00:01
Now when I started my critical
care career on weekends,
a lot of times the
physicians weren't in house,
the cardiothoracic surgeons were at
home or the intensivists were at home.
00:11
And the scariest thing to
do was having to call them
and let them know something that
was going on with their patient.
00:17
I was worried about what
they were going to ask me
and worried about if I was going
to have the correct answer.
00:22
Well, let me help you build a foundation
of these critical care concepts and values
and how to apply that so you're
prepared to talk to these physicians,
they're at home expecting you
to have the right answers.
00:35
The first value we're going
to talk about cardiac output,
the normal cardiac output is
between 4 and 8 L per minute.
00:42
So what cardiac output is
basically how much blood
is coming out of that
left ventricle per minute,
how much blood is squeezing out
that left ventricle per minute.
00:53
Now, cardiac output is stroke
volume times heart rate.
00:58
It's difficult to talk about cardiac
output without understanding stroke volume.
01:02
What stroke volume is how
many milliliters of blood
is ejected from that
left ventricle per beat.
01:10
So cardiac output is stroke
volume times heart rate.
01:15
Now, the determinants of
cardiac output are heart rate,
preload, afterload, contractility,
and Frank Starling law.
01:24
With heart rate,
preload and afterload,
we're going to discuss those a
little bit later in this series.
01:29
So it makes a little
bit more sense.
01:31
But I want you to remember
Frank Starling law.
01:34
Frank Starling law is
like a rubber band,
that myocardial tissue,
if you stretch it,
the further you stretch it,
the more snapback you're gonna get,
the more contractility.
01:44
The greater squeezed, the more
stretch, the greater the squeeze.
01:47
So I want you to remember that when we're
talking about our left and right ventricle.
01:52
What decreases cardiac output such things
as hypovolemia, brady and tachycardia,
dysrhythmias, too high of afterload,
systemic vascular resistance.
02:03
Specific cardiomyopathy (restrictive
or dialytic cardiomyopathy).
02:07
Sometimes our ventricular
walls are too stiff,
and they can't stretch,
or maybe they're too dilated,
and they lose that
Frank Starling law.
02:16
You can have incompetent valves
causing regurge or stenosis,
which is reducing
our cardiac output.
02:23
Cardiac tamponade
and pericarditis.
02:25
Basically, remember,
tamponade is having too much pressure
on the outside of the
heart, not letting it fill.
02:31
And pericarditis is an
infection of the tissue.
02:35
So there, it's inflamed,
it's losing that Frank Starling law
and that squeezing capacity.
02:40
You can have a ventral septal defects
which is a hole in that septum,
where blood flow isn't going out to
the heart or going out to the aorta,
it's actually coming across the
septum into the right ventricle.
02:53
So you're losing some
of that cardiac output.
02:55
A high PEEP if the patient
is intubated and sedated.
03:00
A PEEP is positive
end-expiratory pressure.
03:04
So when they're breathing out,
we have pressure going back in
to keep those air sacs open.
03:10
So, if we increase
that PEEP too much,
we actually reduce the flow going
back into the heart, the blood flow,
because we're putting a lot of
pressure on that superior vena cava,
basically squeezing it down,
not letting blood get back into the heart
and back to that left ventricle to
eventually come out to the body.
03:29
But I'm talking about PEEPs that
are up in the term of the amounts
of like, 16, 18, 20.
03:37
That's what we're looking
at with a really high PEEP.
03:39
And it's specific medications can
cause a decreased cardiac output.
03:43
This are specific beta-blockers and
selective calcium channel blockers
that just reduce
that contractility.
03:51
Now, what can increase
your cardiac output?
Well,
the early stages of sepsis,
the early stages of sepsis
is called hyperdynamic stage.
04:01
And that's where
the body is sensing
that we're having a decrease
in our blood pressure.
04:06
And to compensate for it,
it's increasing our cardiac output.
04:09
We can see a hyperdynamic left
ventricle and in this sense.
