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Pulmonary Function Tests and Alveolar Ventilation

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Introductory Human Physiology

Duke University

4.7 (1,918 ratings) | 220K Students Enrolled

In this course, students learn to recognize and to apply the basic concepts that govern integrated body function (as an intact organism) in the body's nine organ systems.

Skills You'll Learn

Metabolic Pathways, Biology, Organ Systems, Medicine

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4.7 (1,918 ratings)

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DH

Oct 11, 2016

I gained a deeper understanding and greater appreciation for how my body works. Thank you to the Teams at Duke and Coursera for making such a wide body of information available to the motivated.

WL

Apr 01, 2016

Lectures are very concise. This course can help you grasp the most important core concepts and key woking mechanisms of human physiology. But I don't know why it do not have the immune system.

From the lesson

Respiratory System

We hope that you are enjoying the course! This module considers the respiratory system. In these lessons, we explore topics such as how we get air into our lungs, the role of airway resistance in ventilation, the transport of oxygen and carbon dioxide between the lungs and tissues, and the regulation of breathing. There are a couple of demonstrations of lung function in the videos! The things to do this week are to watch the 8 videos, to answer the in-video questions, to read the notes, and to complete the Respiratory System problem set. We suggest that you read the notes, watch the videos, and answer the in-video questions before you start on the problem sets, which are not graded. Take a deep breath and have fun with it!

Anatomy and Mechanics15:24

Lung Volumes and Compliance19:52

Pressure Changes and Resistance17:49

Pulmonary Function Tests and Alveolar Ventilation16:24

Taught By

Jennifer Carbrey
Assistant Research Professor
Emma Jakoi
Associate Research Professor

Transcript

Welcome back, we're going to consider this time some pulmonary function tests.

So, we're going to look back again at some of the volumes that are flowing in and

out of the lung, and how those can change with diseases.

And then, we're going to start to consider more about the actual composition

of the air in the alveoli, because in the next session we're going to start

talking about oxygen transport and talking about the pressure of oxygen and

carbon dioxide in the alveoli versus the capillary.

And so we're going to start moving in that direction during this session.

So, pulmonary function tests, so these are again going to be used in

helping to diagnose patient with obstructive versus restrictive

lung disease and also monitoring their disease progression.

And so one thing that can be measured is the vital capacity or

more specifically, the forced vital capacity,

which is really what we've talked about before where you're going to

completely fill the lung, and then see how much air you can get out, so

that you get down to the only thing that's left, is residual volume.

Then, there's another thing that can be measured,

which is how much you can expire in one second.

So completely fill your lung, and

then see how quickly you can get the air out, and how much it gets out in a second.

So if you take the ratio of these two numbers how much you can get out in

a second versus how much you can get out over an unlimited period of time.

That should, for a normal person, be 80%.

You should be able to get 80% of the air out of your lung in 1 second.

Of the air that you're going to be able to get out of your lung,

this is going to exclude residual volume.

So in our two types of disease states then these numbers are going to change.

And this should be somewhat predictable that someone with an obstructive

lung disease, they have a problem getting their air out,

then this ratio is going to be less than 80%,

they're going to get less than 80% of their air out of their lung in one second.

Their vital capacity, their forced vital capacity is going to be normal.

They have a normal lung capacity.

In a restrictive lung disease where they have a problem getting the air in,

they have no problem getting it out.

So their FEV1 to FVC ratio should be normal.

They should be able to get 80% of their air out in one second.

However, it's the actual numbers of those two capacities that should be different,

because they can't, their vital capacity is smaller, and

then that mean the actual number, the volume for

their FEV1 will also be smaller even though their ratio should be normal.

And we're going to see that in this next slide where Y is going to be

this pulmonary function test for a normal person where here at the beginning you

can see they're taking a normal breath, it's about a half a liter.

So they're breathing in, breathing out normally.

