Continue forward. We have differentials now,
for acute type of hypercapnea. Ventilatory.
So this would mean that something is causing
your absolute shutdown of the respiratory drive
to blow off carbon dioxide. What is this?
Maybe a demyelinating disorder. So from the
CNS maybe stroke, maybe herniation, multiple
sclerosis type of issue or perhaps even drugs.
So this is then, for example, think about
opioids that we talked about, knocking out
the respiratory centre. What happens? From
the CNS you can’t properly do what? Blow
off your carbon dioxide. Herniation. Think
of something like your subfalcine type of
herniation, or something like a uncal herniation,
right? Some of those herniations in the brain
may then bring about, well, damage to the
respiratory centre. What’s my topic? Acute
hypercapnea, failure to blow off carbon dioxide.
Continuing further with demyelinating disorders.
Guillain-Barre, right, we’ve talked about, where
diaphragm can’t properly work. Myasthenia
gravis is a big one. So, therefore, here you’re
looking at possibly, a female, autoimmune disease,
and she wakes up in the morning and she feels
great, right? And then she tells you “Hey,
doc, in the middle of the day I’m
having a hard time looking at my computer
and stuff. And as the day progresses and I
get into 3 or 4 o’clock in the afternoon,
oh, I can’t even move. And then I go to
sleep at night, I can barely even crawl into
my bed. I have to drag.” Not that
bad, but I’m just being dramatic here. Wake
up in the morning and that cycle continues.
This is myasthenia gravis. Botulism,
what’s going on here? It’s the fact that,
well, those patients that you might get, right,
and of course, cosmetic surgery is a
big deal. And you do what you want, but those
patients that are coming in and they want
to get rid of their wrinkles. What do you
do? You are injecting, what’s that called?
Botox, right? And so, therefore, now, how
are they walking around? Oh, my face is groggy.
So, I mean to say that they have that type
of face in which their wrinkles are gone,
but at what expense? But, anyhow, I’m just
having fun there. It’s the fact that you’re
inhibiting the release of acetylcholine from
the neuromuscular junction. There you go.
Myopathies, these include things like muscular
Airways. You can have even issues like
bronchoconstriction, such as from asthma, in
which it may result in difficulty with
blowing off carbon dioxide, obstructive patterns.
Often seen in acute respiratory failure as
patient tires. That’s a big one. So, for
example, say that you have a child who just
had a asthma attack,
and at this point comes in and huffs and puffs,
breathing really fast.
My goodness gracious, intercostal muscle.
All the accessory muscles
of respiration are going at full steam. This
is a child. And then, what happens? Well,
patient comes to you and intern perhaps gives
treatment, whatever that may be, some type
of bronchodilator, and the child starts quieting
down. Intern feels as though that he or she
has just saved the life of the child. Well, come
back with the [Inaudible 00:12:21] the child
is dead. What just happened? This is
what happened. Often seen in acute respiratory
failure as patient tires. So, the reason that
the child was tiring, was why? Because the
actual muscles got tired and then what happened?
Oh, my goodness, there is no energy left to
blow off that carbon dioxide. Isn’t that
my topic? Yes, it is. That is no joke.
You're better off breaking off
a few teeth with intubation than knowing that
you might have killed the patient, a child
on your clock. Could I be any more dramatic?
Hypercapneic respiratory failure ultimately
leads to hypoxemia. Why? As we said earlier,
carbon dioxide, wherever it may be, is going
to then displace the oxygen,
especially in the alveoli. Not a good thing.
Now, there is something from physiology that
I wish to bring in to play with dealing with
hypercapnea, okay? There is a difference between
rapid shallow breathing, which students tend
to confuse with rapid deep breathing. And
students never seem to get this straight.
Well, let’s organise our patterns and get
it straight, once and for all. Now, I’m
not going to go through every single one,
but I’m going to set up the table, where
you understand as to how you are breathing
from patient to patient to patient.
Let’s begin. So, on the ventilation side
are your different patients. The Vt is your
tidal volume of different types. The f is
frequency, the number of breaths or respiratory
rate that you have. Then, you stop here. Then
you have two different types of ventilation.
We have total ventilation and we have alveolar
ventilation. You keep them separate, please.
Why? Total ventilation is not taking your
dead space into consideration. Is that clear?
Is that space always pathology? Not at all.
Remember, when you’re breathing in, and
is it possible some of this
air then may get trapped? Sure. Anatomically.
And how much is this dead space that we're
referring to? This dead space, you should
know from physio, is 150. So, you noticed,
let’s do the following.
First, total ventilation for patient A, normal
patient, normal. 500 times 10 gives you a
total of 5000. Wow, that seems fantastic.
