Cardiomyopathy | Clinical Medicine

foreign what's up Ninja nerds in this video today we're going to be talking about cardiomyopathies within our clinical medicine section if you guys like this video you benefit from it please support us and the best way that you guys can do that is by hitting that like button commenting on the comment section and also subscribing another way that you can help us is go down in the description box below we got a link to our website at our website we have a lot of other things that we can offer for you great notes great illustrations

to follow along with during these lectures as well as we're developing courses on those who are preparing for the step one the step two the pants go check that out also we got some merchandise that we actually sell there so go check that out as well all right let's talk about cardiomyopathies so cardiomyopathy is a disease process pretty much of The myocardium that's really what it is and there's three types there's dilated hypertrophic and restrictive what we have to understand is what is the pathophysiological difference between these three when we talk about dilated thus within

the name it's pretty straightforward they're very dilated ventricles but what causes the ventricular dilation we'll talk about that in a second but the concept the pathophysiological concept is that there is some disease process that's causing the contractility to go down and we'll go over those causes now when the contractility of the heart goes down what your body tries to do is it tries to compensate right because you guys know that whenever you drop your contractility what do you do to your cardiac output you guys know this right eventually it'll drop your ejection fraction you may

drop your cardiac output so in cardiac output drops what does that do to your blood pressure it drops your blood pressure how does your body compensate for the drop in blood pressure it increases your systemic vascular resistance if you increase your systemic vascular resistance on your veins you're going to squeeze the heck out of those veins and I'm going to try to push more blood into the heart what does that do to the heart loads it with fluid so now you make it super pre-loaded right and if I increase preload and that sounds like that

may be a beneficial thing but if the heart's weak and it can barely get blood out now you're going to load it up even more and when it does that it has to compensate and so what it does is it dilates and whenever this ventricle dilates over time it thins The myocardium makes it even more weak and you know what that does when you stimulate this dilation process what this will do is is this will lead to a drop in the ejection fraction and these patients often develop what's called systolic heart failure another term that

we use is what's called Hef ref heart failure with a reduced ejection fraction where it usually drops less than 40 percent and this is usually the concept that you'll see here with dilated cardiomyopathy now the question is is this dilation well how does it occur we talk about this in cardiac pathology but just a quick little terminology that I want you guys to be aware of is we use this term it's what's called eccentric eccentric hypertrophy and what does that mean that means that you're adding these particular sarcomeres in a series process and that's what

really is triggering this dilation process that's really what the dilation is now let's actually ask ourselves the question okay we're dilating the ventricles because a reduction in contractility what is causing this reduction in contractility in other words why are these ventricles all jacked up for whatever reason causing these things to be gargantuous that's the question so let's actually remember there's a quick little mnemonic because there's a lot of causes and the mnemonic here are a little kind of helpful trick is a b Triple C D and then we'll add on two more unfortunately after that

but a is for alcohol B is for berry berry which is thymine deficiency C is for cocaine toxicity the other C is for chaga's disease which is a nasty little protozoa right we call that trypanosoma cruisy the other C is going to be very interesting this is usually probably say one of the more common causes of the virus it's called Coxsackie B virus and the last one here is actually a very common chemotherapeutic agent that we use and it's called doxorubicin all right so these are some of the offending agents in exactly the mechanism how

they cause a reduction in contractility we don't completely know but they do tend to do that there's two other ones that I really don't want you to forget as well they don't have an easy mnemonic I just want you to add them on to your mind and these other two are going to be what's called takatsubo and the other one is peripartum I think the peripartum one is a giveaway for itself it's a patient who is usually somewhere around the actual pregnancy process of either getting ready to give birth or they just given birth gutsubo

is usually something that happens when there is a generalized massive stress on the body emotional physical sometimes you can see this in patients develop like intracranial hemorrhages for some reason but it's a massive sympathetic storm but all I want you to know is that all of these particular factors here what are they doing they're reducing the contractility which is leading to this dilated cardiomyopathy okay my friends that covers dilated cardiomyopathy so we have an understanding of this process now let's move on to the next one you have this patient here and look at this look

at this chunky sucker look at this that ventricles all right why is it we'll talk about that in a second but the primary process that is occurring in hypertrophic cardiomyopathy is in the name it's hypertrophy but most of the time it's asymmetric and it usually involves the septum so we're going to say this is what's called septal hypertrophy when you have this septal hypertrophy right here right what does this do all right that's super interesting because I'd say it actually does kind of two things if you want to think about it one is it makes

it almost impossible sometimes to get blood out of the heart right so here let's X this off where it makes it hard to get blood out of the heart we call this a left ventricular outflow tract obstruction this is the left ventricular outflow attract which is the blood trying to get out into the aorta that's completely obstructed by this big old chunky septum that's one really big thing the second thing is look at the space look at how much it's crowding out that left ventricular space it's going to be almost impossible to get blood into

