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0:07
what's up ninja nerds in this video today we are going to be talking about mitral valve disease that includes mitral valve stenosis and mitral valve regurgitation before we get started if you guys like this video you benefit from it it helps you it makes sense please support us by hitting that like button commenting down the comment section and most importantly subscribing also down in the description box we have a link to our website where you guys can check out some awesome notes some
0:28
amazing illustrations to follow along with during this video so go check those out without further ado let's get right into it and start talking about mitral valve disease so basic definition of mitral valve disease there's mitral valve stenosis when we talk about mitral valve stenosis what's the issue with this okay basic terminology not using too much words and verbage it's simple whenever you have someone who has mitral stenosis the primary issue with these is that the
0:52
valve the mitral valve so the mitral valve is the valve that's usually separating between the left atrium and the left ventricle this valve it's really really fibrotic it's really really stenotic it's very calcified and when it's like that it reduces or slows or affects the flow going from the left atrium into the left ventricle so the big thing that i want you guys to remember in mitral stenosis in patients who have mitral stenosis the primary issue is you have a fibrotic
1:27
or some type of calcified valve and that calcified valve the issue with that valve is it does not allow for a good flow from the left atrium to the left ventricle this is hindered in that process we have to think about what causes this valve to become fibrotic and calcified and then what's the problematic issue that occurs whenever you aren't able to get enough blood flow from the left atrium into the left ventricle that's what we gotta talk about so we'll do that in a second
1:58
before we do that though we also should talk about mitral regurgitation and compare and contrast it in mitral regurgitation the problem is again the mitral valve but you see these valves here their problem is they have a poor seal they're not good at actually coming together coacting together so whenever the ventricles go through their particular cardiac cycle and contract and relax you know whenever they contract the left ventricle goes into a period of contraction it should want to
2:25
do what so here's your left ventricle here's your left atrium you want to push blood from your left ventricle out into the aorta that's the goal you don't want blood to go back into the left atrium so when the ventricles are going through systole they actually push blood in this disease from the left ventricle back up into the left atrium and so that's important to remember so in this disease mitral regurgitation the issue is you have a poor seal between the actual mitral valve
2:55
and this causes a backflow this will cause a backflow from the left ventricle to the left atrium so the question that we have to ask ourselves is what causes this pore sealed valve and then what are the issues that we run into whenever there's a back flow of blood from the left ventricle into the left atrium the last thing that we want to talk about is when are these problematic issues occurring so mitral stenosis mitral regurgitation in their cardiac cycle when would this problematic issue be
3:26
occurring would it be occurring when the ventricles are relaxing and getting filled with blood during diastole or is it occurring during systole when they're contracting and ejecting blood out so in this case think about the problem mitral stenosis is problematic flow from left atrium to left ventricle that means blood are going into the ventricles so this issue would be a diastolic problem so this issue that you would see in this disease is a problem with that's
3:49
occurring during diastole whereas in this situation the left ventricle is supposed to be contracting and ejecting blood out through the aorta but blood goes back into the left atrium so this is occurring during systole so that is another important differentiating factor for the basic definition all right my friends we've covered the basic definition we've talked about what's the problem we talked about what can lead to these issues particularly the left atrium to
4:18
left ventricle flow is slow during diastole and during regurgitation there's backflow from the left ventricle and the left atrium the next thing we got to talk about is what causes this fibrosis and calcifications of the valve and then what causes the poor seal that you see associated with these diseases so first thing up mitral stenosis what causes this dangled mitral valve to be super fibrotic sclerotic calcified in some way i'm glad you asked because you know what
4:46
the most common kind of condition that you'll see here you know there's a condition in which your body um you have like a strep infection you know streptococcus infections like particularly group a streptococcus beta-hemolyticus type of bacteria in those situations you produce antibodies against the bacteria but sometimes people produce antibodies not against the bacteria only but they produce bacteria against tissues in their body and some of those tissues tend to be the valves of the heart
5:12
this condition that you see is called rheumatic heart disease so in rheumatic heart disease you develop auto antibodies that cause attack and actually cause inflammation of these mitral valves and all that inflammation over time causes fibrous deposition on the valves that causes them to become very stiff and not wanting to open and allow for blood to easily flow from the left atrium to left ventricle that's one cause now interesting thing with rheumatic heart disease is that you
5:40
see this not only with mitral valve stenosis you may see this with mitral valve regurgitation and you can also see this with aortic stenosis and aortic regurgitation so sometimes you see this involving not just the mitral valve but also the aortic valve and it can cause both stenosis and sometimes regurgitation in the severe stages all right beautiful so we have rheumatic heart diseases one of the particular causes for that sclerotic fibrotic valve what's the second one the
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second one is also really interesting so you know in patients who are really really old so you have some elderly patients in elderly patients they have high risk you know they just have lots of issues where they can cause lots of calcium deposition into particular vessels and and other tissues and so they get lots of calcium deposition so lots of calcium the depth deposits into the actual cardiac valves particularly the mitral valve you know another condition in patients who have end-stage renal
6:38
disease in these situations they develop something called secondary hyperparathyroidism you know a pyrothyroid hormone what does it do it increases your calcium levels in the blood and if you increase calcium levels in the blood you again can increase the deposition onto these valves so if you cause lots of calcium to deposit onto these valves you make them very stiff you make them very less pliable and they're not good at allowing for blood to move easily from the left atrium into the left
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ventricle because these valves just don't want to let it go that way all right so that's a particular reason right so it's some type of calcifications and this calcifications that you can see in these patients are particularly in high risk in patients who are elderly or in-stage renal disease patients okay one more particular cause to be thinking about this one's not super common but it can happen there's a condition called carcinoid syndrome particularly in carcinoid syndrome you see this more
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likely to involve the tricuspid valve more than the mitral valve however it's possible so you know carcinoid syndrome generally there's a cancer there's generally some type of tumor that forms usually within the gastrointestinal tract first so usually what happens is you get some type of tumor within the gastrointestinal tract and that tumor may spread to the liver and then from the liver it may go to the right heart and from the right heart it may spread into the lungs and cause some
8:01
actual tumor to deposit within the lungs either way what's the problem with either of these tumors whether it be in the gi tract or in the lungs the problem with these tumors is they release a lot of something called serotonin so one of the things that they release is they release something called 5-hydroxytryptomy lots of serotonin and that serotonin loves to deposit cause fibrosis it causes a fibrotic reaction on the mitral valve and if it causes it to become fibrotic it reduces the normal
8:30
flow from the left atrium into left ventricle because the valves don't want to open as well and they don't want to allow for blood to flow easily in this direction so that's another particular reason carcinoid syndrome and again this is usually due to neoplastic cells that are releasing 5-hydroxytryptamine and this is causing fibrosis okay beautiful so the three particular causes that i want you guys to remember from mitral stenosis is rheumatic heart disease but just big thing to remember
9:00
is you can see this in mitral valve disease and aortic valve disease second one is calcifications and third one is carcinoid syndrome but don't forget these two let's talk about mitral regurgitation now come down here all right so mitral regurgitation in this condition again we know that there's a poor seal what is causing that poor seal what's not leading to the valves nicely coapting together because when the ventricles contract the pressure should rise in the ventricle
9:27
enough that it's higher than the pressure in the atria and the valve its purpose its literal function is to snap shut and prevent backflow into the left atrium it's not doing that why we gotta think about the anatomy of the actual mitral valve the apparatus itself there's three primary components of it one there's actually four components of it we'll talk about that that fourth component over here but there's the annulus ring okay so there's the annulus ring which is this black ring right here
9:54
and then off of that actual ring is your leaflets and then off of the leaflets there's these little cords that are made up of collagen and other types of connective tissue called chordae tendineae and then the chordae tendineae are connected to these little muscles that are extensions of the myocardium that hold on to the little chordae tendon and pull them tight to keep the valve leaflets close to one another those are called the papillary muscles so there's technically four components
10:24
of the actual mitral valve apparatus that is the annulus the leaflets the chordae tendineae and the papillary muscles if there's some disease process that is affecting one of those four structures that can definitely lead to mitral regurgitation because it's going to cause a poor seal we're affecting that valve apparatus let's talk about those things now primary mitral regurgitation is usually going to be conditions that cause an effect of the leaflets the chordae tendineae or the papillary
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muscles usually so what are some things that can actually cause destruction or issues with the leaflets you know there's a one condition which you definitely don't want to forget you know there's these nasty like bacteria sometimes that can actually accumulate on the valve and they can release nasty like types of destructive molecules and lead to the actual destruction of these valves and if i erode these valves away do you think that this is going to be easy now you have a little nub of a
11:20
valve and when these are supposed to come together during ventricular systole is that going to be good at being able to block the flow up into the left atrium when the left ventricle contracts no because now i got a nub and i got a long valve leaflet so that's one of the issues what is that disease process where you cause destruction of the leaflet due to bacterial infections this is called infective endocarditis so anytime someone has infective endocarditis this is a very severe cause
