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CV Response || Boards and Beyond || Cardiology

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0:05Hello everyone and welcome to our module

0:07on the cardiovascular response to

0:08exercise.

0:10In this video I'm going to go through

0:12the cardiovascular response to exercise.

0:14And by that I mean I'm going to discuss

0:16the physiologic changes that occur in

0:18the vascular system when you exercise.

0:20This is a very important application of

0:22basic principles of cardiac physiology.

0:25It's also commonly tested and very high

0:27yield for the USMLE step one exam. So

0:29when you exercise, the body's overall

0:31goal is to maximize the profusion to

0:33skeletal muscles in the heart and to

0:35minimize the profusion to all other

0:36areas of the body. The initiator for

0:39this response is muscle hypoxia. When

0:41you begin exercising, your tissue beds

0:43in your muscles become hypoxic and that

0:46triggers the body's response. And the

0:48mediator of that response is the

0:49sympathetic nervous system. It is what

0:51drives all the different changes that

0:53occur in the cardiovascular system. The

0:55process of the body's response to

0:57exercise begins with muscle contraction.

0:59When you start exercising, you contract

1:00your muscles and this leads to the

1:02consumption of ATP. When you consume

1:04ATP, you then consume oxygen because you

1:07need more ATP for your muscle tissue.

1:09The result is local hypoxia in muscle

1:11tissue. And this leads to vasoddilation,

1:13which is a very important intermediate

1:14step in the body's response to exercise.

1:17Vasoddilation results because of

1:19multiple mediators that are released

1:20into the plasma in muscle tissue, which

1:23is hypoxic. This includes adenazine

1:25generated from ATP consumption also

1:27lactate, carbon dioxide and potassium

1:29among other mediators. The net result of

1:32the vasoddilation in muscle tissue is a

1:34lowering of total peripheral resistance

1:36which is a very important physiologic

1:38change that occurs with exercise. The

1:40fall in peripheral resistance leads to

1:42activation of the sympathetic nervous

1:44system which leads to many of the

1:45physiologic changes associated with

1:47exercise. There's a rise in

1:49contractility and stroke volume. The

1:51heart rate goes up. The net result of

1:52both of these changes is a rise in

1:54cardiac output. When the cardiac output

1:56goes up, you push more blood into the

1:58arterial system. This leads to a rise in

2:00the systolic blood pressure. In

2:02addition, there's vasoc constriction to

2:04some areas that are not important during

2:06exercise, areas like the gut and the

2:07skin. This helps to redistribute blood

2:09to the important areas like the heart

2:11and the muscle. The blood pressure

2:13changes that occur with exercise are

2:15very high yield. So, let's review those

2:17on this slide. The systolic blood

2:19pressure usually rises with exercise. is

2:21this is because the cardiac output goes

2:22up that drives more blood into the

2:24arterial tree and that raises the

2:26systolic blood pressure. Always remember

2:28that the primary determinant of the

2:29systolic blood pressure is the cardiac

2:31output. When the cardiac output goes up

2:33the SBP usually rises and when the

2:35cardiac output falls the systolic

2:36pressure usually falls. The diastolic

2:39blood pressure with exercise decreases

2:41slightly or stays normal. Why does this

2:43happen? Well, as we discussed, there's

2:44local dilation of skeletal muscles. And

2:47remember that the primary determinant of

2:49the diastolic blood pressure is the

2:50peripheral resistance. So that dilation

2:52can lower the peripheral resistance and

2:54that can decrease the diastolic blood

2:56pressure. So because you've got systolic

2:58pressure going up and diastolic blood

3:00pressure staying flat or going down, the

3:02net result is that you will have a

3:04widening of the pulse pressure which is

3:06the difference between the two. So the

3:07pulse pressure goes up with exercise and

3:10as we discussed previously the total

3:11peripheral resistance goes down because

3:13of dilation of vessels in skeletal

3:15muscles.

3:17There are important changes to coronary

3:19artery profusion that occur as part of

3:21the response to exercise. This is

3:22because the faster heart rate shortens

3:24diastily. Recall that coronary arteries

3:26are profused during diastily, not cy

3:29like most arteries in the body. This

3:31means that when the faster heart rate

3:33shortens diastily, there is less

3:34coronary filling time. As a result, the

3:37coronary arteries must vasoddilate in

3:39order to increase their blood flow. This

3:41is the only way to get more oxygen to

3:43myioardial tissue. Myioardial tissue

3:45cannot extract more oxygen because it

3:47already extracts the maximum oxygen from

3:50red blood cells at baseline. Other

3:52tissues in the body can take more oxygen

3:54from red cells when they need it. But

3:55the heart cannot do this because it is

3:58always extracting the maximum amount.

