Valvular Heart Diseases | Clinical Medicine

foreign what's up Ninja nerds in this video today we're going to be talking about valvular heart disease also abbreviated vhds this is going to be part of our clinical medicine section if you guys like this video you benefit from it please support us hit that like button comment down the comment section also subscribe you guys I really suggest if you guys have an opportunity to go down the description box below we got a link to our website we got great notes great illustrations we have a lot of awesome merchandise and we're developing something really cool

a lot of test prep courses on those preparing for the step one the step two the pants Etc go check that out all right let's get into vhds so valvular heart diseases there is a couple more that aren't really listed here they are just super uncommon they're not very high yield so I'm not going to spend time on those that's your tricuspids stenosis your tricuspid regurg pulmonary stenosis pulmonary regurgitation those aren't super calm and the left heart disease those valvular disorders are much much more common and more likely to be tested on so let's focus

on those that includes your mitral stenosis regurgitation aortic stenosis aortic regurgitation and then we'll talk about this like little random guy here called rheumatic fever one little note tricuspid regurgitation may be the only one that could potentially be mentioned on your exams only thing to remember for that one it's as highly associated with IV drug abuse other than that that's really it let's start talking about these so mitral stenosis within the name it's telling me that there is some fibrosis there's tough there's sclerosis of this mitral valve so this is the valve that is actually

between the left atrial and left ventricle that's the basic anatomy right what I want you to associate with mitral stenosis is there's difficulty in being able to get blood where from the left atrium to the left ventricle because this valve is not allowing that that is honestly the basic pathophysiological process so there is a decrease blood flow from where blood flow from the left atrium to the left ventricle and really that's about as simple as it needs to be but the question then kind of arises what generally causes this valve to become supersonatic and tough

and hard and not just allowing it to open normally it should open allow blood from go over the left atrium to left ventricle it's not opening properly why by far the most common cause of this is going to be rheumatic fever so that's why I will mention rheumatic fever a little bit later all right this is going to be the associated causes that are particularly associated with mitral stenosis all right good enough let's talk about mitral regurgitation miter regurgitation is a little bit more interesting and what happens with mitral regurgitation is the opposite the mitral

valve is not functioning and it's causing blood to go from the what left ventricle into the left atrium that generally should not be happening now the valves mitral valves should open during diastole allow blood to go from left atrium to left ventricle should snap shut during systole blocking blood from going to left ventricle to left atrium the question then arises all right so we know that from this pathophysiological process there is a increased blood flow from the left ventricle to the left atrium and that's the pathophysiological process that occurs in both of these diseases right

so this is the concept here now what I want us to be able to ask theselves the question is is what is causing these valves to not function and block blood from going back up one of the causes for this particular cut thing is you have some type of dilated left ventricle causes all right so there's a dilated left ventricle what are diseases that would cause dilation of the left ventricle systolic heart failure systolic heart failure what's another terminology just so we're clear for systolic heart failure this is also known as heart failure with a

reduced ejection fraction what happens is you dilate these ventricles and if they dilate look they're dilated it's going to stretch these valve flaps farther away from one another now there's not there's too much distance between them to snap shut during systole that's one cause another one is called dilated cardiomyopathy this is another particular cause that I want you guys to associate it with but basically the whole concept is they're diluting the ventricles and not allowing for the valve flaps to come together nicely this one is there some type of mitral valve damage or like destruction

generally but in in general there's direct damage to the mitral valve the question that we have to ask is what are the reasons why there is mitral valve damage and there is a couple the biggest one is sometimes you can get an infection and if you have an infection particularly something called infective endocarditis it can destroy these valves it can literally chew them away and now you don't have a valve flap that can actually meet the other one and completely close so I want you to remember a big one here is going to be infective

endocarditis super common especially in the IV drug use of population are those who have some type of underlying cardiac surgery or prosthetic valves the other one here is that the mitral valve has some type of like underlying genetic connective tissue dysfunction so it's naturally weak and it's degenerate we call this myxomatous degeneration remember that from pathology so the valve is naturally weak that it can pop it can prolapse and when it prolapses it can bow up into the left atrium you guys know what that's called we call that mitral valve prolapse this is extremely common