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and can lead to very destructive lesions of that valve and cause acute mitral regurgitation which is disastrous sometimes another thing that damages the valves now this is remember i was talking about rheumatic heart disease it's a weird one where it can cause both stenosis and regurgitation here's what happens so when rheumatic heart disease right you can also destroy those leaflets now it's a weird way that it does it if you kind of imagine here that we have
12:19
these valves let's imagine here we have the annulus so here's our annulus for the rheumatic heart disease example here's our annulus right there right and then off of that annulus ring is your leaflets and for the mitral there's the anterior leaflet and then the posterior leaflet now generally these should kind of come together nicely and coax together right and generally block blood flow from going into the left atrium during ventricular systole when you get a lot of inflammation
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and fibrosis of these valves okay what starts happening is yes you kind of really cause them to become stiff and narrow and they don't allow you to easily open up the valves to push blood down that's that's definitely one issue this can be affected but if these valves are super stiff and super not pliable and they just don't want to move because they're super fibrotic when you push blood it's supposed to cause this and this to coap together but if they're super stiff and not
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pliable and you try to push blood against these and snap them shut they may not snap shut instead they'll run through that little space that's still open because the valve leaflets just don't want to touch one another because they're so stiff and so non-pliable when you hit them they're supposed to close but you hit them and they just kind of still stay open so it creates a little orifice for blood to jet into the left atrium and that can happen with rheumatic heart disease particularly on
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the severe stages of them so that's things that you definitely want to think about that involve the leaflets there's another condition it's generally believed to be like you know familial or sporadic and there's lots of deposition like lots of actual kind of like what's called proliferation of parts of the actual leaflet it makes it kind of like easy to bow and bend and this is called mitral valve prolapse so this is actually due to what's called mixomatus proliferation of
14:12
what's called the zona spongiosa which is kind of like this inner tissue inside of the valve leaflet it becomes really really floppy and it becomes really easy to bow and that creates an opportunity if it's bowing like you actually are supposed to be like this and it's bowing now you create a little space for the blood to actually regurgitate right back into the left atrium and so that's one particular condition to think about okay now what about the chordae tendonity
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what can cause some issues with these so imagine that the chordae tendon are not very good at their job they're supposed to anchor those leaflets and pull the valve leaflets closer together now if for some reason the chordae tendineae have some issue where they aren't able to pull down tautly on those leaflets and keep them close together and they're loose for some reason there's some issue with them then now this could potentially hang and that could allow for an opening for blood to
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regurgitate back in what are diseases that could damage the chordae tendineae you know these are particularly connective tissue diseases you know you can see this in mitral valve prolapse but these particular conditions that you want to be aware of is something called marfan syndrome or you know what else ehlers-danlos syndrome and then sometimes there's another condition called osteogenesis imperfecta but these are the big ones that i want you guys to think about so there could be some type
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of connective tissue diseases that are causing weakening of these chordae tendonitis they're not as strong they're not able to generate a nice tautness of that leaflet and they don't give you a good seal what else okay not only could it be the problem with the lethal it's not only going to be a problem with the chordae tendineae but there's something wrong with the papillary muscles my friends what could that be due to you know good old papillary muscles sometimes
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in patients who develop really nasty myocardial infarctions so you know if someone develops a really nasty myocardial infarction particularly these tend to affect more of like the posterior leaflet than anything but if you get like a myocardial infarction and the particular territories that you'd want to be worried about is if someone had like what's called a posterior mi that could be one or because that usually affects the posterior leaflet or if they have an inferior mi
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those sometimes can also give you destruction of the papillary muscles that anchor the the posterior leaflet but either way you get a myocardial infarction and that causes some destruction of this portion right here okay let's say you get some destruction of the papillary muscles that are in the posterior portion you infarct these areas the myocardium and the nearby papillary muscles if they're infarcted are they able to pull down on the chordae tendon and keep them taut no if
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they're not pulling on the cortex can they keep the leaflets nice and coapted together properly no and so now it opens up an opportunity to blood flow to regurgitate right back into the left atrium so again in a patient who has an mi this can cause the papillary muscles to potentially rupture so an mi may cause papillary rupture and this is a big thing to think about you want to know why there's two particular conditions that can cause acute mitral regurgitation
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which is a hemodynamic emergency it can be cardiovascular emergency infective endocarditis is a really really scary one and a papillary rupture is another particular scary one these can cause acute mitral regurg sometimes dramatic heart disease if you get a really bad acute attack it can as well but these other ones like mitral valve prolapse some of these connective tissue diseases they're rarely going to be leading into any kind of like acute mitral regurgitation they're more likely going
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to be a chronic issue okay the secondary mitral regurgitation so this comes back to the annulus so there's a disease process that's causing stretching so you know here's your annulus right this is one of the components this is your annulus ring and this is one of the components of the valve apparatus so the annulus ring you know it's really interesting because it obviously holds onto the leaflets and then from the leaflets you obviously have to remember that these are
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connected to the chordae tendineae and then from the chordae tendineae these are connected to your papillary muscles so we we know all of these things at this point what happens is imagine a patient has a disease process that stretches the annulus ring and if you stretch the annulus ring you pull the leaflets that are anchored to it farther away from one another and if these are farther away from another you lose a good seal you're not able to get those valve flaps close together
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that can create a regurgitation what are conditions that cause the annulus ring to be stretched anything that causes the dilation of the left ventricle so something that's causing dilation of the left ventricle what could that be due to my friends so things that would cause anes ring to stretch so we'll say this is usually due to the annulus ring and the problem is that we are increasing the stretch this would be conditions that cause left ventricular dilation so this is due to left ventricular
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dilation okay what could that be due to what are some things that cause left ventricular dilation so first things first is if someone has aortic regurgitation that can cause blood to actually get larger volumes inside of this actual left ventricle and that can cause it to distend to get bigger to accommodate those volumes so one particular reason could be aortic regurgitation a second one is you develop what's called dilated cardiomyopathy and there's many different reasons for
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this but the actual ventricles become damaged and they undergo a modeling process where they get thinner and the ventricles get larger to accommodate larger volumes it could also be due to some type of systolic heart failure of some kind in these situations these are very common reasons for someone to have left ventricular dilation and so think about that because this is a secondary cause of their mitral regurg and again secondary causes of mitral regards are
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unlikely to produce an acute type of my triggers these are going to fall in the category of more of a chronic there's one more type of mitral regurgitation that is secondary because it's not due to any of the leaflets none of the chordae tendineae not the papillary muscles not even the annulus ring this one's an interesting one you know there's a condition called hypertrophic obstructive cardiomyopathy and hypertrophic obstructive cardiomyopathy their problem is that they have this very
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hypertrophic septum and when blood is actually supposed to be squeezed and run through this area it's very narrow and it creates something called the venturi effect and that yanks this anterior leaflet of the mitral valve towards that left ventricular alpha tract it obstructs it and so then you can't get blood out through that way but it also if you pull this valve leaflet this way what are you doing you're creating space between the posterior leaflet and the anterior
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leaflet guess where the blood can go right back into the left atrium this is a very interesting type of mitral regurgitation this is a mitral regurgitation that is secondary to due to something called systolic anterior motion of the mitral valve so remember this is another type of thing that you can see what's called hypertrophic obstructive cardiomyopathy it's not due to a problem with the leaflet not due to a problem with the chordae tendon and not due to the problem with the papillary muscles
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it's not due to stretching of the annulus ring it's due to a weird type of yanking of that anterior leaflet in the mitral valve during systole in this condition so we've covered the causes we've covered the definition of mitral stenosis and mitral regurg let's now talk about why is this a problem to have little flow going from the left atrium to the left ventricle and mitral stenosis and then let's talk about what's the problem with having backflow from the left ventricle into the left
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atrium and mitral regurgitation all right so let's talk a little bit about mitral stenosis particularly the pathophysiology and how that leads to the clinical features their physical exam findings so mitral stenosis so let's say here we have a normal kind of like opening of the mitral valve right so here's the two leaflets of your mitral valve you have like your posterior leaflet and your anterior leaflet and then here's the the opening or the orifice by which blood is
