Aortic stenosis and aortic regurgitation | Circulatory System and Disease | NCLEX-RN | Khan Academy

Aortic stenosis and aortic regurgitation | Circulatory System and Disease | NCLEX-RN | Khan Academy

January 4, 2020 26 By Bertrand Dibbert


– [Voiceover] Here we actually see the LV, or left ventricle,
contacting into the aorta, and the red arrow’s looking
at the aortic valve, which is actually not opening very much if you can see that. So this is aortic stenosis. What is aortic stenosis? Very basically, it’s having a tight aortic valve so not enough blood can get through. You’ll see our label here,
the LV, the left ventricle, and then I’ll label the aorta here. Blood normally flows from the LV through the aortic valve into the aorta, and then supplies the rest of the body. So, to take you through the
progression of blood flow, you have blood that returns to the left atrium from the lungs, goes into the left ventricle
through the mitral valve, leaves through the aorta, and then goes and oxygenates tissue in the rest of the body. Now, if it can’t get
from the left ventricle to the aorta due to something
such as aortic stenosis, then you’re going to have blood backed up in the left ventricle, and you’re going to have problems profusing, or supplying, enough blood and enough oxygen to the rest of the body’s tissues. Let’s talk about some of the major causes of aortic stenosis. The first thing we want to talk about is having a bicuspid aortic valve. This a congenital condition, meaning you’re born with it, and this means that you only have two cusps to the aortic valve. Let’s demonstrate this here. Normally, the aortic
valve has three cusps. I’m going to label those
one, two and three. But a certain portion of the population actually has a congenital
bicuspid aortic valve, only having one and two cusps. The reason why a bicuspid aortic valve is more likely to get aortic stenosis or is more likely to become stenotic, is because you actually have two cusps doing the work of three, and so these bicuspid valves actually get damaged quicker and can become calcified over time, and are thus more likely
to become stenotic and more likely to do
so at an earlier age. Another cause of aortic stenosis is age-related calcification. As you get older, the
valve actually calcifies and gets hardened, and
can actually obstruct, or stop, the valves
from opening all the way and causing a stenosis. The risk factors for having calcification of the aortic valve are very similar to the process of coronary artery disease. So when we talk about
risk factors for this, we talk about things such as smoking, high blood pressure, or hypertension, hyperlipidemia, or high cholesterol, and diabetes mellitus. Another cause of aortic stenosis could be rheumatic fever. Generally, the mitral valve
is more commonly affected, but the disease process of rheumatic fever and rheumatic heart disease can actually affect the aortic valve as well. The way that you can remember
the signs and symptoms of aortic stenosis is
with the acronym SAD. S stands for syncope, meaning fainting. A stands for angina, which is a type of chest pain. And dyspnea, meaning shortness of breath. Other things that you can
look for are things like pulsus parvus et tardus. Now, this sounds kind of
funny and kind of weird, but all it means is that you have a small or weak pulse, parvus meaning small, and tardus meaning like tardy, slow. So it’s a small or weak
pulse that is slow to rise, because if you think of blood coming out of a very tight valve,
you’re not going to have the normal rise in pressure
that you normally do, that you feel when you’re
feeling someone’s pulse. Another thing that may occur is LVH, or left ventricular hypertrophy. What you can do on physical exam is you can actually palpate
what’s called the PMI, or the point of maximal impulse. This should normally be in
the fifth intercostal space in the midclavicular line, so similar to what we call the mitral area when you’re auscultating, or listening with a stethoscope. In people with LVH, this PMI can actually move medially, or towards the sternum, and that would be a sign of
left ventricular hypertrophy, meaning the muscle has
kind of gotten thicker. Another thing that you
can see in aortic stenosis is MAHA, or microangiopathic
hemolytic anemia. What happens here is that red blood cells actually get sheared as they go across the really tight valve, and so the cells are actually broken apart and you can get an anemia that shows red blood cells that have
kind of been broken apart, and that’s due to the aortic stenosis. Finally, you get a
systolic ejection murmur on auscultation, and this
systolic ejection murmur is best heard in the aortic area, or the right upper sternal border, and that may or may not
have an ejection sound as the valve pops open. So, to explain the angina real quick, angina is basically chest
pain that is related to ischemia, or lack of oxygen. There are kind of two
good reasons why you get angina in someone who has aortic stenosis. Someone may have pre-existing
coronary artery disease or they may have left
ventricular hypertrophy. With coronary artery disease,
we’ll draw an artery here, or a coronary artery, one of the arteries that supplies the heart. Here in this orange we’ll draw a plaque that’s kind of pushing into the lumen, or the inside of the artery,
where the blood flows. If we say that this plaque is occluding, or blocking, 65% of the artery, when someone has aortic stenosis and can’t get enough blood out, this blockage that is actually 65% may feel like a 75% blockage and cause chest pain to become apparent or cause more chest pain. In someone with left