The ventricle as well so there's going to be some type of impaired filling process so there's going to be a decrease in the filling process but at no point in this disease process does it reduce the contractility it just impairs filling it makes it a little bit harder to get the blood out this my friends is an example of what's called a heart failure where the preserved ejection fraction so sometimes this can be in the category of what's called a half half heart fail with a preserved ejection fraction where it's greater than 40 percent and

so this is something that I want you guys to think about and we'll go over these in a little bit more detail when we get at the complications but that's the basic concept of hypertrophic cardiomyopathy but the question usually comes here is why is there so this was dilation this is septal hypertrophy and they're both hypertrophy you'll notice right so why is this one completely different well if you guys remember from pathology the way you add the sarcomeres in the septum is usually kind of like on top of one another in parallel and we call

that what concentric hypertrophy so that's that big pathology difference there okay question then arises what causes the septal hypertrophy and believe it or not it's usually a genetic mutation if it's pretty much the septum not generalized left ventricular hypertrophy because left ventricular hypertrophy can be generated from hypertension aortic stenosis anything that really increases the afterload in true asymmetric septal hypertrophy it's usually a genetic mutation and so in this particular scenario I want you to remember that this is the heavy chain myosin gene mutation oh that's actually kind of nice because this is HCM hypertrophic cardiomyopathy

that really kind of helps me a little bit to remember this whole process so this is a mutation of some sort generally involving the heavy chain of myosin that's the concept I want you to understand about hypertrophic cardiomyopathy all right last one here my friend says restrictive cardiomyopathy this one actually tends to be kind of the the interesting one super rare if you had to go from the most common to least common it goes dilated then it goes hypertrophic then it goes restrictive all right so most common to least common now with that being said

what happens here well you'll notice that there's not much of a difference here in the look of it there's no dilation there's no acceptable hypertrophy what happens is there's an infiltrative process so some kind of like substances deposit into the ventricles and when it does that it makes these ventricles super rigid and kind of like fibrotic if you want to think about it like that so now naturally muscle wants to stretch and distend this infiltrative tissue does not want to stretch or distend and so that's the big concept is there some type of myocardial infiltration

and this will reduce The Filling process so this is the concept that I want you to understand you get myocardial infiltration and what do you do to the filling process you make it very very difficult why because blood wants to come into these ventricles right and they will come in blood will come into the ventricles but what will happen is it'll feel kind of like relatively quickly and then it'll stop because the ventricle will allow for some filling but then it doesn't stretch it has no give because it is infiltrative process so because that's kind

of similar to this one and that is there's no reduction in contractility the contractility is generally for the most part preserved but it's really hard to fill it that sounds like a half path so usually in these patients they have what's called half path for the most part where it's greater than 40 for their ejection fraction and that's the big kind of difference here now you'll notice there's no hypertrophy here of any type no concentric no eccentric hypertrophy it is a infiltrative process Into The myocardium so we don't need any other pathological terms to go

here but the question is what is infiltrating right that's the cause that's what you gotta think about and generally for this one it's three particular things that I want you to remember by far the most common is going to be amylitosis so here let's write the infiltrative disease these are usually infiltrative diseases and by far the most common one that I want you guys to remember here there's going to be three of them first one is going to be amyloidosis this is going to be by far the most common the second one is going to

be hemo chromatosis and the third one is going to be sarcoidosis these are generally going to be the infiltrative processes that lead to this reduction in ventricular filling all right so now we have a good understanding my friends of the different types of cardiomyopathy when it comes to the pathophysiological differences so now what I need to do is like okay let's take these cardiomyopathies and say why are they dangerous what's the complications or issues that arise alright my friend so off to the complications of the problems that arise whenever a patient has cardiomyopathy so let's

go through each one of these so dilated cardiomyopathy that sucker is huge big ventricles due to the reduction reduction in contractility what happens with this one is they primarily present with biventricular failure so left and right heart failure this is actually should be pretty simple when a patient has left heart failure what happens is in this particular scenario their cardiac output stinks so their forward flow especially since this is systolic dysfunction is actually going to be not very good and so what happens is it's hard for them to be able to get blood out of

their heart because of the reduction in cardiac output because there is a reduction of cardiac output what happens then is the blood will actually start to back up because the pressure in the left side of the heart is going to be high and that will transmit to the left atrium and then that will transmit to the pulmonary vessels then to the pulmonary capillaries remember what that pressure is that usually arises the pulmonary capillary wedge pressure will rise when the pulmonary capillary wedge pressure Rises what that leads to is something very interesting so the pressure in

the capillaries are so high that it actually causes the hydrostatic pressure to increase and push fluid out into this interstitial space so now you have all this fluid that accumulates in the interstitial space and then into the alveoli what is this called pulmonary edema now pulmonary edema may be a finding that you have on chest x-ray but it can also be potentially evident in the way that these patients present symptomatically so one of the ways that pulmonary edema may present is you may have a patient who whenever they lie down flat when they're sleeping or

