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.
And the scariest thing to do was having to call them
and let them know something that was going on with their patient.
I was worried about what they were going to ask me
and worried about if I was going to have the correct answer.
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.
The first value we're going to talk about cardiac output,
the normal cardiac output is between 4 and 8 L per minute.
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.
Now, cardiac output is stroke volume times heart rate.
It's difficult to talk about cardiac output without understanding stroke volume.
What stroke volume is how many milliliters of blood
is ejected from that left ventricle per beat.
So cardiac output is stroke volume times heart rate.
Now, the determinants of cardiac output are heart rate,
preload, afterload, contractility, and Frank Starling law.
With heart rate, preload and afterload,
we're going to discuss those a little bit later in this series.
So it makes a little bit more sense.
But I want you to remember Frank Starling law.
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.
The greater squeezed, the more stretch, the greater the squeeze.
So I want you to remember that when we're talking about our left and right ventricle.
What decreases cardiac output such things as hypovolemia, brady and tachycardia,
dysrhythmias, too high of afterload, systemic vascular resistance.
Specific cardiomyopathy (restrictive or dialytic cardiomyopathy).
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.
You can have incompetent valves causing regurge or stenosis,
which is reducing our cardiac output.
Cardiac tamponade and pericarditis.
Basically, remember, tamponade is having too much pressure
on the outside of the heart, not letting it fill.
And pericarditis is an infection of the tissue.
So there, it's inflamed, it's losing that Frank Starling law
and that squeezing capacity.
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.
So you're losing some of that cardiac output.
A high PEEP if the patient is intubated and sedated.
A PEEP is positive end-expiratory pressure.
So when they're breathing out,
we have pressure going back in to keep those air sacs open.
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.
But I'm talking about PEEPs that are up in the term of the amounts
of like, 16, 18, 20.
That's what we're looking at with a really high PEEP.
And it's specific medications can cause a decreased cardiac output.
This are specific beta-blockers and selective calcium channel blockers
that just reduce that contractility.
Now, what can increase your cardiac output?
Well, the early stages of sepsis,
the early stages of sepsis is called hyperdynamic stage.
And that's where the body is sensing
that we're having a decrease in our blood pressure.
And to compensate for it, it's increasing our cardiac output.
We can see a hyperdynamic left ventricle and in this sense.
Other things that cause increased cardiac output,
exercise, anxiety and stress, hyperthyroidism,
a really decreased SVR, really, really low afterload.
And then specific medications such as inotropes
and vasodilators can increase our cardiac output.
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.
And I want you to keep in mind that a hyperdynamic left ventricle
is a cardiac output that's greater than 8L/min.
We see this really, really healthy athletes and healthy hearts.
We also see this in the early stages of sepsis.
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.
So if you actually add fluid, you can actually slow it down.
So it's not contracting, everything it has, it's a little bit backwards in that sense.
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.
Now, we've talked about cardiac output,
let's talk about cardiac index.
Cardiac index normal is 2.2 to 4.0 L/min/m2.
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.
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.
So here's an example.
Take a seven foot basketball player and a five foot gymnast.
Both of their cardiac outputs are 5.0.
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.
But to that basketball player, it is not going to be enough to perfuse everything.
So the cardiac index of the gymnast is going to be 2.5, maybe 2.8.
And that's definitely enough.
But the cardiac index of the basketball player is going to be 1.8 to 1.5,
which is not enough to perfuse everything.
So we'd like to look more closely at cardiac index,
as it's the same for every single patient.
The last part I want to talk about is atrial kick.
This is very important and it can account to 5-30% of cardiac output.
When atrial kick is basically the last part of diastole.
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.
It's also what we call a priming force
contributed by the last of the atrial contraction.
Just keep in mind, atrial kick accounts for 5-30% of cardiac output.
Now, when do we lose atrial kick?
We lose atrial kick, and anything that causes AV dissociation.
So anything that loses that association of atrial contraction, ventricle contraction,
atrial contraction, then the ventricles contract.
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.
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.
Take a look at your ECG rhythm.
It could be that the patient went into atrial fibrillation
and you've lost your atrial kick.
Also, take note, if you have a pacemaker that's only pacing the ventricles,
then you'll lose your atrial kick.
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.
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.
And that's because we're losing our atrial kick.