Cardiovascular disease has been the number one killer in the world for over a decade
and statistically, it’s the number one most likely thing to kill me, so I’m definitely
interested in learning more about it. It brings to mind one phrase you may have heard now
and then, “clogged arteries.” And I’m going to be completely honest, before I got
to college and learned the mechanism behind this disease, I thought clogged arteries were
a direct result of diet. Like if I put too much butter on my potatoes, that butter was
clogging my arteries. But it turns out that’s not what happens. The term Cardiovascular
disease is a catch-all for a bunch of different diseases, and there are a ton of factors that
go into what causes each kind. But the structure we need to learn to understand these diseases
isn’t the heart necessarily, it’s those arteries. These things are complex, ever
changing organs that deliver blood throughout the body and play a role not just in disease,
but in experiencing different climates, exercising, and maintaining homeostasis.
In the last few videos, we’ve been talking about the components of blood,
which includes a bunch of specialized cells.
We’ve got red blood cells for carrying and delivering oxygen to hungry body parts,
and the white blood cells that make up a big part of our immune system. But we haven’t
talked about the hardware that contains them and moves them. That’s where the cardiovascular
system comes in. If you prefer calling it the circulatory system, that’s fine too
— they’re the same thing. In this video, I’ll use cardiovascular because the name
gives away its pieces: the heart, hence the cardio portion, and all the blood vessels,
which is the vascular part. Now, the heart is an incredibly complex organ and we could
dedicate an entire series to it, but for now, we’re going to focus on the blood vessels,
those tubelike structures that transport blood around the body. When you take a big picture
look at the cardiovascular system, you’ll notice two distinct loops of blood vessel
networks, like a figure eight. One of those loops carries deoxygenated blood from the
right side of the heart to the lungs, picks up some oxygen, and circles back to the heart.
This loop’s pretty straightforward, only one organ to visit. This pulmonary circulation
is where important gas exchange happens, letting us do something with all the carbon dioxide
waste we’ve built up in our blood and capture that oxygen we breathe in. Once our blood
is nice and oxygenated it comes back to the left side of the heart to be pumped into systemic
circulation, the loop that hits everything that isn’t the lungs. As you can imagine
from the everything about this, the systemic circulation has a little more going on. Right
after getting ejected from the left side of the heart, blood passes through the aorta,
the biggest artery we have. This artery is going to branch off into smaller arteries
up into the neck and brain and down the body into the limbs and abdomen. As they get closer
to individual tissues and organs, they’ll branch off into tiny arterioles, and then
into microscopic blood vessels called capillaries. Some of those capillaries are so tiny that
red blood cells have to line up cell by cell to get through.
Not all of our arteries
are built the same. Big arteries close to the heart, like the aorta are under a lot
of pressure. And I don’t mean their parents are hovering over their shoulder checking
their math homework, I mean physical pressure from the pumping heart muscle. To cope with
this pressure, they’re built to be more elastic, letting them expand along with the
pressure. As we get to the arteries of the arms and legs, we see them become more muscular,
giving them more control of their diameter. This is where we start seeing the arteries
as more than just static tubes. An artery itself has three main layers, or tunics: the
tunica externa, media, and intima. Literally the outer, middle, and inner layers of the
artery. They all serve a different purpose, and they all come up again in understanding
cardiovascular disease. The tunica externa, also called the adventitia, gives the artery
its general shape and structure. The tunica media is built of a protein called elastin,
which, as you could tell by the name, gives the artery some elasticity. But it’s also
got a layer of contractible muscle around it. Now, this is a different type of muscle
from the skeletal muscles in your arms and legs. This smooth muscle surrounds the entire
blood vessel which provides a little more support, but more importantly, it regulates
how wide the artery becomes. Why is this so important? Well, the ability to shrink or
expand our blood vessels comes in handy in different situations. Let’s take a look