in patients who have some type of like connective tissue disorder do you guys remember some of them things like marfon syndrome ehlers Don low syndrome these are big things to remember here all right so to recap this mitral stenosis decrease blood going from the left atrium to left ventricle because of a synotic valve rheumatic fever happens to be pretty much one of the most common mitral regurg increased blood flow going back into the left atrium because you dilate your left ventricle or you damage the mitral valve pretty straightforward we'll come back to this in a

second so over to aortic stenosis aortic stenosis is this valve it's supposed to allow blood to go from the left ventricle into the aorta during systole and then block the blood flow from the aorta into the left ventricle during diastole aortic stenosis it's not allowing blood to flow forward so it's supposed to go here and it is not allowing for that process to occur and the reason is there's some type of hardening or sclerosis or just intense fibrosis of the aortic valve and the problem with this disease is there is a decreased blood flow from

the left ventricle to the aorta and that is really the pathophysiological process that I want you guys to understand here but then the question then arises like all of these what is causing this valve to become supersclerotic and hard and difficulty being able to open up and allow blood to leave the left ventricle the causes here is it's twofold I want you to remember it like this those patients who are less than 70 years of age and those that are greater than 70 years of age and those who are less than 70 years of age

they may have a gen some type of problem with the valve development and we call this a bicuspid aortic valve a bicuspid I'm going to put aortic valve that's an abbreviation for the aortic valve for those greater than 70 it's just calcification over time this happens to be probably one of the most common causes it's just dystrophic calcification so we call this dystrophic calcification and this is just wear and tear on the valve over time and that is generally the problem for this disorder the last one of these left ventricular valvular heart diseases is aortic

regurgitation for this one it's very interesting so what happens in this disease is again aortic valve should open during systole close during diastole during diastole for some reason the blood decides to shoot back into the left ventricle from the aorta shoot back from the aorta sorry aorta into the left ventricle that's the correct terminology so again with these particular scenarios what's the pathophysiological process there is an increase in blood flow from the aorta to the left ventricle and that is the pathophysiological process that I want you guys to understand now with that being said we

then say okay there's something wrong with the valves pretty straightforward for my regurgitation it was a dilated left ventricle aortic regurgitation it's a dilated aorta so anything that causes dilation of the aorta so dilated aorta causes it doesn't take a genius to figure out these what's the dilation of the aorta called an aortic aneurysm so when patients have a ascending aortic aneurysm this is a very very common cause and anything else that causes dilation there is a it is not very common and I want you guys to worry too much about it but anything that

causes aortic inflammation so there is some Rarities out there like syphilis and things like takayasus arteritis and reactive arthritis which you can see sometimes and writer syndrome but this is by far going to be much more common for you have an ascending aortic aneurysm and it's pretty straightforward if this aorta is super dilated just like it was for the left ventricle and my triggerge it's pulling the valve flaps farther away from another they can't completely close in this particular scenario it was damaged mitral valve aortic valve damage so there is some type of aortic valve

damage and so we have to ask ourselves the question what is causing this aortic valve damage and it's relatively similar one is infective endocarditis right infective endocarditis can damage the mitral valves it can damage the aortic Valves and remember I told you that little Pearl the only thing pertinent for tricuspid regurgitation is in MRSA and IV drug abusers that can attack the tricuspid valve but generally these are the most commonly attack valves so infective endocarditis is an infection of those valves where the bacteria literally I'm not even kidding can chew away the actual valve another

one is this one's an interesting one sometimes if patients get aortic dissections like ascending aortic dissection is or proximal aortic dissections it can literally tear away in the media and then move into the valve and cause it to literally dysfunction so sometimes another one would be a a proximal aortic dissection or a Stanford a proximal aortic dissection these would be some of the big things that I would really want you guys to remember for the causes of aortic regurgitation so with that being said we've covered all the valvular heart diseases but I got this Rando

thing here mentioned you're like okay I saw rheumatic fever particularly with mitral stenosis it can attack other vowels it loves the mitral valve we'll talk about that then it loves the aortic valve so let's talk a Teensy bit about this because you can see this in some of these valvular disorders rheumatic fever usually this happens in younger patients who get strep throat alright so they get a bacteria that causes an infection here so here we're going to have an infection here of the actual pharynx here's the bacteria that's wreaking all this Havoc this is called