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supposed to move through so imagine like if i had blood coming it was coming this way whoop and then out that way right nice little orifice there that's a normal type of mitral valve so this would be kind of fitting within your normal type of mitral valve and then one of the ways we look at this is we look at like what's called the mitral valve surface area right so we look at what's called the mitral valve surface area which normally you know it's somewhere between like
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four to six centimeters squared that's about how large the orifice should be and a patient who starts to have something called mitral stenosis now look look at the blood that you're trying to squeeze through that tiny little area there that's going to be a very small orifice and so the mitral valve surface area in this patient who has mitral stenosis they're going to have a very narrow area and what happens is their mitral valve surface area starts dropping below this
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point particularly when it starts to become diseased it's at least less than two centimeters squared and that's enough to start really reducing the blood flow from the left atrium into the left ventricle so you see the whole process here is that this valve becomes so fibrotic so calcified and stenotic in a way that it reduces a lot of flow because you're narrowing the space of the mitral valve orifice now how does that look like here's what i want you to think imagine you have an issue here
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where in this patient you have less blood that's able to get from the left atrium into the left ventricle right so if that's the case you're not filling the left ventricle appropriately with the volume that you want to during diastole when the ventricles are supposed to be getting their blood so if that's the case this causes a low left ventricular in diastolic volume right the amount of volume that's in the left ventricle when it's relaxing before it actually pumps blood out if that's
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the case then that's called what the volume of blood is in the heart that potentially can affect stroke volume that's called preload so there's a reduction in the preload and if you drop your preload you drop your stroke volume if you drop your stroke volume you drop your cardiac output what's the issue with this this can cause forward heart failure problems so if you get less blood that's filling into the actual left ventricle you're going to potentially drop the amount of blood
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that you want to go out into the systemic circulation and that's problematic because some of the ways that this could potentially present is this may present in a patient who may have something like hypotension right and if they're hypotensive and they're not able to perfuse particular organs they may have like cool and clammy types of extremities right and that may be one particular sign and they also may have potential if you're not able to get enough blood flow out of the actual heart
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that also could lead to other particular manifestations many many different things but these are things that we would want to think about right so this is a very nasty kind of situation and this may present similar to kind of like a problem of a heart failure type of presentation we're not able to get blood out of the heart because actually not not a problem getting blood out of the heart we just don't have enough volume that's coming into the left ventricle
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because of the stenotic valve so i'm not actually pumping enough volume out the left ventricle is probably good enough not having any issues it's just i'm not getting the volume that i'm supposed to be getting from the left atrium so that becomes an issue potentially all right what's the other issue that kind of goes along with this forward heart failure so they may present with some hypotension they may have some cool clammy types of extremities due to this reduction in diastolic volume but the
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other issue here is think about this if the left ventricle is not getting a lot of blood filled into it right so there's supposed to be blood coming from the left atrium into the left ventricle supposed to go this way now if it's not getting it's not able to do this process blood will start accumulating in the left atrium right so blood will start accumulating into the left atrium so there'll be a high blood volume
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and whenever the left atrium has a lot of volume and it can't actually expand or distend to accommodate that volume the pressure in the left atrium will also start to go up so it'll be a high blood volume and they'll also be a high pressure in the left atrium the problem with that is that if there's all of this volume that's accumulating within the left atrium what it's going to do is it's going to start causing a backflow and when it starts backflowing it backflows into the nearest vessels
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and this is your pulmonary vessels particularly the pulmonary veins and it'll backflow into the pulmonary veins and then eventually into the pulmonary capillaries and when it does that it actually starts third spacing into the tissue layers between the actual alveoli and the pulmonary capillaries and this can lead to pulmonary edema so the clinical presentation of this is they may have pulmonary edema and this may present with things like dyspnea that may be on exertion so
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whenever they're having some shortness of breath walking because they're not getting enough oxygenation across the lungs they may have something called peroxismal nocturnal dyspnea where they get short of breath when they're laying down flat because their actual hypoxia can worsen or they may have something like orthopnea where their difficulty breathing can occur when they're laying flat so a lot of these things could be potential clinical features here so
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these are something else to remember for these patients you know what else because this volume and pressure's so high it can cause a lot of backflow a lot of backflow enough that it can congest some blood vessels in the lungs to the point where the pressure in those blood vessels increase and actually cause them to rupture if they rupture because they're holding onto too much volume that can cause blood to actually enter into the airway and that's to cough that up what's that called hemoptysis
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so this can lead to hemoptysis so these are also particular findings that you can see in these patients from a lot of pulmonary venous congestion so because of the problem with getting blood into the left ventricle we dropped their stroke volume because we dropped their preload that can cause them to maybe have some hypotension some cool clammy poor perfused extremities if they're not getting blood from the left atrium with the left ventricle it's accumulating there the pressure is
29:22
increasing it's going to backflow into the pulmonary venous circulation and cause pulmonary edema cause some congestion of some of the blood vessels in the lungs to the point where they may rupture and cause hemoptysis what else can potentially happen they can develop right heart failure particular symptoms why let's come down and talk about that you're causing some issues here where again the problem is that you weren't able to get blood from the left atrium into the left ventricle right
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and so the problematic issue here is that the blood accumulates the blood volume accumulates the blood pressure accumulates with inside of the left atrium and it causes backflow and it back flows into your pulmonary veins now here's the thing when it backflows into the pulmonary veins it backflows into the pulmonary capillaries and into the pulmonary arteries and so then the blood pressure and the pulmonary arteries will start to go up imagine the pressure here in these
30:15
pulmonary vessels being higher so now imagine i'm going to put here their pulmonary artery pressures are higher because of this backflow from the pulmonary venous circulation because of a back flow from the left atrium because that valve isn't letting blood get through if the pulmonary artery as pressure is higher that means that this poor old right ventricle which is pumping blood into the pulmonary arteries is going to have to work harder it's going to have to do some steroids
30:44
and get all kinds of jacked up to be able to push blood out of the right ventricle into that high pulmonary artery system so because again you get a back flow into the pulmonary veins that increases the pulmonary artery pressure and that increases the right ventricular strain and so now the right ventricle has to start working harder to actually push against this high pressure so what does it do guess what the right ventricle gets ready to go get steroided up and so
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it undergoes something called right ventricular hypertrophy so when it actually causes the strain what's really happening is it's causing right ventricular hypertrophy to thicken up to push blood against that over time though this can lead to failure right because now if you're causing this ventricle to have to work harder you're narrowing this lumen you're not able to fill the right ventricle pop properly and if you can't get blood into this right ventricle as well because now the
31:46
sucker is huge then blood's going to start backing up into your superior vena cave and inferior vena cava and so because of that you may start getting failure symptoms and they'll start actually backing up into the supreme cave and inferior vena cava so if it backs up into the superior vena cava what could be some particular issues with that well it'll back up into your jugular veins and cause those puppies to get all puffed up and so it may cause something like jugular venous distension if it
32:14
backs up into the ivc it may cause some swelling or accumulation of fluid around the liver and around the spleen the patio swinomegaly may accumulate in the parasitic cavity ascites made third space into the tissues of the lower extremities pedal edema so these may be findings you may see something called hepato splenomegaly
32:39
you may see something called ascites and you may see something called pedal edema and the whole purpose to understand this is that it was left-sided heart failure that led to right-sided heart failure and what caused the left-sided heart failure that dang old stenotic mitral valve not letting blood get into the left ventricle and then it's just gonna back up okay symbol all right so we're gonna talk about left atrial dilation but again make sure that you understand the
33:08
problems was you have forward heart failure you have problems going into the left ventricle blood flow getting into the left ventricle so we're not getting enough out that's causing that forward heart failure also the blood isn't getting from the left atrium into the left ventricle so it's back flowing it's causing the venous vessels in the pulmonary system to get congested causing edema potentially hemoptysis and that congestion in the pulmonary circulation can cause the pulmonary
33:32
artery pressures to go up so high it can lead to right-sided heart failure now here's the last thing to think about we talked about because the blood flow going from the left atrium into the left ventricle is halted right it's reduced because of these stenotic valves the blood volume and what else the pressure inside of this left atrium increases whenever there's high volume generally whenever there's higher volume states inside of the left atrium what it'll do in the left atrium what
34:07
the left atrium will try to do is it'll actually undergo a process called dilation to accommodate that volume so it'll cause left atrial dilation now here's the issue the left atrium is a big son of a gun okay so it's a big son of a gun a couple different things can happen it may cause compression symptoms so compress on things nearby and we'll talk about what are those things and what things we should be thinking about the other thing is is it stretches the electrical circuit so you
