Mechanics of Breathing

"But I thought I already covered all this?" was my first thought when I saw the title.

But then I saw the Flow-Volume loops, and I knew that I was wrong. So wrong.

Protip for any future lecturers discussing respiratory physiology: I know it takes time, but it might be worth spending that extra minute or two discussing what the hell is going on in the flow-volume loops. Otherwise students (like me!) might miss out what you're saying on the next slide because their minds are still spinning around trying to work out what happened. And that's not nice. This goes double for if flow-volume plots aren't covered in the textbook.

Describe the flow-volume plot

Alright so here's the flow-volume plot that I ripped from the lecture slides, with the original source in the corner because I'm not that much of a thief. Let's start with volume, because volume is easy. Ish. Note that volume goes backwards, from 6 down to 2 rather than the other way around. Don't know why they do that, I guess that's just the people who made up the convention being mega trolls. This person has a maximum lung volume (TLC- total lung capacity) of around 6 litres, and a residual volume (RV) just below 2 litres.

Now let's have a look at the flow! Positive values indicate flow out of the lung (expiration) whereas negative values indicate flow into the lung (inspiration). Let's have a look at expiration first. The steep part is, to my understanding, the forced expiration that is reliant on patient effort (so I'm not sure why "forced expiration" is written on the right of the graph rather than the left). The peak, where the air is flowing out as fast as it can, is the PEF, or peak expiratory flow. (It's sometimes denoted by PEF(R)- I think the R stands for "rate" but I'm not quite sure.) After the PEF the flow rate decreases. This part is not patient-directed. (I think it's basically the air that continues to leave your lungs after you've already contracted all your extra breathing muscles.)

The bottom part is all about inspiration. As you can see from the graph, it's a bit shallower and flatter than the top, probably because of the inspiratory "ramp" signal that makes us breathe more gradually (I'll cover this in a later post). The PIF (peak inspiratory flow) is when the flow is as negative as it can get.

Oh, and I should probably talk about that small circle in the middle. That represents tidal breathing. As you can see, no drastic changes happen here, and the circle is pretty small because tidal breathing only spans around half a litre or so.

Now for a quick note on how this all changes in disease states! The two main categories to consider here are obstructive and restrictive lung disease. Obstructive lung disease is when air has trouble getting out whereas restrictive lung disease is when air has trouble getting in.

Patients with mild obstructive lung disease have the same functional vital capacity as a healthy person: it's just that they take longer to breathe it all out (i.e. get from maximum inspiration to maximum expiration). (However, a person with severe obstructive lung disease have a reduced functional vital capacity.) Since air has trouble getting out of the lungs, they tend to have a reduced FEV₁ (see my previous post for all the terminology). As for the graphs: the PEF tends to be pretty similar to normal (except in severe obstruction, where it might be a bit lower), but the significant part is that the flow rate rapidly drops right after that. This shape is known as "coving" and is deeper in more severe obstruction.

Patients with restrictive lung disease are the opposite: their FEV₁ values tend to be pretty normal, but their functional vital capacities are reduced as they can't get as much air in to begin with. Their graph looks kinda normal in that it doesn't have the "coving" characteristic of obstructive lung disease and that the PEF is pretty much the same, but other than that the curve is somewhat "shrunken" in all sides to reflect the reduced FVC.

If you want to know more about flow-volume loops and such, here's a pretty good video that I found on Youtube:

And here's a shorter one for those of you who don't want to sit through 15 minutes (video quality is not the best, but it explains things pretty simply):

Understand the factors that determine flow: compliance, resistance, muscular effort

Compliance

Compliance is a measure of how much the volume of the lungs changes for a given pressure difference. Even more simply put, it's a measure of how easily the lungs inflate. This is because pressure difference (in inspiration, at least) has a lot to do with effort (i.e. how much your diaphragm and other muscles contract), and so if your lungs inflate a lot for a small pressure difference, it'll be easier to inflate your lungs.

Anyway the formula for compliance is quite simple. C_L = ΔV/ΔP. It is measured in L/cm H₂O. The usual value for compliance is somewhere around the ballpark of 0.2 L/cm H₂O. It increases in obstructive lung disease (since air won't get out) but decreases in restrictive lung disease.