I'm an abbreviated group a beta hemolyticus Streptococcus bacteria so this is some type of bacteria and it causes a nasty infection of the pharynx now naturally what will happen is your body will have these things called plasma cells that'll become eventually activated and what they're going to try to do is is they're going to try to pump out some Auto antibodies right some anti-strepto lysine antibodies some anti-dnas B antibodies a bunch of these puppies and when they try to pump these out these are supposed to go and eradicate or destroy let's put a little inhibitory

sign inhibit the actual group a beta hemolyticus Streptococcus bacteria destroy it but sometimes what happens is these Auto antibodies like to go and Destroy other tissues and one of those tissues that we have discussed here is particularly what the heart and with that being said the most commonly affected valves that when it actually goes these Auto antibodies they go and attack the heart they love to attack a couple different valves the most prominent valve that they love to attack is going to be the mitral valve then after that it would be the aortic valve so

with that being said what you're going to see is you're going to see some type of valvular heart damage you're going to see a lot of damage to the actual valves but it's going to prefer to hit the mitral valve and then after that hit the aortic valve so sometimes what you may see in certain textbooks is that rheumatic fever which can lead to rheumatic heart disease so this is eventually what happens is if you damage the actual Hearts we actually give this a terminology here and we call this Rheumatic heart disease once you actually

start exhibiting some cardiac destruction when we see this you may see oh this causes mitral stenosis and it causes mitral regurgitation yeah and it can even cause aortic stenosis and sometimes aortic regurgitation but I just want you guys to remember that it really loves to attack the valves all right my friends that covers the pathophysiology of valvular heart diseases now I want you guys to understand what happens when these values of the heart diseases wreak havoc on our body all right my friends now let's talk about the complications associated with valvular heart diseases so first

thing mitro stenosis we already know there's a problem going from left atrium to left ventricle right rheumatic fever is a big trigger here what I want you guys to understand though is that if we can't get blood from the left atrium to the left ventricle the problem is is what it's going to kind of start backing up from the left atrium into the pulmonary veins and so what happens is is these patients generally have like a very high left atrial pressure that transmits to a high pulmonary capillary wedge pressure and that leads to that hydrostatic

pressure being high and pushing that fluid out into the interstitial spaces into the alveoli when fluid accumulates there what is that called pulmonary edema and then that pulmonary edema depending upon the severity of it can cause features of dyspnea peroxismal nocturnal dyspnea it can cause orthopnia and in certain severe cases it may cause respiratory distress causing hypoxia increased work of breathing increased respiratory rate Etc but it's again a concept of this pathophysiological process so again blood can't go from here to here because of that the pressure in the left atrium Rises that then transmits to

what the pulmonary capillaries which causes their pressure to increase that then stimulates fluid to accumulate here which leads to pulmonary edema which leads to the symptomatic features of left heart failure which you may see all right the other concept here is that because you can't get blood from the left atrium into the left ventricle again blood will stay in this area right but you know what else will stay in here a lot of that blood will actually start causing the left atrium to say hey man left neutral pressure is pretty high and the volume inside

of the left Atria is pretty high I need to dilate and so what happens is is because of all of this you develop something called Left atrial dilation now look at how honking big this dang Atria is it's gargantuous and because of that big old Atria now you stretch out The myocardium when you stretch the atrial tissue it Alters the circuitry there and it increases the risk for patients developing atrial fibrillation so then this causes atrial fibrillation to be way more prominent in these patients now what's the problem with atrial fibrillation it doesn't contract very

well because of those re-entrant circuits and it causes clots to begin to form in the left Atria and then those clots can flick off and you can form emboli and these emboli can travel via the systemic circulation so look at this some of these are going to slip out here they're going to run out here and into the systemic circulation if they run into the systemic circulation what is that called they're called embolic phenomenon so then you're going to get these thromboemboli which are going to go and spread to multiple areas of the body some