3:59Thus, the only way it can increase the

4:02oxygen delivery is by increasing the

4:03blood flow. And the only way it can do

4:05that in the setting of a shorter

4:06diastily is to increase the amount of

4:08coronary vasoddilation. Your preload

4:10rises with exercise. This is because

4:12sympathetic stimulation leads to venus

4:14contraction. As we discussed previously,

4:16this will increase the preload and the

4:18end diastolic volume and this is another

4:20contributor to the rise in cardiac

4:22output seen with exercise along with the

4:24increased heart rate and the

4:25contractility. The left ventricular

4:27ejection fraction increases dramatically

4:29with exercise. If you look at the two

4:31moving images on the bottom of the

4:32screen, the left side is a patient

4:34before exercise, the right side is after

4:37exercise. You can see that before

4:39exercise, the left ventricle thickens

4:41and the walls come in, but there's still

4:43plenty of black left in the middle. On

4:45the right side, the heart is contracting

4:46so vigorously after exercise that almost

4:48all the black in the middle is

4:50eliminated. I show you these pictures

4:51because it's an easy way to remember

4:53that the left ventricular ejection

4:54fraction goes up with exercise. The

4:57reason this happens is because there's

4:58more vigorous contraction in the setting

5:00of exercise and sympathetic stimulation.

5:02The major impact is decreasing the ends

5:05systolic volume as a result of increased

5:07contractility. There's minor changes on

5:09the end diastolic volume. The reason is

5:11because there's more preload which tends

5:13to raise the end diastolic volume.

5:15However, there's less filling at fast

5:16heart rates. Thus, the change in the end

5:18diastolic volume tends to be relatively

5:20minor and somewhat variable. However,

5:22the ejection fraction if you look at the

5:23top right side of the screen is dictated

5:26by the end diastolic volume minus the

5:27ends systolic volume over the end

5:29diastolic volume. So if the ends

5:31systolic volume goes way down, it will

5:33make the EF go way up by this equation.

5:36There's one additional concept in

5:37cardiac physiology that we haven't

5:39discussed yet and it's particularly

5:40important in exercise and that's the

5:42concept of lucotropy. Lucotropy is

5:44myocardial relaxation. It's the opposite

5:46of contractility. Contractility is how

5:48vigorously the walls of the left

5:50ventricle come together to push blood

5:52out of the ventricle into the aorta in

5:54cy. Lucotropy is how vigorously the

5:56walls of the left ventricle come apart

5:58in diastily. When they come apart, they

6:01suck in blood and raise the preload,

6:03which raises the cardiac output. Thus,

6:05when the degree of lucotropy increases,

6:07the left ventricle relaxes more

6:08vigorously. This pulls in more blood and

6:10raises a preload and raises

6:12contractility. And just like

6:14contractility, lucotropy is increased

6:16with exercise. This contributes to the

6:18increased preload seen with exercise,

6:20which leads to the rise in cardiac

6:21output. The key regulatory protein of

6:23lucotropy in the heart is called

6:25phospholaman. This regulatory protein is

6:28an inhibitor of a very important enzyme

6:30called circa. Circa stands for the

6:32cycoplasmic reticulum calcium ATPAS. And

6:35this enzyme regulates lucotropy in

6:37ventricular myasytes. To understand

6:38this, imagine we have the cycloplasmic

6:41reticulum inside a ventricular myasy. In

6:43order for relaxation to occur, the

6:45cycloplasmic reticulum must pull calcium

6:48from the cytool so that the myasy can

6:50relax. Circa facilitates uptake of

6:53calcium from the cytool into the

6:54cycoplasmic reticulum and it is normally

6:56inhibited by phospholamand. However,

6:59betaadronurgic stimulation via the

7:01sympathetic nervous system can

7:03phosphorolate phospholamand. This makes

7:05it stop inhibiting circa and it allows

7:07circa to take up calcium more vigorously

7:10out of myioytes in the left ventricle.

7:12This leads to more rapid and more

7:13vigorous relaxation and an increase in

7:16lucotropy. Here's a picture to make this

7:18more clear. here circa in the membrane

7:19of the cycloplasmic reticulum. It is

7:21normally inhibited by phospholamban.

7:23However, sympathetic stimulation

7:25phosphorolates phospholamand via beta

7:27adinuric stimulation. This inactivates

7:30phospholamand. It relieves the

7:31inhibitory effect. It allows circa to

7:33take up more calcium and thus there is

7:35more vigorous relaxation of the left

7:37ventricle that leads to a rise in

7:39lucotropy and an increase in preload.

7:41I'll finish this video with this concept

7:43map which summarizes all the changes

7:45that occur in exercise that you need to

7:47know for the step one exam. So when

7:48exercise begins this leads to muscle

7:51hypoxia which causes vasoddilation.

7:53Vasoddilation lowers the TPR. It lowers

7:56the afterload and that activates the

7:58sympathetic nervous system. In addition

8:00the lowering of afterload can decrease

8:01the diastolic blood pressure. At this

8:04point, the sympathetic nervous system

8:05becomes the mediator for all the

8:07physiologic changes that occur with

8:09exercise. In the peripheral vessels,

8:11there will be constriction of arterials

8:13to unimportant areas like the skin and

8:15the gut. There will be venus

8:16constriction which will send blood back

8:18to the left ventricle, raising the

8:20preload and raising the end diastolic

8:21volume. In the heart, the sympathetic

8:24activation will increase contractility

8:26and heart rate. The increased

8:27contractility will lower the ends

8:29systolic volume and raise the ejection

8:31fraction as we saw in those echo

8:32cardiogram images earlier. The higher

8:34heart rate plus the increase in

8:36contractility plus the increase in

8:38lucidotropy all contribute to a rise in

8:40cardiac output and that raises the

8:41systolic blood pressure. And that

8:44concludes our video on the

8:45cardiovascular response to

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