There's some other stuff on this lecture slide that looks like stuff I should understand, but I don't understand it fully. I might have to watch that part of the lecture again. Joy. By the looks of things it's saying that compliance tends to be lower when lung volume is higher and vice versa, but at the same time I thought I read somewhere that collapsed lungs (with 0 volume) are highly resistant and difficult to inflate (so low compliance). Hmm.

The effect of compliance on lung inflation is counteracted by the elasticity of lung tissue, which causes the lungs to recoil following inspiration. Elasticity is inversely proportional to compliance. Elastic fibres can become overstretched in obstructive lung disease, causing them to lose their elasticity. (Maybe this is why compliance tends to be higher in obstructive lung disease. Hmm.)

Another opponent to compliance is surface tension. The alveoli are wet and all those water molecules want to stick together. The issue is, water molecules sticking together causes alveoli to collapse (though there is pulmonary surfactant opposing this- more on this later). This inward-directed pressure can be calculated by using the LaPlace equation, which is P = 2T/r. P is the pressure, T is the surface tension measured in dyne/cm, and r is the radius of the alveolus in question.

If you're sharp you might have noticed that this seems really unfair to the smaller alveoli, since they have a smaller radius and therefore P will be higher. But never fear- pulmonary surfactant is here!

Pulmonary surfactant is made of lipoproteins such as DPPC (dipalmitoylphosphatidylcholine) and is secreted by type II alveolar cells. (Type I cells make up the walls of the alveoli.) They break up water molecules and so oppose surface tension (which opposes compliance... I guess this is a case of "the enemy of my enemy is my friend"). The effect of pulmonary surfactant tends to be more pronounced for smaller alveoli as their smaller surface area means that the surfactant molecules are more densely packed. Ultimately, all of the alveoli end up with roughly equal inward-directed pressure.

Resistance

To talk about resistance and why it matters, first I'll give a brief note about flow. Air flows from an area of high pressure to an area of low pressure, and the rate of flow depends a lot on the pressure gradient. Opposing this is the resistance of the airways. Hence the equation of flow is Flow = ΔP/R, where P is pressure and R is resistance.

Resistance is largely dependent on airway diameter. R is inversely proportional to r^4 where r is the radius. Note that it's raised to the fourth power. That means that the radius has a helluva big effect on resistance. That's also why bronchioles have the highest resistance: while they have larger radii than, say, terminal bronchioles and alveoli, there are fewer of them so their total cross-sectional area is less.

Bronchioles also have smooth muscle which can change the resistance of the airways. The smooth muscle constricts under PARASYMPATHETIC stimulation (when you're resting, you don't need to be taking in as much air). Neurotransmitters that stimulate bronchoconstriction (airway smooth muscle constriction) include acetylcholine and histamine. Bronchodilation is the opposite: it occurs under sympathetic stimulation from adrenaline and noradrenaline.

Aside from these factors, mucus can affect radius and therefore resistance. This is more of a problem when excessive amounts of mucus are secreted.

I'm going to quickly go back to talking about pressure, because that's what they did in the lecture slides for some inexplicable reason. I've mentioned the negative pressure (well, negative compared to atmospheric pressure) in the pleural cavity before, but it can become positive during forced expiration. This is the only time when this happens, and its purpose here is to help push out the air (I think...). Also another point worth mentioning is the equal pressure point, or EPP. This is the point at which the pressure difference between the airways and pleural cavity is equal to 0. I don't know why it's relevant, but it's in the slides, so there you go.

Muscular Effort

Last main point! Thank goodness for that, because I'm getting sick of this post already.

Firstly, an equation: W = P * ΔV. W is the work of breathing, which includes compliance/elastic work, tissue resistance work and airway resistance work. P is the transpulmonary pressure (i.e. the pressure gradient between the airways and pleural cavity) and V is lung volume. Obviously more work is required the more you want to inflate your lungs.

Breathing doesn't really require that much effort. At rest, tidal breathing only requires around 3% of our total energy due to low resistance and high compliance. Even during exercise, in which our pulmonary ventilation increases (see my previous post for a definition on pulmonary ventilation), this percentage doesn't change much: more energy is being used up in total, and our lungs are only using around 5% of this new maximum.

One other condition that can increase workload is disease. In some disease states, compliance can decrease and/or resistance can increase.

Aaaaand I think I've finally written down everything relevant to this lecture topic! Hope I haven't overwhelmed you all by the length of this post and sheer volume of information covered. I've almost overwhelmed myself. (Let's just ignore the fact that I have some more anatomy posts to do, which are probably even more dense...)