of those under the brain this is the most terrifying you can end up with a stroke it can go to the gut and cause acute mesenteric ischemia it could go to a vessel in the leg and block off the blood flow of the leg and cause acute limb ischemia so these are all potential features that can happen in a patient who has mitral stenosis now this type of aphid that they usually develop will talk about it more in the afib lecture but I'll put it here in kind of like a little parentheses if you will

it's like a little little spacer it's called valvular valvular atrial fibrillation very important because that determines the type of treatment we'll give to these patients all right cool mitral stenosis remember pulmonary edema due to high left atrial pressure left atrial dilation increasing risk of afib and thrombo and Bly all right what's next Nitro regurgitation with mitro regurgitation the problem is blood is pumping back up into the left Atria from the left ventricle so now look two things happens here normally when you contract your left ventricle blood should go this way should not be going this

way but both of these things have become Unfortunate Events here where this occurs pretty rapidly so then what happens to your left atrial pressure goes up what happens to your pulmonary capillary wedge pressure goes up what do you then stimulate pulmonary edema so all of these things happen because of this flood of blood this jet backing up into the left atrium left atrial pressure goes up pulmonary capillary wedge pressure goes up you stimulate pulmonary edema and this present presences we'll just put for now but the same thing is above dyspnea peroxismal nocturnal Disney orthopnea or

in severe cases it can cause respiratory failure so then again fluid will accumulate here and all in these particular areas here precipitating this which may precipitate this or worsening respiratory failure the other downside of mitral regurgitation especially this is acute so if a patient develops an acute mitral regurgitation what happens is is a lot of blood backs up here and causes overt pulmonary edema but also you have less blood there is a decrease per se and the volume of blood that is leaving the heart within each heartbeat your stroke volume that thing can drop the

cardiac output can drop the blood pressure and can lead to shock these patients may go into overt cardiogenic shock if it is acute so this is more prominent and patients who have acute mitral regurgitation whereas those who are more of the chronic mitral regards they may compensate in some type of way they may dilate their ventricles to try to have a bigger preload but in these scenarios of acute mitral regurgitation it can progress to a type of shock which we call cardiogenic shock so these are the big things that I want you to watch out

for with my regurgitation is the possibility of cardiogenic shock and pulmonary edema okay we're going to come back to rheumatic fever in just a second all right remember that this is a big trigger of mitral valve disease aortic disease but what's the most common one mitral valve first like mitral stenosis all right aortic stenosis this is a really interesting one it's similar to one of those we call hypertrophic cardiomopathy similar pathophysiology just a little bit difference in the underlying cause and hypertrophic it was a big septal hypertrophy and aortic stenosis the valve is super hard

and sclerotic and not allowing blood to leave so it's the same concept if you will so in this disease it's hard getting blood out right so there definitely will be a reduction in the amount of blood leaving the heart so we'll call this the cardiac output which will lead to a reduction in your systemic perfusion now in patients who have this we like to call this like you know how we said that this is kind of like your left ventricular outflow tract this can act it can act as what's called we're going to call this

a l v o t o a left ventricular outflow tract obstruction so it's kind of preventing blood from getting out of the left ventricle into the aorta that leads to this reduction in cardiac output that leads to the reduction in systemic perfusion and this can be very quick and so because of that this can affect tissues very abruptly some of these are very interesting first one here is the carotids so a patient who has aortic stenosis when you palpate their carotid during systole it's very weak because it's hard for them to get blood out of

the heart and it's also delayed because the heart is really having to squeeze and squeeze and squeeze so it takes a longer time for them to push out the appropriate volume of blood into the Carotid so it's a delayed and weak pulse we always got to make things more difficult though and so we use a term we call it pulses parvis at TARDIS all we're saying is is its weak and delayed pulse that's all it is and that's usually because again very little blood is reaching the carotids all right the next concept here is that

it also can cause a transient reduction in perfusion to the brain and sometimes these patients can transiently lose Consciousness what is this called this is called syncope another very very common feature here that we can see and the last one here is whenever you don't perfuse the coronaries the aortic stenosis is a really powerful trigger if you can't get blood out of the left ventricle into the order you won't be able to perfuse those coronaries which is right off the base of the aorta and so this can cause a reduction in coronary perfusion which may