ventricular hypertrophy, this is when the heart
becomes more muscular, and so you have increased muscle mass and you have an increased
oxygen demand from the tissue. If you have an increased oxygen demand and you can’t meet that demand because you have aortic stenosis, you can get chest pain. Now, let’s talk about the
opposite of aortic stenosis, and that’ll be aortic regurgitation. What you can see here is I’ve
labeled the aorta for you and the left ventricle,
and what the arrow’s pointing to is actually
regurgitation of blood flow. You can see that part
of the valve is actually kind of just flopping there from all this blood coming
back into the left ventricle. That’s aortic regurgitation. This is kind of a floppy aortic valve. Here we’ll label the
LV, the left ventricle, the LA, the left atrium, the aorta, and you’ll see that
normally the blood goes out of the aorta into the rest of the body like we showed before. But in the case of aortic regurgitation, when the heart is supposed to be relaxing and filling with blood from the atrium, the blood can actually come back through the aortic valve and
into the left ventricle, when really that valve should be shut and not letting any blood back. So the flow of blood would be normally from the left atrium
to the left ventricle, and then out of the
aortic valve to the aorta and to the rest of the body. But here, blood is actually coming back from the aorta into the left ventricle through the regurgitant aortic valve. Let’s talk about some causes
of aortic regurgitation. One way that this occurs is when you get a widening, or aneurysmal change. An aneurysm is really just a ballooning or an out-pouching of a vessel, so widening or aneurysmal
change of the aortic annulus. The annulus is really just
a ring of fibrous tissue that surrounds the aortic valve. Any time that becomes widened, the valve area becomes widened and the valve can’t close as well. This happens in conditions such as tertiary syphilis, or some of the connective tissue disorders such as Marfan Syndrome
and ‎Ehlers-Danlos, which are both disorders
relating to collagen, which is a connective
tissue protein in the body used for structural
support of blood vessels and other things. Another reason that this can occur, aortic regurgitation, is due to endocarditis. You can get an infection of the valve that can lead to the
formation of a vegetation and this big ball of
platelets and bacteria that can actually stop a valve
from closing effectively. Finally, rheumatic fever. As we’ve already seen, rheumatic fever normally affects the mitral valve, but it can easily affect
the aortic valve as well. Let’s talk about some signs and symptoms of aortic regurgitation. Patients may experience fatigue. This is because all the blood that’s being pumped out to the aorta is
not exactly staying there. Some of it may come back into the heart. They may have syncope for similar reasons. Shortness of breath and palpitations. Other things that you may want to look for on physical exam or when
you take a blood pressure would be something called
wide pulse pressure. The pulse pressure, let me
just define that for you. The pulse pressure is
the difference between the systolic blood pressure, SBP, and the diastolic blood pressure, DBP. Let’s go ahead and draw this for a second. Here you’re going to see the aorta, and then we’ll make the valve, an open valve, an open
aortic valve, in white. When blood comes through,
this is at a systolic pressure of 120 millimeters of mercury. That’s the blood getting
ejected from the heart. Now, when the heart goes to relax and the valve closes as a result of the elastic recoil of the aorta against a closed valve, the pressure in the system actually stays pretty high, around 80 millimeters of mercury. A normal systolic over
diastolic blood pressure would be something like
120 millimeters of mercury over 80 millimeters of mercury. If this aortic valve was regurgitant, and a lot of blood backed through, you wouldn’t be able to maintain that normal pressure of about 80, which is due to the elasticity and recoil of the aorta on a closed aortic valve, but now you would have
something like about 50, because that blood would be flowing back through that aortic valve. In addition, because more blood is flowing back into the left ventricle, this actually increases
what’s called the pre-load, or how much blood that
ventricle is filled with. Then due to something
called Frank–Starling’s law, or Frank–Starling’s curve, if you have increased pre-load, the heart actually contracts harder and better to put out all of that blood that it’s receiving, and so
that systolic blood pressure will actually increase. So if you have an increase in pre-load, you’re no longer going to have that 120 millimeters of mercury, but now maybe 140 millimeters of mercury. So you went from a pressure of, let’s say, 120/80 to about 140/50, which is going to increase your pulse pressure. Another thing that you may
notice on physical exam is left ventricular dilatation, and this can be recognized through a couple of different things. You can see this on echocardiography or you can have an S3,
an extra heart sound, which signifies volume overload. The blood is getting too much volume back from the aorta when
it’s not supposed to. This may also displace the
point of maximal impulse. When we talked about left
ventricular hypertrophy earlier, the PMI would
actually move medially towards the sternum, but in a case where the heart is volume overloaded, it will actually move laterally, and possibly inferiorly. An aortic regurgitation can be heard on auscultation as an
early diastolic murmur along the left sternal border.