>>Dr. Ketchum: The purpose of this video lecture is to learn about cardiac output and the factors
affecting cardiac output. To begin, let’s define cardiac output, abbreviated CO. Cardiac
output is defined as the rate at which a ventricle pumps blood; the units are expressed as liters
per minute. The normal cardiac output is five liters per minute. Cardiac output can be calculated
by multiplying heart rate times stroke volume. Let’s talk about each of these variables—first,
heart rate. Heart rate is measured as beats per minute, abbreviated BPM. The average heart
rate is about 70 beats per minute. The heart rate is set by the SA node. Second is stroke
volume. Stroke volume is the volume of blood pumped per beat or stroke, and that’s about
70 milliliters per beat. The abbreviation for stroke volume is SV. Stroke volume can
be calculated by subtracting the end-diastolic volume, the EDV, minus the end systolic volume,
ESV. So let’s go ahead and define these terms.
For end-diastolic volume, first think about the word “diastole.” What does that word
mean? It means relaxation of the ventricles, and we use the word “end”—and we use
the word “end.” So end-diastolic is the end of relaxation, which is right before the
heart muscle contracts, and the world “volume” pertains to the volume of blood in the ventricles.
So when we put all these words together, EDV, end-diastolic volume, means the maximum
amount of blood in the ventricles before contraction. Now for end-systolic volume, again, first
think about the word “systole.” What does that word mean? It means contraction of the
ventricles, and we use the word “end.” So end-systolic is the end of contraction,
which is right before the heart muscle relaxes. And again, the word “volume” pertains
to the volume of blood in the ventricles. So when we put all these words together, the
end-systolic volume, ESV, means the maximum amount of blood in the ventricles after contraction.
So before we proceed any further, let’s make sure that we are all on the same page regarding
the right and the left ventricles. The volume of blood that is pumped by each ventricle
(meaning the right and the left ventricle) is the same. The volume of blood coming out
of the right and the left ventricle is the same. That’s an important concept. The pressures,
however, are different. The pressure in the left ventricle is higher than the pressure
in the right ventricle. But again, remember, the volume of blood is the same. Now let’s
return to cardiac output and explore how heart rate and stroke volume affect cardiac output.
Remember that we calculate cardiac output by multiplying heart rate times stroke volume.
So if heart rate increases, cardiac output increases. Or if stroke volume decreases,
cardiac output decreases, and so on.
So let’s go ahead and zoom in on these factors. We’re going to begin with heart rate. So
here are the factors that regulate heart rate. Neural control via the autonomic nervous system
can regulate heart rate. More specifically, the parasympathetic nervous system will lower
heart rate, while the sympathetic nervous system will raise heart rate. But it’s not
just the autonomic nervous system that regulates heart rate—hormones are also involved.
These hormones include epinephrine, which you already know is released as a result of sympathetic
stimulation, but there is also thyroid hormone.
Thyroid hormone actually enhances the effects of epinephrine. So if you have chronic hyperthyroidism
—meaning an abnormally high level of thyroid hormone—this can actually weaken the heart, because thyroid
hormone not only increases heart rate, it also increases force of contraction. Those
are the factors that regulate heart rate. In a separate video, we will discuss the mechanism
for the sympathetic and parasympathetic effect on heart rate. So now let’s focus on stroke
volume. Stroke volume is regulated by two different factors: the end-diastolic volume
and ventricular contractility. So let’s focus on end-diastolic volume first. Remember
to always define the terms; this will help you a lot. So end-diastolic volume is the
maximum amount of blood in the ventricles before contraction—this is influenced by
Starling’s Law. Starling’s Law is the rate at which blood flows into the heart;
some people will refer to this as preload. So if I increase the rates of blood flow into
the heart, that means I have increased venous return. If I increase venous return, that
will increase end-diastolic volume. Now let’s focus on the factors that affect ventricular
contractility. Remember, this is the other factor that affects stroke volume. Ventricular
contractility is affected by the sympathetic nervous system.
The sympathetic nervous system increases the force of contraction; we will discuss the
mechanism for that in a separate video. There are also hormones that can affect ventricular
contractility: insulin, glucagon, thyroid hormone, and epinephrine will all increase
the force of ventricular contraction.