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  • 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 arteriesThese 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 steadyaround 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 vasodilatingthe 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 jobprovide

  • 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 arterySome of these conditions get

  • names with a little more pizazz though, a little more oomph where you're likeohh

  • dang, I don't want thatbut 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 likelysmoking,

  • 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.

Cardiovascular disease has been the number one killer in the world for over a decade

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