If you're seeing this message, it means we're having trouble loading external resources on our website.

If you're behind a web filter, please make sure that the domains *.kastatic.org and *.kasandbox.org are unblocked.

Main content
Current time:0:00Total duration:12:07

Video transcript

so here actually see the LV or left ventricle contracting it to the aorta and the red arrow is looking at the aortic valve which is actually not opening very much if you can see that and so this is a or text enosis so what is aortic stenosis well very basically it's having a tight a ordered valve so not enough blood can get through and so you'll see our label here the LV the left ventricle and then I'll label the aorta here and 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 a or text enosis then you're going to have blood backed up in the left ventricle and you're going to have problems perfusing or supplying enough blood and enough oxygen to the rest of the body's tissues so let's talk about some of the major causes of aortic stenosis so the first thing we want to talk about is having a bicuspid aortic valve now this is a congenital condition meaning you're born with it and this means that you only have two cusps to the aortic valve so let's demonstrate this here normally the aortic valve has three cusps so 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 now the reason why a bicuspid aortic valve is more likely to get a or text enosis or is more likely to become stenotic is because you actually have two cusps doing the work of three and so these valves these bicuspid valves actually get damaged quicker and can become calcified over time and are thus more likely to become sonata and more likely to do so at an earlier age and then another cause of aortic stenosis is age-related calcification so 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 now 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 now another cause of aortic stenosis could be rheumatic fever now 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 so the way that you can remember the signs and symptoms of aortic stenosis is with the acronym sad and S stands for syncope meaning fainting a stands for angina which is a type of chest pain and dyspnea meaning shortness of breath so other things that you can look for are things like pulses parvis at tardis now this sounds kind of funny and kind of weird but all it means is that you have a small or weak pulse Parviz meaning small and TARDIS meaning like tardy slow so it's a smaller 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 so another thing that may occur is LVH or left ventricular hypertrophy and what you can do on physical exam is you can actually palpate what's called the PMI or the point of maximal impulse and 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 auscultate in or listening with a stethoscope and 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 Erikson OSIS is maja or micro angio Pathak hemolytic anemia and 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 and 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 engine in real quick angina is basically chest pain that is related to ischemia or lack of oxygen and so there are kind of two good reasons why you get angina in someone who has a or texts enosis so someone may have pre-existing coronary artery disease or they may have left ventricular hypertrophy so with coronary artery disease we'll draw an artery here or AB coronary artery one of the arteries that supplies the heart and here in this orange will draw a plaque that's kind of pushing into the lumen or the inside of the artery where the blood flows so if we say that this plaque is occluding or blocking 65% of the artery when someone has a auric 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 now 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 and so if you have an increased oxygen demand and you can't meet that demand because you have a or text enosis you can get chest pain so now let's talk about the opposite of aortic stenosis and that'll be a or decree Gurjit ation so what you can see here is I've labeled the aorta for you and the left ventricle and what the arrows pointing to is actually regurgitation of blood flow and 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 and so that's a or decree rotation and so this is kind of a floppy a or take valve so here we'll label the LV the left ventricle the la2 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 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 a or take valve so let's talk about some causes of aortic regurgitation so one way that this occurs is when you get a widening or aneurysmal change in an aneurysm is really just a ballooning or an outpouching of a vessel so widening widening or aneurysmal change of the aortic annulus and the annulus is really just a ring of fibrous tissue that surrounds the aortic valve so anytime that becomes widened the valve area becomes widened and the valve can't close as well so 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 so another reason that this can occur a auric regurgitation is due to endocarditis so 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 the valve from closing effectively and finally rheumatic fever and as we've already seen rheumatic fever normally affects the mitral valve but it can easily affect the aortic valve as well so let's talk about some signs and symptoms of aortic regurgitation so patients may experience fatigue and 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 and so the pulse pressure let me just define that for you the pulse pressure is the difference between the systolic blood pressure SVP and the diastolic blood pressure DBP so let's go ahead and draw this for a second and here you're going to see the aorta and then we'll make the valve an open valve and open aortic valve in white and 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 into a normal systolic over diastolic blood pressure would be something like 120 millimeters of mercury over 80 millimeters of mercury so now if this a or DIC valve was regurgitant and allowed blood back 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 and in addition because more blood is flowing back into the left ventricle this actually increases what's called the preload or how much blood that ventricle is filled with and then due to something called frank starlings law or frank starlings curve if you have increased preload 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 preload you're no longer to have that 120 millimeters of mercury but now maybe about 140 millimeters of mercury so you went from a pressure of let's say 120 over 80 to about 140 over 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 different things you can see this on echocardiography or you can have an s3 an extra heart sound which signifies volume overloaded the blood is getting too much volume back from the aorta when it's not supposed to and this may also displace the point of maximal impulse so 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'll actually move laterally and possibly inferiorly an aortic regurgitation can be heard on auscultation as an early diastolic murmur along the left sternal border you