04:13
Other things that cause
increased cardiac output,
exercise, anxiety and
stress, hyperthyroidism,
a really decreased SVR,
really, really low afterload.
04:25
And then specific
medications such as inotropes
and vasodilators can
increase our cardiac output.
04:32
A little bit later in the series,
we're going to dive into those medications
so we can understand what they're doing,
how they increase our contractility,
how they decrease our afterload.
04:41
And I want you to keep in mind
that a hyperdynamic left ventricle
is a cardiac output that's
greater than 8L/min.
04:49
We see this really, really healthy
athletes and healthy hearts.
04:53
We also see this in the
early stages of sepsis.
04:56
This is usually an indication that the
patient needs for fluid administration,
basically any fluid that's
going into that left ventricle,
they're just pumping it
out as fast as possible.
05:07
So if you actually add fluid,
you can actually slow it down.
05:10
So it's not contracting, everything it has,
it's a little bit backwards in that sense.
05:15
But it's usually an indication that
they need a little bit more fluid
to help slow it down and
contract a little bit easier.
05:23
Now, we've talked
about cardiac output,
let's talk about cardiac index.
05:27
Cardiac index normal
is 2.2 to 4.0 L/min/m2.
05:34
What's the difference between
cardiac output and cardiac index?
Well, cardiac index takes into
account a person's body surface area,
which is a calculation between
their height and their weight,
when you enter it into the computer,
it'll give you a body surface area.
05:49
As for cardiac output is just
how much liters per minute
is that heart pumping out,
we don't know if it's
enough for the patient.
05:58
So here's an example.
05:59
Take a seven foot basketball
player and a five foot gymnast.
06:03
Both of their cardiac
outputs are 5.0.
06:07
For that gymnast, it's going to
perfuse everything from the brain,
to the kidneys, to the gut,
to the toes and everything in between.
06:15
But to that basketball player, it is not
going to be enough to perfuse everything.
06:20
So the cardiac index of the gymnast
is going to be 2.5, maybe 2.8.
06:25
And that's definitely enough.
06:27
But the cardiac index of the basketball
player is going to be 1.8 to 1.5,
which is not enough
to perfuse everything.
06:35
So we'd like to look more
closely at cardiac index,
as it's the same for
every single patient.
06:41
The last part I want to
talk about is atrial kick.
06:45
This is very important and it can
account to 5-30% of cardiac output.
06:50
When atrial kick is basically
the last part of diastole.
06:54
When those atria are at
their end of of contraction,
the ventricles are
beginning to contract,
and the pulmonic and aortic
valve are beginning to open,
it basically is a kickstart to
the blood flow out to the body.
07:09
It's also what we
call a priming force
contributed by the last
of the atrial contraction.
07:14
Just keep in mind, atrial kick
accounts for 5-30% of cardiac output.
07:19
Now,
when do we lose atrial kick?
We lose atrial kick,
and anything that causes AV dissociation.
07:26
So anything that loses that association of
atrial contraction, ventricle contraction,
atrial contraction,
then the ventricles contract.
07:35
So that would be atrial
fibrillation, aflutter,
and all of our heart blocks,
anything that messes that up,
you're going to lose
your atrial kick.
07:45
So when you're in practice,
and the patient is doing well,
the map is great,
your cardiac output doing well,
and all of a sudden the map has dropped
and the cardiac output has dropped,
but everything looks normal.
07:57
Take a look at your ECG rhythm.
07:59
It could be that the patient
went into atrial fibrillation
and you've lost
your atrial kick.
08:04
Also, take note, if you have a pacemaker
that's only pacing the ventricles,
then you'll lose
your atrial kick.
08:13
So in my practice,
we'll have patients
that are heart patients,
they just had heart surgery,
they'll always come out with
pacemakers that are epicardial leads.
08:26
So sometimes we just have
been trickier pacemakers,
and those patients become bradycardic
will turn on the pacemaker
and actually the pressures
will even further drop.
08:36
And that's because we're
losing our atrial kick.