And then they're told, okay, inhale as much as you can, and

that's where they are right here.

And then they're told, okay, breath out, push out that air as fast as you can.

And all of your air, and so that's when they exhale,

do that forced expiratory volume for one second, and

you can see here after one second, they've gotten 80%

of their forced vital capacity exhaled, and they have just a little bit left.

So they're forced vital capacity is of course normal, and FEV1 is normal.

Now we can consider someone with an obstructive lung disease,

let's say like emphysema, which is this X curve where here,

in this example, they're breathing with their lung being more inflated,

which is probably going to be a good compensation to help them exhale.

So, they take a normal breath, and then they're told fill up your lung,

and then they're told, okay, exhale as quickly as you can.

And that's when they're pushing and

pushing out the air that you can see after one second, they've only gotten

a small portion of their forced vital capacity out.

And it takes many, many seconds for them to get to that 80% point.

So that's going to be typical of an obstructive lung disease.

In a restrictive lung disease, curve Z, then you can see

that they when they do their inhaling,

it's a much smaller volume that they're able to bring in.

So for instance, they may have scoliosis, and

they just cannot expand their chest wall any more to let in any more air.

But then when it's time for them to exhale, it's no problem.

They can get the air out, and so

they're still going to get the vast majority of their air out.

But you can see that their forced vital capacity is about two liters here,

and their FVC should be at about 80% of that.

And so the, if you look at the actual volumes that are being measured,

they're much smaller, even though the ratio of the two numbers is still 80%.

Okay, so we're going to really switch gears now and

start to consider what is the composition of the air in the alveoli.

And this is an important thing to keep in mind is that when we're breathing,

we are not completely replacing the air in our lung, not even close.

And so that's what this is supposed to point out, we're going to have our

conducting volume and our respiratory volume about 150mL vs 3L and

let's say here we have a total volume of 450mL.

Pretty typical.

We're going to bring that into the lung.

The last, into the respiratory system sorry, and

the last 150 mLs however is going to fill the conducting volume,

which means that only 300 mLs of that 450 is

actually reaching the respiratory portion that can actually exchange with the blood.

So by taking in a normal breath, we have only replaced

about 10% of the air in our lung.

So, that's an important thing to keep in mind that we're only replacing a small

portion of our air when we're breathing in in a normal breathing like this and

that a lot of what we're doing is filling the conducting volume.

That means that we have to really consider how much that conducting volume is,

which is also the same thing that we're going to refer to as dead space.

So, we already talked about what minute ventilation is.

That's going to be how much

air you're bringing into the respiratory system each minute.

So we're going to calculate it using the tidal volume

multiplied by the respiratory rate.

So we've got three different scenarios here, all three have the same

minute ventilation, multiplying the respiratory rate times the tidal volume.

However, we know now that we really need to consider alveolar ventilation,

that's what we care about is how much fresh air is getting to the alveoli.

So to calculate that, we're going to take the tidal volume and

subtract the volume of the dead space, which in this case we're going to assume

is just the same as the conducting space volume of 150 mLs,

and then we're going to multiply it by the respiratory rate.

And so if we do that for scenario one, we're seeing this person is

basically breathing 50 times a minute, but only bringing in a hundred milliliters.

It's basically like they're panting, and

so in that case they're only bringing a hundred mLs.

They're not even filling their conducting space or their dead space.

Zero liters of this air is getting into the alveoli, so

the alveolar ventilation is zero.

If we have someone that has really a normal breathing pattern of 10 breaths

a minute of 500 ml, then their alveolar ventilation 500 minus 150,

which is 350 times 10 is going to be 3500 milliliters.

And then if we have someone that is breathing only five times a minute,

but taking deeper breaths,

then we'll subtract 150 from 1,000 and multiply by 5.

And so we have actually a greater alveolar ventilation,

if we're taking deeper less frequent breathes, so

that we can have the same minute ventilation, but yet

have radically different alveolar ventilation.

