Now, we need to discuss in a little
bit more detail what some of those
receptors were that give
feedback besides chemoreceptors.
So one of the big ones
were irritant receptors.
So these are located not only
in the mouth, in the throat,
and down some portions of
the respiratory tract,
that will sense things like dust,
cold air, various chemicals.
But when they’re engaged, the
big process that happens is
you either cause coughing
So coughing would be to try to get
that substance out of the lungs.
Bronchoconstriction would decrease
the diameter of the bronchus.
In that way, you have less
airflow travelling down it.
The joint and muscle receptors that
are located in the various muscles,
these help you to determine
what the chest wall position is
as well as the amount
of muscular tension.
These usually will help give you
feedback on the depth of breath
and how hard the
muscles are working.
When you look at
these are going to be in
response to lung inflation.
And the important thing
is to terminate inflation
before you overinflate certain
portions of the lung and damage them
Finally, J receptors.
These particular ones are very interesting
because they respond to
both chemicals and stretch
but I think even more importantly
from a clinical perspective,
they are responding for or
responding during pulmonary edema.
So if a person has pulmonary
edema, they are engaged
just like if there was overstretching
that happens or a chemical response.
This causes a shallow
breathing such as this.
Bronchoconstriction, which decreases
again the luminal diameter of the airway
and increases the amount of mucus that is
secreted into those particular airways.
So another problem with pulmonary edema
is this effect with the J receptors.
So here’s an overall view of all the
different receptors from irritant
to stretch receptors to joint and
muscle receptors to J receptors.
And I think you should have
this question in your mind,
is why in the world do you have
all these particular receptors?
I think the important thing to think about
here is you want to protect the lungs
and you want to protect what gets into the
lungs because the lungs are very delicate.
There’s a very, very
small diffusion distance
and you can very easily
get things or particles,
bacterial or viruses across the
lung membrane and cause infections.
The final clinical aspect that I’d like to
discuss has to do with respiratory control.
There is something
known as sleep apnea,
which is becoming more
prevalent in our population.
And in obstructive sleep apnea,
here are two different diagrams.
One denotes airflow and the
other is pleural pressure.
Pleural pressure is going
to be the drive to breathe.
So as pleural pressure goes down,
there should be airflow
coming in, right?
However, during obstructive sleep
apnea, something blocks the airway
so even though you’re trying to breathe in
and you’re even breathing in more and more
and more, you’re not getting any airflow.
And this is a very problematic condition
in which you could cause a hypoxic
and hypercapneic environment.
But we can compare and contrast
obstructive sleep apnea
to something known as
central sleep apnea.
In central sleep apnea, you don’t
have the drive to breathe.
There’s no problem with
obstruction of the airways.
You simply stop that drive
to want to breathe.
And this is also a dangerous
condition which can cause
both hypoxia as well
Comparing and contrasting centeral
versus obstructive sleep apnea
helps register in your mind the importance
of the control and regulation of breathing
versus simply blocking
in an airway.
Showing both of these graphs here,
looking at this obstructed airway
versus this periodic cessation
of airflow due to the lack
of ventilatory drive.