34:39
know when you stretch out the left atrium now you're having problems sending electrical activity because then you have your sa node then you got your av node bundled branches what happens is when you stretch out this left atrium it creates an opportunity for electrical kind of like circuits to develop and generate increasing types of atrial arrhythmias so they're also at risk for a very significant atrial arrhythmia you know what that's called atrial fibrillation
35:04
so now they're at risk for what's called atrial fibrillation what's the problem with these two things well compression wise there is the esophagus nearby so if the esophagus which is running right behind us is getting compressed by that big old left atrium it may cause dysphagia so there may be dysphagia and that is due to the esophageal compression right so this could be due to esophageal compression the other thing is it may compress on other nearby structures uh
35:39
you know there's a nerve right near this area there's a nerve that kind of comes underneath the aorta the recurrent laryngeal nerve sometimes it's big enough to actually compress onto that and that may cause hoarseness of the patient's voice so it may not only cause so another thing is compression it can cause dysphagia and the other thing is if it causes something called hoarseness and this may be due to the recurrent laryngeal nerve being compressed okay so we got that idea down the next thing
36:10
is the afib what's the problem with afib well now here's the thing you got this big old left atrium you obviously can cause electrical alterations and lead increase the risk of afib obviously the worry with afib is that you increase the risk of emboli you increase the risk of emboli you're not getting effective atrial contractions and so blood can kind of stay within this area and like here let's do it in black it can cause clots to form right it can cause clots to form
36:39
here in the left atrium which is going to increase the risk of that popping off and if that pops off and goes into the systemic circulation it can go up into the brain and lead to an embolic stroke that's one particular thing the other thing is that look at this is blood getting from the left atrium into left ventricle because of the stenotic valve no so another particular issue here is not only do you have an increased risk of atrial fibrillation causing the emboli
37:03
but you know what else increases the emboli another problem with this is just the stasis of blood flow due to the stenotic valve not letting blood go from the left atrium to left ventricle so more blood stays within the left atrium that is another particular problem so again afib increased risk of emboli so you can get strokes splenic infarcts renal infarcts mesenteric ischemia tons of complications but these are the things to think about so now that we've covered mitral stenosis their
37:34
clinical features their physical exam findings now what i want to do is i want to move on and talk about mitral regurgitation it's pathophys it's clinical findings it's physical exam findings all right so with mitral regurgitation we got to think about again the issue is blood is going back from the left ventricle into the left atrium right and there's something that's not forming a good seal so again in this situation here just to compare here's our normal mitral valve
37:56
so this mitral valve we got blood in this issue you know this situation we want blood to again naturally do what naturally whenever the actual ventricles go into systole these leaflets will come close together and when they come close together their job is to come close together enough that they don't allow for blood to go back into the left atrium so this should be the normal situation there should be no regurgitation of blood back into the left atrium so this would be the normal scenario
38:30
okay so there should be no regurge jet that's flying back into the left atrium and someone who's got mitral regurgitation they got this big old gaping hole here due to the valve leaflets not actually having a good connection or sealed between one another so when the left ventricle contracts and pushes blood as supposed to go into the aorta it'll just move through this area here and then jet back into the left atrium so this would be a patient who has mitral regurgitation because they're having a
39:06
a jet going from the left ventricle into the left atrium during systole so that's the problem is we have a large kind of opening here now here's the thing here's what you want to think about and a patient who has mitral regurgitation they can develop it acutely and again when i talk about acutely what were the two scenarios that i wanted you guys to remember one was infective endocarditis and the second one was an mi so they had papillary muscle rupture these were the two particular
39:35
indications sometimes acute rheumatic heart disease like rheumatic fever you may also develop this acute type of mitral rig urge this is very nasty condition here's why in mitral regurgitation imagine your left ventricle right it wants to contract and its job is to push blood into the aorta right and then obviously onto your systemic circulation inadvertently due to this valve issue these suckers ain't working blood will go back into the left atrium during systole so it'll go in these two
40:07
directions so blood is supposed to go where left ventricle into the aorta but let's say that just to give a number let's say 75 of that blood went out into the aorta and let's say 25 of that blood went back into the left atrium okay that means that the amount of blood that you're getting out of the heart is reduced so we can say that in this patient here they have a reduction in their left ventricular stroke volume because some of the blood is being regurged back into the left atrium
40:42
if there's a reduction in their left ventricular stroke volume there is a reduction in their left ventricular cardiac output and this can lead to hypotension to the point where it can actually be in a shock kind of state the point where they can actually be in what's called cardiogenic shock so that's one very scary situation where they can be extremely hypotensive here's the other thing to think about when the left ventricle pumps this blood back into the left atrium
41:13
now here's the issue that's going to happen the blood it's going to go back into the left atrium when the ventricles are in systole but when the ventricles get ready to go into a relaxation phase and get blood back from the left atrium this blood is going to flood right back down so all the blood that was actually pushed from the left ventricle into the mitral into the left atrium it's just going to come right back down during diastole so think about that 25 of the blood that was supposed to go
41:41
out into the aorta is going to come right back down into the left ventricle and plus on top of that it's also going to get the blood that's supposed to be coming from the pulmonary veins as well so it's going to get a lot of blood that's coming into that left ventricle so the next particular issue here is that you end up what's called a left ventricular end diastolic volume they're going to fill these ventricles full because blood is continuing to just keep going back and forth between the left
42:07
ventricle left atrium left atrium back to the left ventricle this is going to keep happening so they're going to get volume overloaded inside the ventricle when that happens this imagine like this imagine it kind of looking like this i think this is the best way to kind of think about it here the blood is now going to keep kind of flowing down here because you're pushing it up and it's just flowing back down imagine all this blood just continues to keep accumulating inside of the left
42:36
ventricle and these valve flaps aren't really kind of being very helpful and so blood's starting to push back into the left atrium because it's just getting overfilled if it continues to keep getting overfilled it's going to eventually start pushing this blood back into the pulmonary circulation because normally what your ventricles would do is they would say oh man there's too much volume i have to dilate in an acute situation you don't have time to be able to dilate and so what
43:00
happens is that pressure starts increasing because you're not dilating to accommodate the volume and so when there's this high left ventricular endostatic volume it causes high left atrial pressures and that causes a backflow into the pulmonary veins and that will lead to pulmonic congestion particularly in the form of severe pulmonary edema to the point where they can be extremely hypoxic they can have disney on exertion disney at rest they can have proximal
43:33
nocturnal listening orthopedists so on and so forth so these are two of the particular presentations that you can see in the patient with acute mitral regurgitation is cardiogenic shock and very severe pulmonary edema don't forget that okay this is really really important finding and a acute mitral regurgitation that you would see in a patient secondary to infective endocarditis or an acute mi okay now let's take this scenario now where you say okay the left ventricular stroke volume is reducing
44:07
they're not getting as much volume out of the heart right that was one of the issues that we were running into because a lot of the blood is getting pushed back into the left atrium what are the ways that our heart tries to accommodate for that i'll talk to you let's explain that how all right so the primary issue here is the left ventricle is just filling and filling and filling and filling with blood so it's getting super overloaded okay so the left ventricular in diastolic volume is just
44:36
very high now in a patient who develops mitral rig they have mitral regurgitation they start having a lot of this fluid overload kind of say volume overload state what we do to accommodate for this is you will dilate the left ventricle you'll undergo what's called like it's a very specific type of process you know there's two different types of hypertrophy one type of hypertrophy is where you actually add sarcomeres you know you have sarcomeres let's say here let's say here i have a muscle cell
45:06
and in this i have sarcomeres okay if i add the sarcomeres in a linear fashion like in a series it's going to cause the muscle cell to get longer and that's called eccentric hypertrophy that'll cause the actual ventricular walls to be thin but the ventricles to be dilated and a patient who i take like a sarcomere for example though like here's a muscle cell and i take the sarcomeres like these and i add them in parallel to one another then it's going to cause them to become
45:39
bigger and thicker this is called concentric so what happens in these patients is they actually develop eccentric hypertrophy that's their problem their actual muscle cells get longer and cause their ventricles to get thinner but their actual the actual lumen the cavity of the ventricle to get larger to accommodate all that volume so they dilate their left ventricle let's just write down this purpose here this is called eccentric hypertrophy now when it does this think about what
46:15
happens now as a result of this and what that that does is it allows a higher volume to be in the ventricles right so now if we dilated we can allow all that volume to be accommodated to where it's not actually backing up as much into the left atrium so it can kind of stay within the left ventricle we're just increasing the size the pocket of that actual left ventricle so more blood can stay here and less of it back flows into the actual left atrium less of a back
46:44
flows into the pulmonary circulation and so because of that if you allow more volume to be within the left ventricle two things happen here's where it's really interesting our ventricles are very smart if you have a higher left ventricular end diastolic volume now because you've actually allowed for this dilation you have a much higher preload if you have a much higher preload you'll produce a higher stroke volume and if you have a higher stroke volume you'll have a higher cardiac output so
47:22