Now, actual alveolar ventilation. Take a look
at the equation, please. It’s VA, in other
words alveolar ventilation equals tidal volume
in our patient A, 500. VD stands for dead
space, which for you clinically is fixed at
150. So, 500 minus 150, 350 times, what’s
your frequency of this patient? 10. What does
that give you? 3,500. That’s normal. Are
we clear? Now, on your own time, you can take
a look at patient B. That’s great. Patient C. Okay.
Now, I want you to pay attention to patient
D and E for me. Patient D and E are both pathologies
in which is compensation
taking place and you’ll see as to who is
who. Here, tidal volume for patient D as in
delta is 300. Frequency is 18. What’s normal?
About 12-16 breaths per minute. We are at 18,
understand that this is now increased respiratory
rate. So, increased frequency. So, now, it’s
rapid breathing, that much we do know. Take
a look at total ventilation. 5400. What was
normal? 5,000. 18 times 300 gives you 5400.
Okay. But, take a look at alveolar ventilation
here. You take the 300 and from this
you subtract what? 150. Wow, that’s really
low. Multiply that by 18, you get a measly
What’s normal alveolar ventilation? 3,500.
We have dropped by 800 in patient D. Who is
this patient? Maybe rapid shallow breathing,
secondary to a DVT, a PE. So, there’s every
possibility in PE that you might have rapid
shallow breathing. But guess what, you might
not necessarily have hypercapnea. Okay? Be
careful. So, now, or should I say you would
necessarily have hypocapnea. So even though
you are rapid shallow breathing, you might
still be retaining to carbon dioxide, because
that alveolar ventilation isn’t great.
That patient D, that’s a relevant patient
for our topic, but, just to make sure we’re
clear, let’s take a look at rapid deep breathing.
Patient E, once again, look at frequency.
15, elevated. Tidal volume, 600. That’s
deep tidal volume. Now, you take a look at
the alveolar ventilation here, please. So,
600 minus 150, multiple that by your 15. You
get a whopping 6,750. Is this effective for
blowing off carbon dioxide? Of course it is.
Welcome to DKA, diabetic ketoacidosis,
metabolic acidosis. How are you compensating?
Rapid deep breathing and every breath that
you then smell, oh, it smells so good. That’s
your sweet odour, right? Welcome to Kussmaul’s
You pay attention to patient D and patient E.
However, make sure you begin with patient
A and little titbit that you wanna know from
physiology, very relevant for our cases.
Let’s go on to now, chronic. With chronic
type of respiratory failure, due to chronic
hypoventilation. So, what’s your A-a gradient
here? Good. Normal. It’s depressed in the
alveoli, therefore, depressed in your artery.
Next, well, if there’s chronic respiratory acidosis,
you can be absolutely sure that
your patient has increase in carbon dioxide.
These tend to be type II respiratory failures.
Type I respiratory failure, not necessarily
have an increased in carbon dioxide, but definitely
have a depressed oxygen. In chronic respiratory
failure, your carbon dioxide will be elevated,
in fact, your body then becomes accustomed.
It’s amazing, isn’t it? Remember, the
central chemoreceptors are very very sensitive,
to whom? Carbon dioxide. But, amazingly in
a chronic setting, they then become dull.
So, therefore, the central chemoreceptors
are not going to respond. So, therefore, now,
understand that your body becomes more responsive
to depressed oxygen over long period of time.
But, yet, the carbon dioxide levels are elevated.
So, therefore, what’s the kidney doing?
Holding onto the bicarb. Please, look for
serum bicarb to be elevated in chronic respiratory
acidosis. Do not memorise any of this. You
put stories, give yourself clinical situations
and you build upon the information that we
have looked at over and over and over again.
I hope point two or that second bullet point
makes perfect sense to you.
Now, diseases that can affect. Well, ventilatory
control. CNS insult. But, we also saw they
were acute? Sure. But, could you have chronic
changes? Absolutely. Obesity-hypoventilation
syndrome is a big problem in the United States.
Obesity, what happens? Oh, boy. Well, obesity,
understand that the patient is not able to
properly ventilate. What is he or she retaining?
Carbon dioxide. So, therefore, your patient
is in a chronic state of hypercapnea.
Not good. Let’s continue.
We have chest wall type of issues. This is
kyphoscoliosis where literally the lung doesn’t
wish to expand. This is chronic. Neuromuscular
diseases, here could also be chronic. Airways
can be chronic and chronic diffuse lung
disease. We’ll talk more about that lung
disease later on, but all these may result
in chronic type of, what’s on this? Hypoxemia.
And, hence, elevations of your carbon dioxide.