lead to a little bit of ischemia and that ischemia may present with angina and so watch out for angenal symptoms here as another prominent feature the last thing that I want you guys to remember here is is if it's hard to get blood out of the left ventricle it's going to start causing blood to unfortunately back up and so it may so this is being inhibited right but unfortunately because it can't get out the blood will start to back up and the left atrial pressures will go up the pulmonary capillary wedge pressures will go up

this will precipitate oh my gosh it's like a a repeat all the time this will be ingrained into your brains forever guys dyspnea peroxidable nocturnal dyspnea orthopnea Etc it can even be terribly especially if it's really really bad it can precipitate respiratory failure right and this is some of the big features here due to that blood backing up into the left Atria right so those left ventricular end diastolic pressures will be really really high and it's hard to fill it okay with that being said the common theme that you want to remember is aortic stenosis

is sad I know that's corny but remember syncope angina in dyspnea tend to be the common features in aortic stenosis due to the left ventricular tract obstruction similar to hypertrophic cardiomyopathy now there will be a murmur that is also present in all of these I don't we didn't we're not skipping over it we're going to talk about it in great detail in a second but for right now that's another really big way to differentiate aortic stenosis from hypertrophic cardiomyopathy is the murmur and also age age is another really big factor one other thing that I

want you guys to remember here with aortic stenosis is whenever this difficulty in getting blood out of the left ventricle occurs the afterload is high right it's hard to get blood out after those High that will trigger The ventricle to have to get thicker and that'll lead to something called left ventricular hypertrophy it'll thicken it you guys remember in the heart failure lecture when The ventricle gets really really thick it doesn't feel well what type of heart failure is that heart failure with a preserved ejection fraction we call that a diastolic heart failure just because

of room here I'm going to put half oftentimes this will be another potential thing that you can see in these patients the aortic stenosis okay aortic regurgitation problem is blood is flooding back in to the left ventricle so you're trying your best to push blood out but a lot of it is just flooding back in what will this do okay well let's focus first on if I can't get blood out so let's say that I'm pushing blood out but a lot of it's flooding back in and the total volume of blood that you're pushing out

of the heart and that one kind of cardiac cycle is what it's reduced because you're pushing it out but A lot's just flooding right back in so that's a reduction and the cardiac output and what the problem with this is is if this is acute so I have to remember to tell you guys this again if this is an acute and I'm going to abbreviate this aortic regurgitation this will drop the blood pressure and this will put the patient into cardiogenic shock very quickly this one's a terrifying one okay so if the patient does have

an acute aortic regurgitation and they drop their cardiac output enough they'll drop their blood pressure and they will present with cardiogenic shock so that's a big thing to be able to remember all right the other concept here is that we're pushing very little blood out because a lot of it's flooding back in so what you're going to start noticing is is that the blood I'm going to do it like this because of room with all these arrows the blood will start to kind of accumulate in these ventricles and they will get plumpy big right so

they're going to start filling up so what's the problem with an increased backflow so whenever you have this increased backflow well one thing here let's actually do it like this with an increase in the back flow into the left ventricle where will it go well I can't get out of the heart so unfortunately it'll start backing up and going into the lungs and you'll start developing oh my gosh what a surprise oh pulmonary edema right so your pulmonary capillary wedge pressure will go up and then what will happen here you'll have pulmonary edema I bet

you guys don't know how this presents just kidding dyspnea proximal nocturnal dyspnea orthopnea and maybe even acute respiratory failure if severe right so these are potential things that could occur because of that backflow all right the other thing is whenever you have this increased backflow into the actual left ventricle it does two weird things all right one is you increase your stroke volume so imagine blood goes out of the heart and then a ton of it flows back in when a ton of it flows back in The ventricle will stretch when it'll stretch what is

that called preload right you increase the preload when you increase preload what do you do to your stroke volume but boom so it'll increase the stroke volume so this will increase preload and we'll put here in like in parentheses stroke volume that'll then cause the heart to literally smash as much blood as it possibly can because it's going to get stretched that'll then cause extreme bounding pulses these pulses will be insane and the membrane all right so you're going to have crazy bounding pulses so during Sicily you'll feel them it's literally like a hammer is

