The last step that we’ll take a look at, as
far as shock where the cardio and the pulmonary
system are affected and, well, with distributive,
what’s going on here? This is septic shock,
okay, distributive. Good name, actually. So
septic shock, or you might have heard of this
being neurogenic shock means that your individual
got exposed to a gram-negative organism, caused
sepsis. Now, what is this gram-negative organism
going to do? Through its mechanism of lipopolysaccharide
and company that you learn from Immunology,
you’re going to have massive vasodilation
caused by cytokines. Now listen. This vasodilation
is going to cause vasodilation of the arteries
and also the veins. So, that means that the
blood flowing through your circulation is
What does that mean? Is it possible that you
might have such high flow through your system
in which, let’s say that I’m the tissue
and, well, let’s say that I’m the person
who’s waiting for the bus to come by, okay?
Now, as long as the bus slows down and stops,
I can get on the bus and then I can be on
my merry way. But, if the bus just goes by
and flies, there it goes. How
am I going to get on the bus? I’m not. So
therefore, I've missed my chance.
Well, the bus is the blood flow and I’m
waiting for my oxygen. So therefore, if the
blood flow, the bus, passes through your capillaries
way too quick, which is what happens in sepsis,
how are you ever going to get on that bus?
How are you ever going to release that oxygen?
You can’t. The doors don't open. Are we
clear? Interesting. So here, you’ll notice
the following. Cardiac output is going to
be increased, but yet, what’s the definition
of shock? The tissues are starving for oxygen.
So, Dr. Raj, you’re telling me there’s
an increase in cardiac output, but yet, the
tissue are dying? That is correct. You would
go ahead and call this high output cardiac
failure. That you’ve heard of in
your medical education
and you will continue to.
So, let’s walk through sepsis now that we've
set the foundation. Number 1, you have massive
vasodilation. So, would you tell me where
you might want to go to first? Let’s go
to SVR first, systemic vascular resistance.
You have massive vasodilation of the arteriole.
What happens to your afterload? Decreased,
severely. That’s where we begin here. Number 1.
So, if you decrease your afterload
severely, making it much easier
for the left ventricle to then pump its blood
into the aorta, then what do you think happens
to the cardiac output? Take a look.
Increased. Wow. Fascinating.
So now, you have all this blood that’s
passing through your blood vessels. What
are you going to do now? That’s a lot of
blood in your blood vessel. Increased or decreased
stretch? Increased stretch, okay. The increased
stretch then, this is then going to fool
who? The medulla. And so, therefore, by fooling
the medulla, now the medulla interprets this
message as increased blood pressure. It is
definitely not going to be sending out the
sympathetic. Are we clear? We can definitely
say that. So, there’s going to be decreased
sympathetic outflow. So, who is going to then
take control? The parasympathetic. So, what
does this mean to you in terms of your diagnosis?
Increased blood flow, not cold, but warm.
You see that? Next, increased
blood flow through your blood
vessels, weak or bounding pulses. Next, bounding
pulses. Next, we have widening
of your pulse pressure. What’s your pulse
pressure mean to you? It’s your systolic
blood pressure minus your diastolic blood
pressure. If you are excessively vasodilating,
what do you think happens to DBP, diastolic
blood pressure? Drastically decreased. Now,
this I can’t help you. It’s just simple
math. If you decrease your diastolic blood
pressure like crazy and systolic blood pressure
is maybe increased, what do you think happens
to pulse pressure? There you go,
widening. Then, well, what about the
sweat? You’re going to be dry here.
Why? Who controls sweat? Oh, yeah, Dr.
Raj, that was one of the exceptions. It was
a sympathetic muscarinic. And so, therefore,
in septic, you have decreased sympathetic.
So, you’re going to be warm and dry, widened
pulse pressure, bound, you can’t miss
this. There’s no way. Is that clear?
So, that’s what you have here and then let's
just make sure we finish up here. What about
preload? Well, all you do, you take a look
at cardiac output. It’s increased. Okay.
So, if there’s increased cardiac output,
how much blood is left in your heart now?
Decreased. So therefore, any test that you’re
going to use to measure the blood in your
heart, you’d expect to be, decreased. Take
a look at preload, pulmonary capillary
wedge pressure, central venous pressure, it’ll
be decreased. Understand it. Don’t memorise
it, when you’re dealing with what’s known
as distributive type of shock. What might
you want to do here for treatment? It’s
still IV fluids because your patient is
in a form of shock and obviously pressors.
So, it’s the combination of the two.
Yeah, so, maybe some type of vasopressin type
of analogue, Angiotensin II, what have you.
So, full table here. Make sure that you are
able to walk through the different types of
shocks. We put together cardiogenic and obstructive
because some of the things that we’re looking
at in terms of tests and measurements are
going to be extremely comparable. Now, the
big thing here is in terms of how to distinguish
the obstructive and cardiogenic and the diagnoses
there and the causes are going to help you