So, the two have to be balanced, of course.
Now, what determines cardiac output- which
is the number of liters of blood that the
heart pumps in one minute, is of course, the
stroke volume which is put out with each beat
times the heart rate. Because stroke volume
stays... let’s say the person is resting and
not exercising, stroke volume stays about
the same with each beat. So, what determines
how much blood comes out of the heart then?
His heart rate! Because cardiac output is stroke volume times the number of beats per
minute. That tells you the number of cubic
centimeters or number of, if you want to express
it in liters, the number of liters per minute.
Usually, the average person puts out about
4 to 5 liters per minute in a resting state
and of course, much more, if they are exercising.
Now, there is another important point that
needs to be remembered about the circulatory
system. It has resistance in it as well as
blood being pumped into it. It’s just like
the famous Ohm’s law in electricity- that
the voltage or the pressure in your electrical
line is equal to the resistance times the
flow in amps. In the cardiovascular system,
it’s the blood pressure is equal to the
cardiac output times the resistance.
In the lung, the resistance is called the pulmonary
vascular resistance and in the systemic circuit,
it’s called the systemic vascular resistance.
So, in the catheterization laboratory, we
often calculate, first of all, the cardiac
output using a variety of techniques and then
we measure the blood pressure and we can then
calculate the resistance in the pulmonary
circuit and the resistance in the systemic
circuit. These two numbers are of great importance
because we can often see when there is disease.
For example, a patient who is markedly hypertensive
will have an elevated systemic vascular resistance.
A patient who has disease in the lung may
have an elevated pulmonary vascular resistance.
And so, with the normal cardiac output you
are going to have higher pressures in whichever
circuit happens to have the increased vascular
resistance. Here we have a very simple diagram of the
three factors that determine ventricular function
during systole. First of all, there is preload.
I’ll tell you what that is in a moment,
then there's afterload and then there's
contractility. So, let’s look at preload
first. Preload is the amount of stretch that
the ventricular muscle is under and it directly
relates to how well we fill the ventricle.
What’s important about preload is that there
is an intrinsic law of the heart that was
discovered by a physiologist named Starling.
It’s called Starling’s Law of the Heart.
I like to call it the Rubber Band Law of the
Heart. The more you stretch the rubber band,
the more it snaps back into place. So, the
more you fill the ventricle, the more it’s
going to squeeze out in the subsequent beat.
This is, therefore, a very important component
because if the patient is dehydrated or having
a hemorrhage and has decreased blood volume,
the ventricle will have decreased filling
and it will decrease the amount of stroke
volume- the amount of blood that it puts out
with each beat. Then there is afterload. Afterload
is the resistance that the ventricle experiences
when it’s squeezing. So, for example, it
could be an increase in peripheral vascular
resistance in the systemic circuit due to
high blood pressure. In which case, the left
ventricle sees a stronger resistance to pushing
the blood out through the aortic valve and
stroke volume may also decrease. We can manipulate
afterload with drugs and we’re going to
be talking about that because in patients
who have an increased systemic vascular resistance,
we can actually make the pumping ability of
the left ventricle better by giving drugs
that decrease the resistance in these blood
vessels and increase the ability of the left
ventricle then to pump again. And then the
final factor is contractility. This is the
intrinsic 'oomph',- the snap of the ventricular
muscle when it squeezes and of course, certain
diseases rob the ventricle of some of its
snap and therefore, stroke volume goes down.
So, you see that there is a real integration
here - you have to have appropriate preload,
you have to have appropriate afterload and
appropriate contractility and most normal
people have all of these going at the right
time when they are well hydrated, when they
have their normal blood volume, when they
have a normal blood pressure and normal contractility.
Now, we have talked already about the Starling
Law of the Heart. It says “the more you
stretch it, the more it rebounds”. So, that’s
really one of the measures of preload. In
terms of afterload, of course, the systemic
arterial blood pressure or the pulmonary artery
pressure determine how much resistance is
seen by the ventricles when they contract.
On the right side, the diseases, for example,
if one has blood clots in the lung, that increases
the resistance and will increase the amount
of pressure that the right ventricle has to
generate to push blood out into the pulmonary
arteries. Often on the left side, the patients
will have high blood pressure, they will have
constriction in the small arteries in the
system, and that will resist the left ventricle
as it tries to eject blood into the aorta.