So, it's important to keep that in mind that minute ventilation

does not necessarily mean all that much,

that alveolar ventilation is also a very important to consider.

So we're going to now that we know the volume of the air that is getting into

the lungs or getting into the respiratory portion of the lungs, then what does that

mean for the actual pressure of the different gases that are in there.

So that's what we're going to start considering where we know that most

of the air that we breathe is going to be nitrogen and only 21% oxygen, and

that in the air we breath carbon dioxide is very low.

We also know that the total pressure is going to be made up

of the sum of the partial pressures of the gases.

And that that means that the pressure of oxygen is going to be equal to

the fraction of inspired air that's oxygen times the atmospheric pressure.

So since oxygen is 21% of the atmosphere, and

the atmosphere pressure is 760, that means in the normal air that we're breathing,

the pressure of oxygen is 160 millimeters of mercury.

Remember that I said that one of the roles of the conducting system was to moisturize

air, and so that means that we're adding the vapor air.

Vapor form of air and so, vapor form of water,

sorry, and so that is going to be the vapor pressure

of water is 47 millimeters of mercury.

And so that has got to be subtracted from 760

millimeters of the pressure of atmospheric air

to calculate now what the new pressure of oxygen

is going to be in inspired air 150mm of mercury.

Okay so that's the number,

the pressure of oxygen in the air once it's entered into the respiratory

system before its been diluted by the air that's already in there.

And that's what we're going to start considering.

So this is what we've just calculated.

We're going to say that we know the pressure

of oxygen in the atmosphere is 160.

Once it gets humidified, it's going to become 150 millimeters of mercury.

We've already said that the pressure of CO2 in the atmosphere is very low.

Once we get to the alveoli that we've got this P big A,

the pressure of oxygen is going to be much lower.

And that's going to be, because remember we said that fresh air is going to

be diluted, we're not going to completely replace the air in the lungs.

So it's going to get diluted by old air, and

the old air is having the oxygen taken out of it continually by the blood, so

that's why the pressure of oxygen is going to be lower in alveoli.

For CO2 we're going to have a different issue where CO2

is constantly being put into diffusing into the lung,

and so that means that the pressure of CO2 in alveoli is going to

be much greater than the almost negligible pressure of the air that's coming in.

Then once we looked at the pressure of oxygen that's dissolved n the artery or

in arterial blood, that's going to be P little a, or

not capitalized, so that's going to be our symbol for

arterial blood is Pa, P little a.

So that's something to keep in mind,

because I'm going to be referring to these abbreviations a fair amount.

So you can see that the pressure in the arteries is basically

matching almost exactly the pressure in the alveoli,

and that's true for oxygen and CO2.

So we're getting basically complete

equilibration between the alveoli and the arteries.

And so that means that the pressure of gas in the alveoli

is going to be what is going to determine the pressure of

oxygen in the blood, and that's what is important.

So then, the arterial blood is going to be taken to the organs, and

the organs are going to take the oxygen, and dump CO2.

And so you'll see that the pressure in veins of oxygen has now

gone down to 40 millimeters of mercury.

So a lot of it has been dumped, and that now our pressure of

CO2 in the veins has increased from 40 to 46 millimeters of mercury.

And we'll be talking much more about these pressures, and

about how these gases are carried in the blood in future sessions.

So, we've talked about ventilation.

We've talked about minute ventilation, but

now we've also considered alveolar ventilation.

How much fresh air is getting to the alveoli, because that's what matters.

We've also talked about how that means you're going to have to

consider dead space where we've got

anatomical dead space, which is the only kind of dead space we've considered so

far, which is just the conducting zone of the respiratory tract.

Later we'll consider a little bit areas of the lungs that are not well ventilated or

perfused, which is also going to be included when we talk about physiologic

dead space, and that's going to occur in just even normal lungs where we

don't have perfect ventilation or perfusion in different areas.

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