In this lecture, we’re going to
cover hypoxemias and hypercapneas.
And our learning goals will be pretty
diffused, but we’ll cover them one by one.
And that is the arterial venous and
then alveolar to arterial O2 gradient.
We’ll then describe hypoxia, which
is different than hypoxemias,
and their potential difference
and underlying mechanisms.
We’ll predict the mechanisms of hypoxemias
and we’ll be able to go through
some clinical scenarios
and some actual test data that will able
to highlight these particular principles.
And then finally, we’re going to go
through the relationship between
So there’s a lot of hypo-
and hypers- today,
but if it has to do with –oxia,
that’s oxygen and –capneas with CO2.
Let’s go through now what normally,
when you breathe in air, what
the different O2s and CO2s are.
So when you breath in
dry air at sea level,
your PO2 will be about 160
millimeters of mercury.
And you might ask, “How in
the world do I know that?”
You take barometric pressure times the
percent of fraction of O2 in the air.
So it’s about 20.93 or we
oftentimes round it to 21%.
CO2 is very low in
Now once you humidify air,
there’s a decrease in the PO2.
And this doesn’t mean that the amount of
O2 has changed in the air, it's still 21%.
But we have to account for the amount
of water of vapor and humidify the air.
Because by the time you get air from the
mouth all the way down to the alveoli,
there is about 99.5%
saturation of that air.
And we have to account for that
and that accounts for about
47 millimeters of mercury
and that difference of 47 millimeters
of mercury lowers the PO2 to about 150.
Once you’re in the air sacs
themselves, PO2 is lower.
In fact, about 100 millimeters of mercury
versus the air sac, CO2 has risen to
about 40 47 millimeters of mercury.
And at first, when you think through this
process, you will always will think,
“Oh, wow! It went from a 150 and 0 down
to a 140. What causes that change?”
Now remember in the air sacs, this
is where gas exchange is occurring.
So you’re removing the O2 and you’re adding
CO2 and that accounts for that difference.
In the blood on the arterial
side of the circulation,
you have a PaO2 of about 95
and CO2 of about of about 40.
On the mixed venous
side, it’ s about 40 O2
and about 46 millimeters
of mercury of CO2.
You’ll notice that we used
the word mixed venous
so this is in the pulmonary artery
and the reason why this is mixed
is all the venous circulation
from the body are
So when you have your
blood returning to the
heart from the inferior
and superior vena cavas,
they will be mixed
together in the right side
of the heart, right
atrium, right ventricle,
and by the time they get into the pulmonary
artery, this is all mixed together
and so this is a general venous
blood across the whole body.
Now with those in place, let’s
talk through our two gradients.
So these gradients will be arterial
to venous, small A minus small V,
or alveolar to arterial, which is
capital A minus small A O2 gradients.
Let’s start off with
systemic venous blood.
This comes in at about a PO2
of 40 millimeters of mercury.
You’ll notice in the pulmonary capillaries,
there’s a dramatic rise
in the amount of PO2.
And that is because there’s
gas exchange occurring
between the pulmonary
capillaries and the alveoli.
In the systemic arterial
blood, it’s a little bit lower
than what occurred at the end
of the pulmonary capillary
and that is because
there’s some blood that
deoxygenated is mixed with
the oxygenated blood.
Where does this blood come from?
It usually comes from a
thebesian veins that
drain the heart and the
So these two circulations will dump
a little bit of deoxygenated blood
into the oxygenated blood and that
accounts for a small decrease
and we call that a shunt
any time there is some deoxygenated
blood mixed with the oxygenated blood.
Then finally, in the systemic
capillaries, you remove that O2.
And therefore, you can see
the dramatic decrease
as you reach down to a
number of about 40.
So what are these two gradients?
That first gradient is A to a.
So that’s the difference between
what is in the pulmonary capillary
minus the arterial blood.
So there’s always a small
gradient that occurs
because that has to do
with physiological shunt.
But it should be a
number less than 15.
If it gets greater than 15,
we’re starting to reach an
amount of an A to a gradient
that is pathological.
The A to V gradient is very
much dependent on metabolism.
And why do we know that?
Is because you’re going to fully oxygenate
your blood at the level of the lung,
but how much you pull out in
the systemic capillaries will
be very dependent upon how
high a person’s metabolism is.