now this ventricle is accumulating all of this blood and it's like guess what baby i'm ready to just plow blood out into the aorta because it's accommodated itself in such a way where it can hold on to more volume and we know that frank starling's law says if you increase preload you increase stretch and increase stroke volume and increase cardiac output now we're going to push more blood out into the circulation and that's going to help to alleviate some of the hypotension so this will help to
47:49
reduce the hypotension in these chronic stages the other thing is that if we dilate if we have this high left ventricular end diastolic volume but we don't allow the blood to back flow what we do is we reduce the backflow now because of the dilation process that will lead to less pulmonary edema
48:20
that can also lessen the actual symptoms that you see in these patients right so that's some of the big things to think about in this chronic mitral regurgitation patients is one of the big things is that they undergo this type of process here called the centric hypertrophy where they dilate to accommodate or allow for more volume into them and if they allow for more volume into them less of it backflows into the left atrium
48:45
and less of that causes less pulmonary edema if we have higher volumes in the left ventricle and the contractility is still good we have more preload more stroke volume and it's going to be very hyper dynamic and we can actually reduce the severity of hypotension that's the big things to think about so sometimes in these patients who have chronic mitral regurgitation they're often sometimes asymptomatic they don't have a lot of symptoms they may have worsening symptoms
49:08
particularly they may get a little bit more hypotensive during situations where you have to undergo like exertion they may get a little bit more short of breath when they're exerting themselves but other than that they're relatively asymptomatic it's when they have this state and they undergo some issue where their contractility drops and they aren't able to maintain a good cardiac output and then they start going into a decompensated state what could that look
49:33
like all right so the problem now is we have a patient with chronic mitral regurgitation honestly they might be very non-specific symptoms really sometimes relatively asymptomatic they may have a little bit of issues with perfusing tissues especially when they're exerting themselves because then they're having to work harder and maintain these higher cardiac outputs and help to prevent you know in these situations they may develop fatigue they may develop disney
49:55
on exertion but relatively asymptomatic it's when they actually go into this decompensated state so what do i mean the problem the good thing about a patient in chronic mitral regurg is that they have a lot of preload and high stroke volumes so they're hyper dynamic right it's when the ejection fraction or the contractility starts dropping so when you get all of these ballooned up ventricles that are accumulating all of this blood the problem arises when the contractility starts dropping
50:26
so if there is a reduction in the contractility that's where you might see some issues so if you have low contractility that's decreasing but you're still having good preload there may be kind of an offsetting thing there but it depends if the contractility goes down you drop your stroke volume and if you drop your stroke volume you drop your cardiac output if you drop your cardiac output you can potentially worsen their hypotension and so this can cause potentially go into cardiogenic shock it
50:58
may cause non-specific symptoms if it's not as severe such as fatigue and disney on exertion cool clammy kind of extremities are decreased like relatively not well perfused extremities but this is something that can happen so if they develop a reduction in contractility in other words they're progressing towards heart failure so sometimes what happens is when you dilate these ventricles so much they get thin they get weak and if their disease continues to progress
51:25
they maybe start developing heart failure to the point where their contractility drops and their output drops and they can become hypotensive on top of that if their contractility drops the other issue here is that if you get less stroke volume out right so less stroke volume less blood leaves the left ventricle the problem now is that we have less blood leaving the left ventricle what was one of the already primary problems in this disease well combine that with them having high
52:03
left ventricular end diastolic volumes them already having a lot of blood within their their left side of the heart now they've accommodated and dilated but if their contractility drops and you're not able to get as much blood out of the heart now you're accumulating even more blood on top of that and so in this situation what you start getting is is that backflow again and if that backflow occurs that's going to lead to again that onset of pulmonary edema
52:34
so basically what this is showing you is that someone who has decompensated chronic mitral regurgitation in other words they're having progression of their heart they're actually developing heart failure this can lead to them kind of presenting like an acute mitral regurgitation patient so they can actually go from a chronic and then convert into a decompensated stage which looks like an acute mitral regurgitation now that's the big things to think about so we have a strong idea now about the
53:02
pathophysiology about kind of acute and chronic and then when someone decompensates they kind of go back into the acute stage the next thing to think about here is what are some other issues particularly with that left ventricular dilation you can actually have some interesting things that you'd want to remember when this left ventricle dilates it's a good it's really good at allowing for blood to enter into it rapidly so whenever the ventricles actually go into
53:27
their diastolic process blood rapidly flows into them during diastole and when blood rapidly flows into these ventricles it produces a turbulent flow when it bounces off the ventricular walls and that can produce a s s3 heart sound so that's one thing that you want to remember in these patients due to their rapid ventricular filling is they may have an s3 heart sound also their left ventricle is huge it's getting really big and so imagine the left ventricle here like just like this right
53:59
imagine how i dilated what am i doing i'm displacing the left ventricle more laterally so you know whenever you're supposed to feel what's called the pmi the point of maximal intensity it's usually near the apex now their left ventricle is dilated it's going to be displaced more laterally and on top of that they're so filled with blood but every time the left ventricle contracts it's got a lot of preload right so it's going to be slanging and a banging clanging and a banging so you're
54:25
going to get very intense thrusting quality that when you're palpating near the pmi they have a very thrusting type of quality and it's laterally displaced that's another big thing here because of the dilation it causes lateral displacement of the pmi the point of maximal intensity and on top of that when you do feel the point of maximal intensity it has a very strong thrusting quality due to it being hyper dynamic it's so filled with blood that it's preloads high and
54:59
if it's stroke volume is really high it's going to keep pounding and pounding and producing that thrusting quality against the chest wall which you'll feel when you palpate near that area so these are big things to remember as well all right ninjas so we got down the mitral stenosis mitral regurg clinical features the physical exam findings we haven't talked about the murmurs yet i want to get into that in the diagnosis section because it's super critical and we've also covered the
55:23
pathophysiology here so now that we've really built our foundation on mitral stenosis mitral regurg let's now get in and talk about the diagnosis starting with the murmurs and then we'll get into some other tests like chest x-ray ekg but looking at the big one which is echo let's do that now all right so when we talk about mitral stenosis we're going to go over the diagnosis right we've really gone over this disease pretty well what we need to now think about in this patient is their
55:46
heart murmurs this is obviously a very important point when we talk about valvular heart diseases that's one of the classic things is you're going you're listening to a patient and you're oh i hear a dang good murmur there something's going on we should be able to identify that murmur and to potentially classified into this category of mitral stenosis or mitral regurgitation so in mitral stenosis you got to go back what do we say the problem with this disease is there's a fibrotic there's a
56:12
sclerotic there's a calcified valve that doesn't allow for good blood flow between the left atrium and left ventricle during what phase ventricular diastole so the problem is is i'm having difficulty getting this blood from the left atrium down to the left ventricle during diastole so s1 begins the onset of ventricular systole so would it occur in between s1 and s2 well that begs the next question what's s2 s2 is the onset of ventricular diastole so when i hear that actual murmur
56:44
between s1 and s2 in other words a during ventricular systole no would i hear it from s2 to s1 which is ventricular diastole yes and when in diastole would i hear it well the problem is getting blood flow right across that valve so once diastole starts the vent the actual atria want to push blood down from the left atrium into left ventricle here's the problem if this valve is really really stenotic and really fibrotic whenever the actual blood flow tries to move across this valve it may
57:17
actually cause the valve to kind of like bow a little bit and when it bows a little bit it can kind of produce like this snapping type of sound which is the snapping open or boeing of the actual fibrotic mitral valve and so sometimes you may have this little like snapping sound and this snapping sound is actually literally called the opening snap it occurs right after s2 now after that happens after you snap it open a little bit more blood is going to rush through this area during the
57:48
early and mid phases of diastole so there's three phases of ventricular diastole there's early there's mid and there's late okay and the early phase is when you try to rapidly fill the ventricles in the mid you're filling the ventricles a little bit and during the late phase the atria is supposed to contract and push down the remaining 10 20 percent of blood into the ventricles so in the opening snap we snap the valve open we get a little acoustic sound there then as blood is
58:17
rushing out it's going to rush out quickly during the early phases so more blood rushing across that valve that stenotic valve will produce the loudest sound so it'll start off loud and as it goes towards like the mid phase here it'll get softer because less blood is going to be running through this as we go through the rapid filling in the early phase and then less blood will be flowing through it through the middle phase of diastole so we call this an opening snap with a diastolic decrescendo
58:49
murmur in like a rumbling fashion so what's the first thing that you have first thing is you have a opening snap then you have a diastolic day crescendo
59:04
murmur and we commonly describe this sound as a rumble rumble in the jungle now that's one of the things that can happen there's another thing that can happen remember i told you early phase is when there's rapid filling so you're gonna have rapid feeling that's why it's the loudest in the beginning then as you go to the middle less filling as you go to the late phase that's when the atria is supposed to contract when the atria contracts it may produce a little accentuation here
59:35
a little pre-ventricular systolic accentuation and we literally call this the pre-systolic accentuation you may hear that a little bit right before you go into s1 big thing to remember though guess what mitral stenosis is at high risk of what disease atrial fibrillation this pre-systolic accentuation is due to the atrial kick in patients who have afib they do not have an atrial kick so if they do not have an atrial kick would they have a pre-systolic situation no so there would be no