at exercise for example. Right now, you’re at rest. Your heart is probably beating nice
and steady — around sixty to a hundred beats per minute. At that rate, about five liters
of blood will pump out of your heart in the next sixty seconds. That’s enough to feed
all of your oxygen-hungry tissues at rest, but they get hungrier when you exercise. So
in order to ship more oxygen to those tissues, your body increases its heart rate, or how
frequently your heart pumps, and stroke volume, the amount of blood squeezed out with each
pump. For most of us, that means the five liters of blood we were pumping every minute
at rest can get up to thirteen liters a minute at peak exercise, and even more if you’re
a trained athlete. That means your arteries have to adjust for two and half times more
blood volume coming through. They do so by vasodilating — the smooth muscle of the
tunica media relaxes, which expands the diameter inside the blood vessel. In a totally different
situation, your arteries can vasoconstrict as a way to reduce loss of body heat and stay
warm in cold temperatures. Those changes in diameter are all possible thanks to the tunica
media, but there’s still one more layer to arteries. The innermost layer, or tunica
interna, has a little more smooth muscle and elastin, but most importantly, it’s lined
with super smooth endothelial cells. These cells have a very important job — provide
a low friction surface and make sure blood gets through circulation as smoothly and efficiently
as possible. So all in all these arteries have a thick outer layer, a smooth inner layer,
and a middle layer that changes the diameter of the vessel, which is amazingly useful.
All of this sets us up to understand how we can go from a free flowing, smooth blood vessel
to a “clogged artery”. Okay, so this process isn’t something that happens all at once.
Arteriosclerosis is the buildup of plaque within an artery to the point where it interferes
with normal function, and it can happen in any artery. Some of these conditions get
names with a little more pizazz though, a little more oomph where you’re like “ohh
dang, I don’t want that” but the pathogenesis is the same. Like when the arteries to the
brain get blocked, we call that a stroke or when the arteries to the heart muscle get
blocked we call that a heart attack. And when those organs don’t get blood, they don’t
get oxygen, and that can cause severe damage or sometimes death.
There are a few different
ways it can begin, but at some point, the endothelial cells become dysfunctional. Remember
from earlier, this layer’s job is to be as smooth as possible so blood can just flow
through. And a bunch of different factors make this condition more likely — smoking,
high blood pressure, diabetes all predispose an artery to endothelial dysfunction.
For instance, smoking reduces the availability of nitric oxide, a chemical that allows the
blood vessels to vasodilate, and increases some inflammatory factors that make the blockage
even worse.
But no matter what causes the dysfunction, now the endothelium lets lipids
from the blood sneak under that layer of endothelial cells and into the intima. That starts a process
where immune cells are called to the scene, where they enter the intima and oxidize those
lipids into foam cells. Foam cells sound cute, but these things are serious. Those immune
cells also recruit more smooth muscle to the area, as well as the tough connective tissue
collagen, which is definitely not supposed to be there. As a result, instead of a soft
bump you’ve got a tough, fibrous plaque. That cycle of plaque stacking can continue
until blood can barely get through an artery and that’s when the tissues it supplies
oxygen to really start to suffer. So again, clogged arteries are the narrowing of arteries
from plaque buildup and not some kind of buttery cholesterol fatberg in your blood vessels.
But that doesn't mean it's not dangerous. That plaque can break open, which means now there’s
a blood clot free floating in your arteries. That’s why a narrowing of the arteries around
the heart is so deadly. If that loose blood clot gets stuck on some plaque in those arteries,
oxygen can’t get to the heart muscle itself and it can die off. And that’s a heart attack.
This is one of the reasons why healthcare professionals recommend exercise for preventing
heart disease. It has the ability to reduce chronically high blood pressure and lower
bad cholesterol, but it also improves your ability to produce nitric oxide, that vasodilator
that improves blood flow. One of the other benefits of exercise is making more red blood
cells, but how does that happen? Tune in to the next episode in our playlist to find out how.
I’m Patrick Kelly, thanks for watching Seeker.