hitting hitting your fingers then what happens is because of this um keep the colors the same look what I did here I jacked all the colors up here guys so it should be an increase in preload here and then this blue area here a little bit of OCD there sorry but the other concept here is whenever I have this increased backflow during the actual diastolic process what's really weird is imagine during systole I push just punch blood into my artery boom bounding pulse so this would be during systole during diastole what happens well generally the

valve should close and blood shouldn't come back into the heart but in this disease it will so in diastole a ton of blood is going to shoot back into the heart and then the pulse will literally drop and when that happens what you're going to notice here is you're going to notice these like weird like wide pulse pressure findings so during diastole I have this wide pulse pressure we're going to put this wide pulse pressure and this is particularly during diastole the reason why I mention this is they use certain um there's all these like

findings like you have the demusset sign you have the Corrigan's pulse or the water hammer pulse there's all these interesting ones the most important one uh like finding here is that it's going to present with what's called a water hammer pulse this is one of the common features of the wide pulse pressure findings and it's basically if you palpate the actual radial artery you'll feel these boom these smashing pulses but it'll just be pop pom it'll be a big poundering systole and it'll go completely flat during diastole it's very very intense and that's usually associated

with aortic regurgitation all right that covers this one so again with aortic regurgitation you'll notice shock what do you notice pretty much out of all of these though pulmonary edema right pulmonary edema could be potential finding in all of these afib is a little bit more specific for mitral stenosis right but you can definitely see cardiogenic shock and aortic regurgitation and mitral regurgitation especially if it's acute the sad features are really the big one that you'll pick up on aortic stenosis but at least of this last one here so we talked about rheumatic fever being

a very powerful trigger of mitral valve disease and aortic valve disease mitral more so than an aortic and again it was due to the group a beta hemolyticus Streptococcus bacteria causing strep throat plasma cells reacted produce antibodies antibodies then try to go and destroy the bacteria in the pharynx but unfortunately produce Auto antibodies that attack other tissue and when they go and attack the tissue they attack the joints they attack the heart they attack the skin and cause these weird nodules or red rash and then they also like to damage the central nervous system and

I want you to remember the tissues that they attacked based upon this little little trick here called Jones and we're going to use the heart we're going to use this like little corny symbol here this is your Jones criteria so first one is you're going to damage the joints so these patients will have joint injury you'll also damage their valves and so they'll have valve damage which one more so mitral valve greater than aortic valve they'll also have these weird bumps on their skin called nodules and we say that this is called like you have

like the erythema nodozum they'll also have this other weird lesion here these red lesions called erythema marginatum so they'll have skin lesions like nodules erythema margin atom they'll also have these valvular disorders and joint pain the last one is they love to have this kind of like Auto antibodies lead to damage to the basal ganglia which leads to side in hands Korea what is Korea Korea not the country we're talking about the weird type of movement that they'll have so they'll have this like weird kind of like jerky movement that they'll exhibit that's common in

these patients so if you have a patient who had strep throat presents with joint pain now valvular disorders you hear a murmur on top of that weird nodules red lat rashes and they have weird movements think about rheumatic fever all right my friends that covers the valvular heart disease complications now what I need us to do is take a second and say how can we differentiate these not just by complications but also by the murmur evaluation I think a patient has a valvular heart disease one of the classic things is the patient presents with a

murmur we talked about this in the heart sounds and heart murmur lecture but I want to quickly recap it so that you guys don't forget it some good space repetition when I auscultate I want to first know location systolic versus diastolic or continuous if I find the location and then I say okay this sounds like it's a systolic murmur then I can automatically think of two particular ones on the left's heart I can think of a crescendo de Crescendo murmur that radiates to the carotids that's aortic stenosis if it's holosystolic and it's at the Apex

and radiates to the axolot that's mitral regurgitation then if it's a diastolic murmur okay then I know I'm left with mitral stenosis and aortic regurgitation so is it de crescendo and if that is the case it's aortic regurgitation even better is it around like that left third intercostal space that also helps next thing is does it have a opening snap with a decrescendo rumble and is that the Apex that supports mitral stenosis so these are easy ways to go about that but maybe you're like I'm still in the fence maybe there's some other murmurs that