1:00:17
pre-systolic accentuation in these patients so potentially if you have someone with mitral stenosis new hairy and then you hear their actual s1 sound that could be they're having a opening snap with a diastolic decrescendo rumbling murmur with a pre-systolic accentuation if they have a-fib they'll just have the opening snap with the diastolic decrescendo rumbling murmur without the prehistosolic accentuation that's what i want you to remember now the next thing i want you
1:00:46
to remember is what's the best area to listen to this the best area in general for mitral valve is usually the left so position wise we like to like the left fifth miss intercostal space the left fifth intercostal space mid clavicular line so we say the left fifth intercostal space mid clavicular line now that's one we can even actually isolate this murmur even better if we put them on their side and what's called the left lateral decubitus position so sometimes
1:01:21
it's even better because we get the apex closer to the chest wall if they're in what's called the left lateral decubitus position so these are things i want you guys to remember remember okay listen in these areas listening for the opening snap the diastolic decrescendo murmur with the rumble potentially pre-systolic accentuation and again it is a diastolic murmur that you need to remember [Music]
1:02:10
okay what else can we do for these patients we can get an ecg is it going to help me no so should i should you guys really really remember this not really i wouldn't focus too much we're going to hit quickly what you could see though in this situation here and a patient who may have again mitral stenosis their left atrium may be enlarged it may be dilated if there is left atrium is enlarged they may have left atrial enlargement evident on there ekg how do we determine that
1:02:37
well you look at lead 2 right and then lead 2 you see a large m wave so you see kind of like this bifed wave that you see in lead 2. or you look in v1 and you see that they'll have a p wave but it'll be a biphasic p wave in their upright portion of it and there's a downward portion of it right they'll have a very deep negative portion so this portion will be much deeper in v1 so again this is their p wave and this is their p wave that you'll see in lead two of a very
1:03:11
bifid large p wave and in v1 they actually have a biphasic p wave with the actual terminal component deeper because that's one thing to remember the other thing that you may have here is again patients with mitral sinuses are very high risk for what condition they're very high risk for atrial fibrillation so you may see a patient with atrial fibrillation potentially present the other thing with mitral stenosis is we cause their pulmonary artery pressures to be high what does that do
1:03:42
to the right ventricle jacks it up when the right ventricle gets super thick it can cause right ventricular hypertrophy so the right ventricular hypertrophy would cause the r waves so this would generally cause the r waves to be greater than the s waves in v1 to v3 because in the r waves in that the determination determines like the depolarization particularly from the right side of the heart so they actually may be larger r waves coming from v1 to v3 then you would actually see generally
1:04:14
there's the s waves should be a little bit larger and then the r waves in particular v1 to v3 in normal patients but in these patients who have right ventricle hypertrophy there are ways maybe greater than their s waves and that's what's generally abnormal so these may be some particular findings again non-specific though right it doesn't diagnose mitral stenosis the murmur tells me something's odd ekg may help you a little bit chest x-ray is it going to do anything for me
1:04:37
not necessarily to be honest with you what could it potentially tell me again what is particularly one of the clinical features that you can see with mitral stenosis you can see fluid backing up blood backing up into the lungs causing a lot of that pulmonary edema so there may be potentially some pulmonary edema present when you get a chest x-ray now another thing is that the left atrium get all kinds of big and dilated so could you potentially see some left
1:05:04
atrial enlargement you may see some left atrium enlargement there may be some left atrial enlargement that's visible on that portion but you know what else is really interesting so the left atrium is near the bronchus the left bronchus it can actually get big enough that it can splay or push the left main stem bronchus superiorly so you may see and sometimes they love to ask this or put this in the actual question stem for your exams is it lifts the left bronchus superiorly
1:05:35
so that potentially could be an additional finding so if there is something off the chest x-ray don't forget this one because sometimes they'd like to add that one in there all right so the gold standard test if you guys don't remember any of the diagnostic steps you guys got to remember this one it's the echo this is what's going to tell us mitral stenosis but it's also going to tell us a lot more not only is it going to diagnose mitral stenosis it's going to tell us the severity of
1:05:54
mitral stenosis which obviously is going to determine our degree of treatment how quickly are we going to accelerate them to non-invasive versus invasive management so it's very important to know the echo so the echo is going to give us a lot of information some of the things that we really want to look at for these patients is we really want to look at these valves right so we want to take a look at these valves you might be able to see that they're very thick and
1:06:13
sclerotic and stenotic but really what i want to know is some of the effects of that actual fibrotic and sclerotic valve one of the things is that again lots of blood and pressure are accumulating volume and pressure accumulating in the left atrium so it has to dilate so the left atrial diameter will increase so that's one of the big things larger that left atrial diameter is the worse that degree of stenosis and also if the left atrial diameter is really high they may have very high left atrial
1:06:42
pressures and again that's kind of a bad prognostic sign as well the other thing to think about is that sometimes if they do have these a lot large like dilated atrium they're likely have an increased risk of atrial fibrillation so also potentially look oh do they have any like left atrial like embolus or thrombus there so again another thing to look for is do they have any left atrial thrombus present okay that's some of the things you definitely want to be looking for the
1:07:09
second thing which is very very important is not just the left atrial diameter but the mitral valve area so in other words this like the area the kind of like the narrowing the space the orifice by which the actual blood is flowing from the left atrium to the left ventricle the smaller that actual orifice is the smaller the area and that determines the degree of stenosis so normally it's about four to six the smaller it gets generally like less than two is diagnostic but severe like
1:07:37
severe is generally we can start off by saying it can be kind of like moderate to severe by less than or equal to like 1.5 centimeters squared but severe is less than one centimeter squared so this may be like moderate to severe and then this one is just full full-blown severe when you see these kinds of situations that's going to tell you that's going to be one of the big things the smaller this is the worse the actual stenosis is and the smaller that is the higher
1:08:07
pressure that the left atrium is going to have to generate to push blood through that tiny little opening so if the actual stenosis is worse meaning that the mitral valve area is really small the pressure which i have to exert to push blood across that area is going to be high and so that's called the mean pressure gradient so the mean pressure gradient the higher it is the worst case scenario mitral valve area the lower it is the worse the scenario so generally we
1:08:34
say whenever the number is getting greater than or equal to 10 millimeters of mercury that's really high and that's kind of indicative of a severe type of mitral stenosis so these are things to be thinking about look at the large left atrium that tells us we have high left atrial pressures look at the mitral valve area the smaller it is particularly getting towards one centimeter squared or less really bad and then the mean pressure gradient the pressure that you're having
1:08:58
to exert to push blood across that valve the higher that is particularly greater than equal to 10 the worse the stenosis
1:09:18
alright so let's now talk about mitral regurgitation so when we're looking at mitral regurgitation it's important to know the murmur okay we have to know the murmur so we have a patient with mitral regurgitation the issue with this disease is that these actual mitral valve leaflets are not going to get good seal blood is back flowing from the left ventricle into the left atrium during what phase of the cardiac cycle during ventricular systole ventricular systole is between s1 to s2 s2 to s1 is
1:09:42
ventricular diastole so it would occur between this phase now when someone has this type of murmur it's very interesting when the blood backflows during the onset of systole okay the actual murmur continues throughout the entire process of systole generally at about the same intensity throughout the entire process so when we look at this you'll see that they have a murmur that is throughout the entire process of systole at the same intensity what is this called we refer to this as a holo
1:10:24
systolic murmur so it's a murmur that is occurring during ventricular systole and it is hollow or pan meaning it's throughout the entire process of systole with the same type of intensity now that is an important one to remember what else is important about this murmur you know what else is important about this remember is obviously we should know different types of maneuvers that increase the intensity of murmur or decrease the intensity of numbers we'll have another video where we actually go
1:10:52
over all the different heart murmurs and all the accentuation stuff but basically what you want to be thinking about in these patients is anything that really increases the venous return into the left side of the heart is going to increase the intensity of the murmur right so if you increase the venous return to the left side of the heart that's going to increase the intensity of the murmur how do you increase the venous return to the to the heart generally
1:11:17
it's going to be through processes like squatting or having them do a leg raise right those would increase the venous return to the right side of the heart and then eventually increase the whenever the right ventricle gets lots of blood it'll pump that to the left atrium right that's one thing the other thing is expiration so whenever you expire that actually causes the lungs to kind of get smaller and squeeze the pulmonary blood back into the left atrium whereas
1:11:40
in inspiration that's when you feel your right side of the heart so an inspiration you increase venous return to the right side of the heart during expiration you increase venous return to the left side of the heart so these murmurs will actually increase with expiration but they would also increase with any venous return mechanism like squatting and passive leg raises the other thing is if we have more blood in this actual left ventricle when it contracts it's
1:12:05
going to push more blood across the actual mitral valve and into the left atrium so we want something that's going to cause higher amounts of afterload so if you also increase the patient's afterload that will also cause them to have a what kind of thing with their stroke volume they'll have a decreased stroke volume and because of that they're going to have more volume of blood in their left ventricle and that's going to also increase the intensity if they have more blood in the
1:12:35
