Okay.
So, last time, we talked about Preload and Afterload.
Today, we re gonna talk about how those two play in to the entire hemodynamic system
and then things that we can do to affect preload and afterload; whether it s elevated or low.
So, before we get started though, remember we talked about preload is a volume and afterload
is a pressure.
So, a little mnemonic for you to remember that is PVAP Preload - Volume; Afterload - Pressure.
Okay, and as we talked through this, that will become kinda clear what that mnemonic
means and then understanding that mnemonic is gonna help you to determine how you can
correct problems in your patient.
Okay, so, first of all, this little chart here basically covers the hemodynamics and
what you need to know about different elements of hemodynamics.
First of all, we have our heart rate.
Okay, our heart rate, and this is our little heart here, atria, ventricles, aorta, tricuspid,
pulmonic valve, mitral valve, aortic valve, okay?
So, atria on top here, ventricles on bottom, here s our little valves.
Okay, so, heart rate originates up here in the atria, in the sinoatrial node, we know.
So, heart rate should normally be between 60 - 100.
There’s a couple of things that could cause that to increase,
to be higher that it should, to be lower than it should.
What our heart rate is, it’s gonna directly affect our cardiac output, okay
Now, these things kind of the y work with each other.
So, it’s not necessarily one causes the other, but it works for verse wise as well.
So, stroke volume is gonna be affected by afterload and vise versa. So, heart rate is
gonna affect cardiac output. And so, our cardiac output is the volume of blood that leaves
the heart per minute. Okay, so, what s leaving this left ventricle every minute? Normal should
be 4 - 8 L/min. Now, what they ve found throughout the years is that, that number varies based
on the patient s size. So, a petite little old grandma isn t going to need as high of
a cardiac output as a much smaller individual. Okay, so, what they did is they decided to
start multiplying that by body surface area. Okay, so they take cardiac output, multiplied
by body surface area, and what you ll come up with is a cardiac index and the normal
for that should be about 2.5 - 4 L/min/m2. Okay, so this is kinda more the number we
re gonna use, what s our cardiac index. Cardiac output is gonna vary based on the patient
s size.
Okay, now, cardiac output is gonna be affected by stroke volume. We talked a bit about stroke
volume in the last video. The stroke volume is basically volume of blood per beat. Okay,
cardiac output is per minute and stroke volume is per beat, okay? Now, the way we calculate
stroke volume is we get end diastolic volume, minus end systolic volume. So, we take what
is left in the ventricles after systole and we substract that by what s in the ventricles
at the end of diastole, the end of filling, what s there minus what s there after contraction.
Okay, so, normal for that will be 60 - 120 mL/beat.
And then, what we talked about in the last video is preload, contractility and afterload.
Okay, so, these are the 3 things that directly affect our stroke volume or the amount of
blood that s leaving our heart every minute, or every beat, I m sorry. So, the 3 things
that are gonna affect that would be contractility first, which is the squeeze of the ventricles.
And then, preload, which we talked about, is the volume. And then, afterload, which
is the pressure that the ventricles must squeeze against in order to push blood out through
the aorta, okay? Okay, with preload, let s talk about preload really quick. We talked
about preload as a volume. It s really basically your end diastolic volume which means the
volume of blood, the volume of blood in the ventricles at the end of diastole, at the
end of filling, the volume that s in there. Okay, and there s two ways to measure that
number. The two ways to measure that number is gonna be CVP and Pulmonary Artery Occlusive
Pressure. CVP is relatively easy to measure. You can actually measure that through a central
line. You place the central line the tip of that sits close to, so, it kinda sits right
in here. And with that, we can actually kinda get a measure of the central venous pressure.
Okay, obviously, we re talking about our central veins here. And that kinda give us our central
venous pressure. And, the number we re gonna get for that, what we re aiming for that is
2 - 6. Okay? So, Central Venous Pressure is basically gonna tell us our preload. It s
gonna tell us how much blood is kinda turning to the heart and what s gonna be available
to fill the ventricles. Okay, so, that s CVP. We also have Pulmonary Artery Occlusive Pressure.