I'm not completely sure about do some accentuation minervous to increase or decrease the intensity to be even more confident in that so then I say okay I'm going to change the position because I'm a little bit confused here I'm going to have them Lean Forward I know that that brings the aortic valve closer to the heart that should increase the aortic Moon murmurs if I put them in left ladder to Cubase that brings the mitral valve closer to the heart that's going to increase mitral murmurs then I'm going to have them Inc kind of change

their Venus return so I'm going to have them increase the Venus return by squat or I do a passive leg raise that brings lots of blood back to the heart that should increase the intensity of all murmurs right the only exception to that is mitral valve prolapse and HCM all right so it increases all murmurs except for HCM and mitral valve prolapse if I decrease the venous return so I have them valzava or I have them stand then it should decrease the intensity of all murmurs except for HCM and mitroval prolapse that's the concept there

then I go to the last thing which is afterload now if I increase the afterload I have them squeeze some hand grips what would that do to this systolic murmurs well in this case it would actually make it harder for blood to move out into this actual vicinity out into the aorta and so that should actually decrease the aortic stenosis murmur the other thing is that it actually should increase the aortic regurgitation the mitral regurgitation murmur why because if the afterload is high the pressure in the aorta is high so now blood will just flood

back from the aorta into the left ventricle so think about that that's going to cause aortic regurgitation to be increased plus you're going to have more volume in the left ventricle so when the left ventricle contracts it's going to push more blood back into the left atrium so that's why Mr and AR would be significantly increased and then if I decrease the afterload then I'm going to do what I'm going to make the aortic stenosis murmur a lot louder and then again flip everything decrease the aortic regurg and mitral regurg murmur all right that's the

concept that I want you guys to understand with the heart murmur evaluation now when a patient comes to you and they have a murmur and you've auscultated you've found okay it's here at this particular location it's systolic or diastolic it changes with this position or with this maneuver and maybe they have some features that are suggestive of that type of ovular heart disease the next thing is to obtain an echocardiogram and consider a cardiac cath I wouldn't say that it's always needed I would say an echo is going to be the first test of choice

what's nice about this is it'll definitely show you which valve is the problem and may even lead you into the cause of that valve problem so if it's aortic stenosis the problem is getting blood out of this left ventricle here into the aorta and I'd be able to see that this valve would not be opening very well so there's decreased blood flow across it and then also usually left ventricular approach look at the thickness there all right the next thing is I did aortic regurgitation I'd be able to see that this blood flow that's going

from the left ventricle up through the aorta which you can't see from this window is shooting right back into it so there's a massive regurgitation jet back into the left ventricle and also I'd be able to see that this left ventricle is pretty dilated to accommodate for that large volume all right with mitral stenosis I'd be able to see again that there's a really difficult time in being able to get blood flow from the left atrium to the left ventricle and this mitral valve orifice would be so tiny and it wouldn't be allowing for me

to get blood flow easily through here plus left atrium should be big as a masaka right mitral regurgitation is I would see look at these valves they're either defective they're chewed up the ventricles are dilated or there's a Pap muscle rupture and I'd be able to see the blood shooting back into from the left atrium sorry left ventricle to the left atrium during systole and that's pretty common now what I did is you could see in each one of these as we correlate again the echocardiogram with the cardiac catheterization and this will show you the

different levels of pulse pressures so you'll be able to see the pulse pressures and where the different pressures in the Atria and The ventricle change all right now after we've done all of this we've diagnostically come to the conclusion hey they have a valvular heart disease and it is this it is this one the question is could it have been because of rheumatic heart disease and again we have to think about that especially in mitral stenosis so if a patient has any of these major criteria at least two of them so any of the Jones

joint pain cardiac valve nodules erythema marginatum inside enhanced Korea if they have two of these you can make the diagnosis of rheumatic heart disease if they don't have two of these maybe they only have one of these then you come over here to the minor criteria is there suggestion of fever an increase at erythrocyte sedimentation rate and increase PR interval or polyarthritis if there is one of these and at least two of these then we can potentially say that the patient has what rheumatic heart disease to add to the diagnosis to make this even better