left ventricle when they contract they're going to push tons of volume of blood back into the left atrium and that's going to cause an intensity intensification of the murmur so these are big things to think about now where would i hear this murmur again it's important to remember that it's best heard at the left fifth intercostal space mid clavicular line but it can definitely be heard a little bit better in the left lateral decubitus position the other thing is
1:13:00
when it's spraying blood backwards into the left atrium it tends to kind of aim it towards that left atrium to where it can actually be sometimes heard in the axilla so sometimes it can radiate to the level of the axilla so these are things to be thinking about so it's a holosystolic murmur it is the best heard of the left fifth intercostal space made convicted of the line or left ladder decubitus and it radiates into the axilla these are big things and anything that increases the
1:13:25
venus return will increase the intensity of the murmur and anything that increases the afterload will increase the intensity of the murmur and any time they go and have an expiration it will increase the intensive murmur mitral stenosis a lot of this stuff would be said similar because again with mitral stenosis you want more blood to go across that mitral valve so if you have them expire it'll increase the blood flow across the valve increasing the diastolic rumble and potentially the
1:13:50
opening snap or if you have them have an increase in venous return so you have them squat or lift their legs it'll increase the flow to the right side of the heart and then eventually the left side and that'll also increase the intensity of the murmur so those are things to think about my friends okay
1:14:23
my friends okay now that we've done that what about the ekg can the ekg help me it's not really going to be super helpful but i can actually go through it what are some of the things to think about well again with these patients their actual left atrium may or may not be dilated and so there could be some signs of left atrial enlargement and again we already talked about what that would look like we said we would look at lead 2 for the m wave and we would look at v1 for the
1:14:50
biphasic but the deeper terminal portion that's something that you could potentially see could they have atrial fibrillation they may have atrial fibrillation again if there's dilation of the left atrium there's a high risk of atrial fibrillation on top of that if you have someone who has as high amounts of pulmonary artery pressure because you're pushing blood back into the left side of the heart and into the pulmonary veins it could increase their pulmonary artery pressure
1:15:16
and cause their right side of the heart to have to work harder so there may also potentially be right ventricular hypertrophy but again a lot of these things aren't super diagnostic so it's not something to super like remember and go crazy about okay what i do want you guys to think about is the chest x-ray is there anything that could help me with a chest x-ray again probably not anything that's going to be super significant i may see some signs of pulmonary edema i may see
1:15:43
some mild signs of pulmonary edema especially an acute pulmonic i mean especially in acute mitral regurgitation in acute mitral regurgitation i may see intense amounts of pulmonary edema so these are definitely things to think about could i see some left atrial enlargement i definitely potentially could see some left atrium enlargement as well but i'd see that really the main finding is just the pulmonary edema you're not really going to see too much else you may see
1:16:09
some left atrial enlargement but again it's a potential plus or minus kind of situation all right so obviously the most important test is the echo right we can think about the ekg and the chest x-ray but they're not going to be super helpful they're not going to tell me oh yeah it is that's my regurgitable baby no you hear a murmur you think it's holosystolic you definitely hear it at the left later the cubitis position or left fifth intercostal space midclavicular line you hear that thing
1:16:30
blowing and radiating back into the axilla so you definitely think oh this could be michael regers get the echo to confirm but also get the echo to tell me how bad and how severe it is so i can determine what my management is so what i'm looking for is i'm obviously looking for a regurgitation jet i'm looking for blood to just jet back from the left ventricle into the left atrium so that's one thing so i know i got a regurgitation jet but what i want to know is how bad is that jet because
1:16:55
that's going to determine if it's mild if it's moderate if it's severe and the ones that are bad is the ones that i got to be thinking about so i got to know the severe stuff so the regurgitation fraction is how much of that actual regurgitation jet backed up into the left atrium and generally whenever that number is greater than or equal to 50 percent it's pretty bad it's pretty bad and they may need some more aggressive management particularly maybe some replacement regurgitation jet width so
1:17:18
what we want to know is the worst case scenario so what is the actual width of this jet and how bad is that and generally whenever it's greater than or equal to 0.7 centimeters that's pretty bad and that's going to be someone again who might need a replacement left ventricular in systolic diameter all this tells me is how dilated my left ventricle is remember i told you that in these patients they have very high left ventricular and diastolic volume they're pushing blood into the
1:17:42
left atrium is going right back down and so their ventricles are big and large and dilated the larger and dilated they are the worst case scenario it could be because it's going to progress into heart failure so in these patients when they're in systolic diameter the amount of blood that's in their ventricles right before they go into systole how big are they they're whopping big and when it gets greater than or equal to 40 millimeters this is pretty bad the last situation here is these
1:18:13
patients with mitral regurgitation they have hyper dynamic hearts so they're they're having very high in diastolic volumes so they're having very high stroke volumes and so they're probably having very high ejection fractions honestly their ejection fractions are probably normally greater than 60 but the problem is is whenever they start getting into that decompensated stage of their actual chronic mitral regurgitation where their ventricles contractility is starting to go downhill
1:18:43
that is a recipe for disaster because then they're not able to maintain that good cardiac output blood in the ventricles stay there they accumulate and again what's going to happen it's going to back up with the lungs cause pulmonary edema if the contractility drops i'm not able to get as much blood out of the heart and so it become hypotensive and so in these situations when the ejection fraction believe it or not is anything less than 60 particularly we kind of say you know
1:19:12
around 30 to 60 percent is actually pretty bad you know for someone who thinks oh ef is 60 that's not too bad but if it is if it's like less than 60 percent generally we say 30 to 60 that's pretty bad regardless of them being asymptomatic or symptomatic that is a significant type of mitral regurgitation
1:19:43
so that's one of the big things to be thinking about here so we've gone through we've talked about mitral rear we've diagnosed we determined severity we have a good idea now of how we're going to approach these patients so let's talk about their approach and how we treat them all right so let's talk about the treatment of mitral valve diseases right so again when we're talking about mitral valve disease we're talking about stenosis we're talking about regurgitation a lot of them can
1:20:02
have some of the similar symptoms right we said a lot of them particularly in these cases they may have symptoms of heart failure right there may be some forward heart failure that's going on in mitral stenosis there may be some backflow that's going on and particularly with both of these situations that's causing pulmonary edema that's increasing their pulmonary artery pressures and it's leading to right side heart failure so they can have biventricular failure
1:20:25
in those situations you want to treat their underlying heart failure and sometimes the symptomatic things that we're utilizing is trying to fluid restrict them so we might try to restrict excessive amounts of fluid and sodium restriction to prevent a lot of the symptomatic problems of what pulmonary edema lower extremity edema society so more of that right side heart failure particular symptoms but again left side heart failure with pulmonary edema we may need diuretics
1:20:54
for these patients as well and then obviously with patients who have heart failure what some of the baseline foundations for these patients is treating them with ace inhibitors and beta blockers if particularly tolerated and sometimes you can even add on something like an aldosterone antagonist like aldachtone or eplernone things of that nature okay so these are basically how we try to treat these patients heart failure now big thing fluid sodium restriction and
1:21:24
diuretics for the symptomatic processes ace inhibitors beta blockers and aldosterone antagonists have been shown to be able to potentially reduce some of the mortality and remodeling that occur in heart failure these are some of the things that you're trying to do because of the patient having mitral stenosis or mitral regurgitation and again particularly this could be mitral stenosis and it'd be more chronic mitral regurgitation atrial fibrillation both of these
1:21:46
patients can have atrial fibrillation what is the concern with atrial fibrillation in patients who have atrial fibrillation they're high risk of emboli so because they're at high risk of throwing an imbolus we need to consider anticoagulation for these patients and usually patients who have some type of mitral valve disease we actually consider them to be more of a valvular type of a-fip and these patients particularly with valvular afib warfarin tends to be the actual preferred
1:22:17
anticoagulant to reduce the risk of throwing symbolic strokes the other thing is patients have atrial fibrillation sometimes they can have issues with their rates and sometimes they can have rapid afib and they can go into these really high rates and so sometimes they may also need additional rate and rhythm control and this may involve multiple medications that we talked about within our atrial fibrillation lecture but i think the big thing to take into consideration is they may need
1:22:44
anticoagulation high likelihood anticoagulation especially which one more commonly so which one would this be a little bit more intense for mitral stenosis more commonly than mitral regurgitations that's a big one to think about okay so we'll treat their heart failure if they have that we'll treat atrial fibrillation with anticoagulation particularly warfarin more likely mitral stenosis than mitral regurgitation the other thing that we have to be thinking about these in patients is
1:23:10
mitral stenosis what are some of the other things that we need to think about so microstenosis they will have potentially have some forward heart failure they have some back flow into the lungs with pulmonary edema some right height side heart failure and increased risk of atrial fibrillation but the problem here is that if we don't fix that stenotic valve that's super super terrible and really bad it's going to continue to get worse and everything that we do is not going
1:23:32
to really help them very much so we need to determine which patients are the best candidates for a particular type of therapy and mitral stenosis you know there's a condition it's called percutaneous mitral balloon commissurotomy all it is is we take like a catheter we thread it through um you know a vessel here and get it into the heart and then what we do is we take this actual catheter we have a balloon that we can inflate once it's near the area of the mitral valve near that synotic
1:24:02
