bigger than 0 – positive (so air can move out towards the lower pressure)

  4. Lungs themselves have no muscles or capacity to open and close of their own accord – they are made to do so through changing the pressures around them

  5. Transmural pressure is what holds lungs open: it is the difference between the pressure in the lung and that in the interpleural space – the pressure in the interpleural space needs to be smaller than that in the lungs


Having understood the important role of the interpleural space in keeping the lungs from collapsing, we are now in a position to understand how eliminating this negative pressure can be dangerous to the lung. If there is a puncture in the chest wall, air can flow into the pleural space (which had a negative pressure), until this pressure is made to be 0 (equal to air pressure outside). Since the negative pressure was what kept the lungs from collapsing (due to elastic recoil and surface tension), the removal of this negative pressure means that the lungs will remain collapsed, and they will not be pulled towards the wall, their volume cannot be increased, and therefore the pressure in them cannot fall sufficiently to allow air to flow in them: you cannot inspire. This is called pneumothorax.

Which are our respiratory muscles?

  1. Main one: diaphragm

  2. External intercostals

  3. Scalenes

  4. Parasternal intercostals

  5. Rectus abdominis, external and internal oblique, transversus abdominis

  6. May also include: sternocleidomastoids


Explain what is meant by the terms elastic and airway resistance; lung compliance

Outline the effects on lung volumes of changes in stiffness of the lungs

Describe the factors affecting airway resistance


This is a resistance of the lung tissues to stretch (outwards force) because of the presence of the lung tissue itself, and because of the surface tension in the air-liquid interface lining the alveoli.


Is the resistance due to friction between the layers of flowing air themselves, and between the air and the airway walls. It is proportional to the changes in pressure in the airways, and inversely proportional to the resistance in those airways.

This is where asthma and wheezes come in: if there is an obstruction, or high velocity of air, or too narrow airways, all these will increase resistance in them: causing wheezing sounds.

These are divided into two groups:

  1. Factors within the airway: smooth muscle tone, inflammation of the epithelium with hypertrophy of the mucus-secreting glands

  2. Pressure across the airway wall: negative interpleural pressure causes the airways to be open, positive intrapleural pressure (in forced expiration) causes collapsing of airways

Where is the main areas of airway resistance?Medium size bronchi: before that the radius is big and beyond that there is so many of them in parallel to one another that the resistance is mall. So generations 3-5 have maximum resistance.


Describes the ability of the lungs to change shape: so it is proportional to the change in volume of the lung, and inversely proportional to the change in transmural pressure gradient.


Explain dynamic compression of airways and outline its effects

Lets explain a full breathing in-and-out cycle:

  1. We start at end-expiration: the pressure in the lungs is 0 (there is no movement of air out or in the lungs).

What do we want to do at end expiration? Breathe. So we want air to go the lungs. So we need pressure in the lungs.

At this point, there are two opposing forces acting on the interpleural space:

  1. The chest has just been deflated: its elastic recoil is now outwards

  2. The lungs want to collapse (as always)

The net result of these two opposing forces and ‘pull’ on the interpleural space, increasing its volume and giving it a negative pressure.

The transpulmonary pressure, PLwill be:

PL= PA– PPL = 0 – (-5) = 5

  1. Now we start active inspiration, contracting the diaphragm.

This further increases both the volume of the interpleural space and the lungs: the lungs now have a negative pressure, and the interpleural space has an even more negative pressure.

2. End-inspiration at maximum chest volume, the pressure inside the lungs equals that of the air outside again, the interpleural pressure is now even bigger.

3. In quiet expiration, the transmural pressure remains negative.

4. Forced expiration also removes the air from the lungs.

At this point the diaphragm starts to relax, and the expiratory muscles contract, this makes the volume of the lungs and interpleural space smaller, increasing the pressure in both of them.

Lung pressure greatly increases to 38, and interpleural pressure to 30.

The pressure in the lungs in now much greater than that outside it, so air will flow out of the lungs.

It is of importance to consider the transpulmonary pressure in the case of forced expiration.

Moving from the alveolus to the mouth, the pressure will change for whatever it is in the lungs to 0, always.

The interpleural space however now has a pressure that is also much higher than atmospheric pressure, this will compress airways: so as soon as the pressure in the airways falls under that of the interpleural space: the airway will collapse.

This usually happens in the bronchi around generation 3 or 4, and these airways do collapse in forced expiration despite their cartillagenous support. What happens next is that the continuous contraction of muscles causes the pressure to build up distally to the collapsed airway, opening it up again. These fluttering walls can be seen in bronchoscopy and produce the brassy note audible when healthy people expire forcefully.

So what are the consequences of this? This means that expiratory airflow is limited at low lung capacity, and volume doesn’t increase even if you try harder: effort independent.


Explain the importance of surface tension forces at the alveolar air-filled interface

Describe the production and role of surfactant

No need to explain the surface tension, same as in physics, presence of water in a water-air interface.

Surfactant is produced by type II pneumocytes, and it has hydrophobic and hydrophilic regions (phospholipid and protein mixture), the hydrophilic regions of which minimizes the hydrogen bonds between the surface water molecules, lowering the surface tension.

The presence of surfactant is extremely important in preventing alveolar collapse and increasing lung compliance, especially in the case of small alveoli, and because it only starts to be produced late in gestation, it is an issue with premature babies – Neonatal respiratory distress syndrome NRDS.

Surfactant proteins contribute to the surface tension lowering action of the phospholipids but also have other functions such as host defence, which is probably why natural surfactants have proved more effective for treating NRDS than artificial surfactant containing only phospholipids.

Another factor that aids in alveolar stability is the connection and mutual pull of neighbouring alveoli: alveolar interdependence.


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