And there are ways to improve the resistance
and therefore, to improve the stroke volume
and the cardiac output. It’s again important
to remember that the right ventricle, because
it’s moving volume at a lower pressure is
very preload dependent. And the left ventricle,
which is pushing blood out at a high pressure,
is more afterload dependent. Now, both of
them are affected by preload and afterload.
But for the right ventricle, preload is particularly
important; for the left ventricle, afterload
is particularly important and we can measure
all of these numbers in the catheterization
laboratory and we know what normal is. Now,
let’s talk a little bit about the measurement
of these hemodynamic values. We do that usually
in the catheterization laboratory, but it
turns out, as I will talk about a little later,
sometimes we can use non-invasive tests such
as the echocardiogram that will also give
us an estimate of cardiac output and an estimate
with the blood pressure of the resistance
in the lung and the resistance in the body.
So, sometimes we don’t have to put a catheter
inside the body to make these measurements.
Here is an important relationship that I referred
to before, just to this graph reiterates that
point, and that is the peripheral resistance
determines how much stroke volume occurs.
You can see in this curve, as the resistance
moves to the right, the stroke volume falls
and as the resistance moves back to the left,
the stroke volume increases. In other words,
when we increase the afterload of the ventricle,
the resistance to which it’s ejecting will
decrease stroke volume. This is an important
hemodynamic point that we often use in patients
with heart failure where we are trying to
decrease the afterload to help a deceased
ventricle empty more completely. So, we are
just going to say for just a few moments some
of things that can increase preload and afterload,
I have already mentioned them. Preload is
very much determined on the blood volume.
Does the patient have appropriate blood volume?
Are they dehydrated? Have they lost blood
somehow through hemorrhage? On the other hand,
in terms of afterload, are the resistances
normal in the pulmonary circuit and in the
systemic circuit? And those can be changed
by disease states, of course, as we have…
as we have talked about.
Here we note the resistance in the lung, so
called pulmonary vascular resistance. We can
actually calculate it in… with a parameter
of (dyne-second-centimeters ^ -5) and we can also
calculate a systemic vascular resistance using
similar parameters. This is done in the catheterization
laboratory, but as I said, you can get a rough
guesstimate of these numbers from the non-invasive
studies as well. Now, what happens when we
are actually in the catheterization laboratory
or sometimes when we have a pulmonary artery
balloon catheter in a patient that’s in
the Intensive Care Unit, we actually try and
correlate the electrocardiogram with the pressure
tracing. Here we see a pressure tracing of
the pulmonary artery and you can see the rise
in the pressure followed by fall to a little
notch and then further decline. That little notch represents the closure of the pulmonary
valve. The same thing happens in the aorta,
there’s a rise in the pressure, then there’s
a fall and there’s a little notch as the
aortic valve closes and you can see the timing
of systole with the QRS above. QRS occurs
and then a few seconds later, you have
the pressure tracing either in the pulmonary
artery or in the aorta. Here it is enlarged,
so you can see it a little better. Notice the
electrocardiogram above the QRS is the big
spike, that’s the electrical activity causing
the ventricle to contract and then there’s
a little delay because the ventricle mechanical
activity doesn’t happen immediately.
It takes a few seconds for the mechanical activity
to build and then you can see the pressure
rising in the aorta or the pulmonary artery.
You can see it falls to the notch, the so called
dicrotic notch, which is either the pulmonary
or the aortic valve closing. And here we see
a… a diagram that’s the.. similar. In this
case, it’s the aortic pressure.
You can see the QRS occurs a little bit before the
aortic pressure. The dicrotic notch isn’t
quite as clear here, but you can still see
the little notch there when the aortic valve
closes. Here is a listing of normal values.
It’s not necessary that you memorize these. These
are all available in tables, but this is a
typical set of normal values. The pulmonary
artery pressure is generally peak systolic
about 25 and diastolic around 12. The peak
aortic pressure is generally about 120/80 mmHg,
that’s the so called normal blood pressure.
Left ventricular diastolic pressure is usually
4-5 mmHg and similarly, right ventricular
diastolic pressure is usually 4-5 mmHg.
And you can see also the normal resistances that gets
calculated from the, if you will, Ohm’s
Law of the heart: blood pressure equals heart
rate… equals cardiac output times resistance.