That s a little bit harder to measure because what we do is, we get a reading in our pulmonary
artery, so we feed the line down like this and up like this. And then we get a reading
in our, and then it can actually fill up a little balloon right here, and what that will
do, is it will get them a reading of the right atria, and with that right atria, it can kind
of estimate Pulmonary Artery Occlusive Pressure which gives them an estimate on the preload
of the left ventricle. So, that s done through much more complicated catheter and generally
you re not gonna have every ICU patients gonna have that. But most ICU patients are gonna
have a central line, so, it becomes very easy to just measure off of our CVP rather that
our pulmonary wedge pressure. So, PAOP, occlusive pressure or wedge pressure means the same
thing. Okay, so really the number we re gonna look at is CVP, and what s that gonna tell
us, is it s gonna tell us our number for our preload. Preload again, is the volume. So,
preload is the volume in our ventricle at the end of diastole, at the end of filling,
it s that volume in there.
Okay, next, we have our afterload. Okay, our afterload, like I said, is the pressure required
to open these valves, your aortic valve and your pulmonic valve and to get the blood out
of the ventricles. That can be measured with two numbers. Peripheral Vascular Resistance,
or Pulmonary Vascular Resistance and Systemic Vascular Resistance. So, SVR is really the
number we re gonna use for that. So, systemic vascular resistance is the resistance in your
systemic vasculature that the ventricles have to squeeze against to get the blood into the
aorta, okay? So, systemic vascular resistance, that s 800 - 1400, and the number is dines
per, something, I don t remember, it s 800 - 1400, 800 - 1200, basically, it s the number
we re looking out for that. Okay, so that s our afterload, the pressure required to
open that valve and get blood out of the heart.
Okay, so, let s look really quick back at preload. So, preload, like we talked about,
is the volume. So, your preload can be elevated, okay, so, what that s basically saying, is
that we have too much volume. And so, if we look at the cures for that, or the things
that doctors might request to lower preload, is things like venous vasodilators, right,
volume coming in, so, venous vasodilators like nitrates, diuretics, ACE inhibitors and
ARBs. So, these are all things that will try to decrease. So, if our preload is elevated,
we try to decrease volume, basically. Okay, if our preload is decreased, if our volume
coming in is low, then what we can do is we can get things like fluid and blood. So, if
it s low, we re gonna try to increase volume. Okay, and if we look over here.
Okay. So, now, let s talk afterload again. Remember, afterload is the pressure required
of these ventricles in order to push blood out into the aorta. So, it s how much pressure
we re working against in our vessels to try to get blood out there. So, if our afterload
is low, okay, so, if we need to tighten up these vessels, if we need to increase the
pressure required to get it out, we re gonna give things like vasopressors. Okay, so, we
ll get things like norepinephrine, neosynephrine, vasopressant or epinephrine. The thing we
use most often on my neurologic floor is neosynephrine. And, usually, you ll give them in specific
order based on the condition of the patient. But basically, if in situations like shock,
sepsis, things like that, we need to increase that pressure, our vessels have dilated dramatically
and we have to get a little bit more squeeze on there and so we ll get things like vasopressors
for that. And that s gonna bring our systemic vascular resistance, it s gonna squeeze those
and we re gonna tighten that up, make it harder to open this aortic valve here and require
the ventricles to squeeze a little bit harder to get through that. Now, if we need to, if
our afterload is too high, if it s too hard for these to open up, if these ventricles
are having to work too hard to get blood into the aorta, we re gonna get things like arterial
vasodilators, right? So, we re gonna dilate our vessels, dilate our arteries, specifically,
with things like hydralazine to try to open that up a little bit easier for blood to get
out and in to the system and profuse the body. So, we can get things like arterial vasodilators,
ACE-Inhibitors, ARBs, and we can use things like intra aortic balloon pumps which is a
little balloon fed up here and during systole, this is gonna.