valve and you can inflate the balloon to basically stretch open that mitral valve and balloon it open and open up that mitral valve orifice if we open up the orifice you can allow for more blood to move through that area and again that's going to help the overall situation what kind of patients is this indicated for there's two particular indications one if the patient is asymptomatic right so they have no symptoms but their mitral valve surface area the area is less than one centimeter squared
1:24:37
remember i told you that was very very bad that was severe mitral stenosis in these patients they likely will need that balloon commisurotomy because they're not going to get much better just managing their heart failure symptoms it's going to continue to progressively get worse the other thing is if they're symptomatic then you can be a little bit more less less intense with the mitral valve area and particularly if their mitral valve surface area is less than 1.5 centimeters squared these are
1:25:01
indications to do a percutaneous mitral balloon kamishirotomy what would be a reason we would not want to do a percutaneous mitral balloon commiserotomy it would be a contraindication or a not a desirable effect if the patient has heavy heavy amounts of calcifications so if they have heavy amounts of calcifications on the mitral valve it's unlikely that you're going to gain any like pliability in that valve and so in these situations it might be better to go for the valve replacement so
1:25:36
when you have a patient with mitral stenosis percutaneous mitral balloon chemistrotomy is the preferred treatment in these two scenarios but if there's heavy heavy calcifications or they fail this treatment they get it and it doesn't really help them they may need a valve replacement so in this situation there's two types of valves that we can actually utilize we can utilize a mechanical valve and replace that actual damaged mitral valve with this one or we can use a bio
1:26:08
prosthetic valve and what is the concerns with these well again with mechanical valves they have a high risk of thrombus high risk of thrombus so they'll need anticoagulation forever for the rest of their life okay so for this patient they're at high risk of bleeding so the preferred to patient to actually do this on is those who are young and those that are on anticoagulation already or they have a low bleeding risk so they're on anticoagulation or they have a low bleeding risk
1:26:43
that's the patient who would be better benefited to get this mechanical heart valve again it's important to remember that the mechanical heart valve is going to last a lifetime so for these patients you want them to be younger so that they have the actual worth of getting that valve that mechanical valve but again it preferably would be less beneficial in patients who are older because again it's it's a long-term valve you'd rather have this particularly on the younger
1:27:06
patients and you have a high risk of bleeding because your anticoagulation needs are absolutely necessary so you want to go with patients who are not only older younger but also lower bleeding risk and maybe on anticoagulation already bioprosthetics are less thrombotic so they don't require lifelong anticoagulation they have a low thrombogenic risk so you may only need anticoagulation short term sometimes just like three months but the thing for this one is is it
1:27:37
doesn't last very long it only maybe gives you about 10 years so because of that we prefer this for the older patients we also prefer this one if they have a high bleeding risk so if they have a high bleeding risk this actually is kind of the better go for type of one and then the last thing is it also has a high risk of infective endocarditis so you can actually get infective endocarditis of the bioprosthetic valve more with these bioprosthetic valves than you would get
1:28:04
with the mechanical heart valves and so that's another particular thing to be thinking about either way valve replacements when would i get it i would get it for two particular reasons one is i would go to the valve replace them for a mitral stenosis if they have a contraindication they have heavy calcifications or the percutaneous mitral balloon commiserotomy failed if that happened in these two scenarios then i would do the valve replacement okay so that's mitral stenosis we treat them
1:28:32
with the above things heart failure atrial fibrillation they're a higher risk though than mitral regurge and then if they have these two particular reasons they get the commiserotomy if they have heavy calcifications or they fail the commiserotomy they get the valve replacement which one they pick is based upon these things we just talked about now let's talk about mitral regurge all right so when we talk about treating a patient with mitral regurgitation remember acute mitral gear just a little
1:28:56
bit more severe pretty scary situation that can happen right and again what were the two scenarios that i want you guys to remember infective endocarditis and mi so post mi in these two situations you can develop a very severe acute mitral regurge that they become hemodynamically unstable remember what i say in these situations you're having all of this blood backflow right into the left atrium and then eventually going back into the left ventricle the left ventricle is getting
1:29:21
overloaded it's getting overloaded and it's flooding back into the left atrium back into the pulmonary circulation this is causing intense pulmonary edema how do we treat the pulmonary edema in these patients well one of the things that we can do is we can actually put them on something called bipap so bi-level positive airway pressure because it helps to push some of that actual edema out of the interstitial spaces the second thing that we consider is things like diuretics so giving
1:29:51
things like furosemide to pull some of the fluid out of those interstitial spaces as well the second thing that's also an issue so one of the problems that we can see in patients with acute mitral regurg is significant pulmonary edema where it can cause hypoxemia so treat them with these two situations here the other situation is again they're having so much blood that's accumulating here and every time they contract to push blood out into the aorta and into
1:30:15
the systemic circulation every time they pump blood out they push a lot back into the left atrium so their stroke volume is dropping and they're getting hypotensive so the other particular issue here is they can be significantly hypotensive to the point where they can be in full blown cardiogenic shock and patients who are extremely hypotensive at the verge are in cardiogenic shock the things that we would like to do for them is get this ventricle to squeeze as much as it
1:30:44
possibly can so i gotta squeeze the ventricles so we might use things like positive inotropes these could be things like dobutamine epinephrine actually less likely epinephrine just because it will talk about why it squeezes down on the actual vessels here and that might actually potentially reduce your stroke volume so particularly we only want the inotropes not as many of the pressers so inotropes particularly like dobutamine or milranone the other thing that we want to do here
1:31:15
is not just get the actual heart to squeeze harder to push more blood out but we should actually try to make it easier for the blood to go from the left ventricle into the aorta how do i do that well i'm making it squeeze harder but what if i make it squeeze harder and i make the pressure in the aorta lower so that it's less afterload what could i do i could actually give reducing afterload reducers and if i want to reduce someone's afterload what are the drugs i can give
1:31:46
them i can give them nitroprusside i can give them hydralazine i can give them nephetipine i can give them a bunch of different things that can help to dilate those vessels ace inhibitors arbs a lot of those drugs that can relax the actual vessels particularly the aortic vessels and drop down the actual pressure the afterload will reduce and i'll be able to push more blood out of the left ventricle and into the aorta and that'll increase my cardiac output and increase
1:32:14
my blood pressure so those are things that you may do the other thing is if these things fail sometimes what we may do until we can get this patient to surgery is we may do something called an intra-aortic balloon pump and it's a thing that inflates during diastole so that we fill the heart with blood well and get coronary filling and then during systole it relaxes and it gives a good way of being able to kind of stabilize the patient until they can get to surgery so this may be something to
1:32:39
consider as well but these are the two therapies that we'll do in the acute mitral regurg and then once we've gotten these things stabilized they need to get a valve replacement asap okay that's their end goal until we replace that valve they are at potential risk of going into complete cardiogenic shock and dying it's the other flavor of this disease chronic mitral reactors that we have to be thinking about so in chronic mitral regurg in these patients they're not
1:33:08
completely pulmonary edema hypoxemic they're not hypotensive at the verge of cardiogenic shock remember i told you they're dilating they're dilating and if they're dilating they're accommodating that higher volume they're having less pulmonary edema less hypotension they're not going to be looking like this they're relatively sometimes asymptomatic so it's those chronic ones that we also have to be thinking about so if they have chronic mitral regurg what do i do i'm treating
1:33:33
their heart failure i'm treating their atrial fibrillation yes but when do i go to replace the valve at what point in time the indications of when a patient with chronic mitral regurgitation will get a valve replacement there's a couple reasons one is the actual left ventricular in systolic diameter what do it's right here actually that's perfect if the left ventricular in systolic diameter is getting really really big because the ventral ventricles are having to accommodate large amounts of
1:34:04
volume that means that it's getting severe to the point where it's greater than or equal to 40 millimeters that is an indication for a valve replacement so one particular reason is their left ventricular and systolic diameter is greater than or equal to 40 millimeters second reason they have any type of secondary mitral regurgitation any of them whether it's dilated cardiomyopathy whether it's some type of aortic regurgitation whether it's systolic heart failure of other
1:34:33
particular reasons regardless they have secondary mitral regurgitation and they have failed medical therapy what is the medical therapy heart failure treatments ace inhibitors beta blockers sodium fluid restriction diuretics adding on aldosterone antagonists digoxin all of those things they've tried all of it it's not working and they're failing to be able to respond to that then they get a valve replacement what's the last particular indication remember i told you that in patients who
1:35:06
have mitral regurgitation their stroke volumes are crazy high because they have such a large preload and they'll continue to keep slamming blood out of their heart their ejection fractions tend to be hyper dynamic if at any point it drops less than 60 percent they are now having very bad left ventricular dysfunction and we say that at any point regardless if they have symptoms or not if their left ventricular ejection fraction is between 30 to 60 percent anything less than 60 percent really
1:35:39
this is again regardless of symptoms so it could be plus or minus symptoms they get a valve replacement these are the three indications in a chronic mitral regurg patient that would get a valve replacement one they're super dilated ventricles second they have secondary mitral regurg or any kind of really thing that where they're failing medical therapy that's a good enough reason and third their ejection fraction is no longer hyperdynamic they have left ventricular dysfunction regardless of
1:36:06
their symptoms boom they get the valve replacement now that we know all of these things we have a very good understanding of mitral valve disease i hope you do i hope you understand and understand just completely got this down pat now engineers if you did i'm so happy and i love you i thank you and as always until next time
1:36:30
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