what about those antibodies that were actually causing these problems test them test them for the strep test to see if they had an infection there test them for the anti-dnas be in the anti-structolycin antibodies okay so again two major or one major plus two minor and you've met the criteria for medic heart disease all right we've determined the patient's valvular heart disease if it's Rheumatic or not how do we treat them this is super straightforward you're not going to get hit with a lot of questions on this but first manage all heart failure symptoms so

again we saw that aortic stenosis can cause diastolic aortic regurgitation can cause systolic heart failure my trigger can cause the solid heart failure and mitral stenosis again doesn't really cause a classic heart failure but you'll notice that in these patients they have specific features of heart failure treat that accordingly if the patient does not improve then you need to consider the potential for a surgical intervention aortic stenosis we do what's called a Taver and we'll go through kind of like a vessel and we'll actually use a catheter and go up there and try to repair

the actual aortic valve or you can do it surgically so savr is a surgical you open them up open up their chest and do it tavr is usually preferred in all of these scenarios because it's less invasive but you have to consider is it severe aortic stenosis because the aortic valve surface area is super small are they really symptomatic despite management with medical therapy and is there lvef dropping because it really shouldn't but if it starts dropping that means that this is not going well and you need to start intervening air degree education same thing

do they need a Savvy usually this is always has to be repaired surgically and again is it acute heart failure is the primary indication so in other words that the the valve just completely get ripped up and now they're in acute heart failure you need to take these patients right away for surgery or do they have aortic regurgitation that's chronic but they're not responding to Medical therapy mitro stenosis same thing we actually do what's called a balloon valvuloplasty where you actually kind of like spread this sucker open a little bit and that's usually if they

have very severe mitral stenosis so their mitral valve surface area is so so tiny the last one is mitral regurgitation this one's also mitral valve repair replacement this is usually if they have acute heart failure or they refractory to all the medical therapy so again I want you to remember if they have aortic regurg or mitral and it's acute that is an immediate indication for a replacement all right but again for the aortic stenosis a mitral stenosis depends upon the severity of the actual patient's disease all right quick thing to add on here with mitral

stenosis I told you that it's the highest risk for atrial fibrillation so therefore they can pop emboli off cause Strokes you need to consider that and determine the patient's Chad vascore and determine if they need anticoagulation usually this is because it's a valvular afib it will require Warfarin and wouldn't be best to treat with the doe ax the other thing here is rheumatic fever if any of these patients have these diseases because of rheumatic fever you have to treat them with Penicillin G and they may be on that for a decent amount of time all

right last thing to discuss is if a patient gets a valve replacement we put in a prostatic valve and this is either mechanical or it's bioprostatic now if they get a mechanical heart valve these are highly thrombogenic so you may have to put them on anticoagulation for the rest of their life and again because it's a mechanical valve Warfarin is the only thing that you can put them on all right and for that you're aiming for an INR of 2.5 to 3.5 remember that what the problem is with the mechanical heart valve is again they

may need to be on Lifeline anticoagulation so they don't want them to be too old because they're going to have a risk of bleeding and again these valves last a really long time so you want them to also be younger because you want to give them a valve that's going to last a decent amount of time if these valves do become damaged It's usually the annular ring so it's on the side where they're actually like the adhesive like that where the surgical incisions are on the side of the valve they start to become weak and

you can develop a leak on the side of the valve where it's actually kind of seated and this can cause blood to regurgitate on the side of that that new healthy valve it's called a pair of alveolar leak very classic from mechanical heart valves with bioparesthetic valves these are not as highly thrombogenic so you do not need to be on lifelong anticoagulation the downside to this one is that the valve can actually get chewed away because it is bioprosthetic and so it can actually get ripped away and eaten and so what happens is you can

actually develop a leak right in the middle of the valve so this is called a transvavular regurgitation if this happens you want to be listening and saying hey do I hear a new murmur that's one of the key features if there is a new murmur that doesn't make sense to them think about the prosthetic valve being dysfunctional if that's not the thing that comes up on the vignette think about weird things such as do they have any anemia especially microangiopathic hemolytic anemia or are they an acute heart failure if any of these things present you

should start thinking about a prosthetic valve that's being dysfunctional and then get an echocardiogram to determine which one of these valvular leaks it is all right my friends that covers valvular heart disease I hope it made sense I hope that you guys enjoyed it and as always until next time [Music] thank you