Ladies and gentlemen, we’ll take a look
at Critical Care in Pulmonology. I do need
you to pay attention to this lecture series.
It will integrate many of the systems that
we have discussed and put it into a table
format in which, for example, if your patient
comes in with lack of proper oxygenation of
his or her tissues, well, what kind of signs
and symptoms are you going to be looking for?
We begin our discussion by looking at this
table and on the first column, we have our
‘Shocks’ that we will walk through and
then everything to the right of this that
you see in the table, are going to be signs
and symptoms and also the measurements and
tests that are going to be relevant for the
type of shock that the patient is unfortunately
Welcome to Critical Care. The first type of
shock, now, in general, when you think
about shock, it’s a fact that the tissue
is not being properly oxygenated for whatever
reason. And we will go through many types
of shocks, but ultimately please understand
whatever that the pathogenesis was, the tissue
was what was suffering the consequences. The
first instance, well, we have Hypovolemic.
What does that mean?
Well earlier, when we had discussed Nephrology
and we were talking about two major wheels
of control or cycles of control. One was dealing
with control of osmolarity, the other one
was dealing with the wheel or cycle of volume.
Do you remember that? If not, then it will
be a good time for you to take a look at those
two cycles where we were monitoring osmolarity
and if it’s physiologically monitoring,
then it is ADH, as you know, that would be
measuring osmolarity. Are you clear? Whereas
if it is volume, then it would be Aldosterone
and company, your RAAS System, that would
then be controlling or monitoring and regulating
your volume. Okay. Every
once in a while, if there’s
such massive volume loss where the patient
is losing greater than 10% of his or
her volume, maybe massive haemorrhage.
Then what cycle or which component of regulation
will then be sacrificed? It will be the osmolarity
because volume becomes of utmost priority
and we discussed that when we had walked through
the regulation of ADH and Aldosterone on osmolarity
and volume respectively. It is imperative
that you have that foundation in your head
firmly implanted before you take a look at
The other big concept that you need to
take away from Physiology would also be your
method of reflex and how the body is desperately
trying to do what? Well, Hypovolemic, you’ve
lost your blood quite a bit. Let's go ahead
and call this greater than 10%. So,
now, at this point, you’re obviously going
to release your RAAS System in desperation.
You’ll have your Angiotensin II. The Angiotensin
II will do it.
Then do that crossover that I was referring
to. Remember the volume becomes of utmost
priority. And what about your blood pressure
in this patient of Hypovolemia? Good, decreased.
Let’s go back to that reflex now. So, there
are a couple of things occurring simultaneously.
The first thing would be the reflex, then
followed by the hormone response, right, in
that order. Reflex is extremely quick and
the reflex that I’m referring to here would
then be the baroreceptor reflex, isn’t it?
So, if your patient comes in, presents with,
number 1, decreased blood pressure. Next,
as soon as that occurs, then where is your
blood? Oh, my goodness! It’s on the floor.
Pick it up. No, you can’t. It doesn’t
work like that. So, there it is on the floor
and there isn’t much blood in your blood
vessels. So, tell me about that stretch, decreased.
Now, before we move on, you tell me, close
your eyes. What kind of outflow would you
want from your autonomic nervous system so
that you could then compensate for the decreased
blood pressure? Good. You want the sympathetic
nervous system, don’t you?
So therefore, you have decreased stretch
and you tell me, are you referring to a sinus
or a body here? Baroreceptors are in sinuses.
Good. Next step, which sinus are you referring
to? Carotid or aortic? Good. Carotid is
more sensitive. Next step. Which cranial
nerve is it? Nine or ten? Glossopharyngeal,
nine. So far so good. So, you have decreased
stretch, glossopharyngeal, decreased firing,
and the medulla is going to then increase
outflow of sympathetic. How can you confirm
that in your patient? I want you to take a
look at the column where it says ‘Diagnosis’.
So, the patient now comes in with decreased
blood pressure. Sympathetic nervous system
is doing everything in its power to do what?
Vasoconstrict. If you vasoconstrict your cutaneous
blood vessels, then how does your skin then
feel? Cold, clammy. Does that make sense?
So, you put all this together
here, didn’t you? Okay, so hypovolemia
– haemorrhage, dehydration, 3rd spacing.
Do not memorise that, understand it. Here,
once again, go back to your basic concepts of Physiology
where you know that you have
excuse me, you have two compartments physiologically
for total body water. The two major components
are or compartments are ICF, two-thirds,
ECF, one-third. What if you pathologically
now introduced a third compartment? What do
you mean? There should never be one, right?
So, let’s say, there is burns or pancreatitis.
This would then mean there’s fluid leakage
into a third compartment, perhaps excessively.
And so therefore, could this result in Hypovolemia?
Sure. Would you have a decrease in blood pressure?
Absolutely. What happens to your stretch?
Decreased. Increased sympathetic and you have
cold and clammy. Okay. Those two down, let’s
go into this concept of preload.
Okay, where’s all the blood? Oh, my goodness!
It’s on the floor. Okay. If all this blood
is on the floor and it’s not in your system,
tell me how full is your heart? Not very full.
You understand the concept? So, preload, we
can safely say, is decreased in Hypovolemic
shock. Next, well, how would you go about
measuring the preload in your heart? If it’s
the left side, you’d be using your PCWP,
pulmonary capillary wedge pressure, and if
it’s the right side, maybe perhaps your
central venous pressure. Point is, if your
blood is on the floor, you don’t have much
of it in the heart, you’ll have decreased
preload. Is that understood?
Next, well, what about that cardiac output?
Once again, it’s not in the heart, decreased
cardiac output. Now, what about your sympathetic
nervous system? We said that it is causing
vasoconstriction. What will then happen to
your systemic vascular resistance? In other
words, TPR is what we’re looking at there,
in that second to last column. Identify it.
And if your TPR increases, another way of
saying this, please know, clinically is, systemic
vascular resistance and with this type of
vasoconstriction, you are then affecting preload
or afterload? Afterload. And what will happen
here? Increased. Clear? What's your treatment
right off the bat?
Patient comes in with Hypovolemia of
such a dramatic fashion, IV
fluids. What might you want to
give that’s cheap and easy? Crystalloids
or colloids? Crystalloid. And this being something
like normal saline, 0.9% saline.
You see as to how this table is integrating
everything that we’ve talked about. So,
as you go through here with critical care
in Pulmonology, understand the
entire system is being affected.