whenever they're lying down flat in general they have shortness of breath and the reason why is that fluid May kind of layer out where it's normally at the the basilar portions or the actual bases now it's going to spread out through the entire lung and worsen the actual shortness of breath so we call this proximal nocturnal dyspnea which is when they're sleeping and lying flat they have shortness of breath or when they're just laying flat orthopnia so these are the two types of features that you may see as a result of pulmonary edema the other

one is that the patient may just have generalized dyspnea so Disney is shortness of breath that they may experience when they're at rest or when they're exerting themselves depends upon the severity but these are the features that you'll see here that would be the left heart failure problems now the right heart failure is actually relatively simple the right heart fails again because there's a difficult time being able to generate enough cardiac output to push blood in this particular scenario out of the right heart so that cardiac output stinks if the cardiac output stinks where does

the blood backflow into the right atrium so the right atrial pressures will rise when the right atrial pressure Rises we use a very particular terminology because in this radiatorial pressure gets transmitted into the cava into the in-free vena cava and the superior vena cavities know what this terminology is called it's called a CVP so when the central venous pressure Rises what this does is is this causes fluid to back up into the superior vena cava when it backs up into the superior vena cava this will then back up into the jugular veins and plump those

suckers up what is that called jugular venous Ascension that's one potential feature the other thing is it backs up into the end fear vena cava plumps up the liver and causes hepatic congestion when you cause this vessel here where you can't get blood out of this dang thing so you get it all congested it causes injury to the liver and this can cause hepatomegaly and potentially even liver failure like cirrhosis so you may see as a result of this hepatic congestion which we can sometimes call hepatomegaly and that can potentially progress to liver failure so

that's one potential way that this CVP being high can cause problems another way is it can go down into the actual lower extremities and cause edema of the lower extremity sometimes when you push into it it actually kind of creates a little divot we call that pitting edema and the last potential feature here that I actually want you guys to remember is sometimes the portal venous pressure becomes super super high and the portal veins whenever they get ballooned up they start leaking fluid into the peritoneal cavity so if your portal hypertension ensues then what this

does is this causes fluid to leak into the actual peritoneal cavity and look at this when you get fluid into this perineal Imperial cavity it causes this big old belly to accumulate and this is called ascites so it's a portal hypertension related ascites these are potential features that you may see and anybody who has right heart failure but the cause of the right heart failure may be dilated cardiomyopathy all right we move on so right heart left heart failure we can also call that biventricular failure is very prominent in patients who have dilated cardiomyopathy hypertrophic

cardiomyopathy is a little bit interesting so remember that thing I told you where they have what's called a left ventricular outflow tract obstruction so it's this septum it's kind of bulging out let's make it even more bulgy we're going to bulge this puppy out it's going to be really hard to get blood out of this thing so now look it's almost impossible to get blood out of the left ventricular outflow tract so because of that they're going to get poor systemic perfusion right if the patient is really like dehydrated or they're working out and they're

really increasing their contractility and their heart rate this creates a really significant problem so what happens is they get a decrease and systemic perfusion but usually this is really really bad in certain States and what I mean is and if a patient is really dehydrated so if they have a very low blood volume or their heart rate is really high then what happens is if their blood volume is low their heart rate's very high these particular problems will really really make it even worse because you have less fluid here that means less blood even getting

out if the heart rate is beating crazy fast that means it's going to be harder for the actual heart to fill properly and then on top of that if you increase contractility that'll also do it so here we'll put in like a little increase and I'll put in Co in but just remember that stands for contractility I'll put clnt all right all of these things are going to worsen that systemic perfusion if it's bad enough where the heart's beating really fast they're hypovolemic and their heart rate's really really high you don't perfuse particular tissues and

the two tissues that I want you to know is the brain and oftentimes this perfusion is so low that it causes a transient loss of consciousness and this is called syncope so this is one potential feature that I want you guys to remember all right syncope is one another one is that you can decrease the perfusion to the heart and that's actually terrifying because now let's say that I have a portion here of the heart that's becoming ischemic so if that ischemia starts to arise what's the actual common clinical manifestation of patients who have ischemic

heart disease angina so they may develop angina due to the actual myocardial ischemic due to poor systemic perfusion so that's one potential feature the more scary feature is sometimes this can be enough ischemia to the heart if they are very hypovolemic super tachycardic high contractility that it actually can cause the patient to go into vtac or vfib so sometimes this is enough to cause the patient to go into vtac refib and sometimes these patients will even go into sudden cardiac arrest and so this is a very common clinical manifestation usually the clinical finance will present

a young kind of like maybe a 15 20 year old person who's out on the football field running around they're dehydrated they're increasing the hurt they're increasing contractility and all of a sudden they syncopize or they have some type of cardiac event that is a very common feature here now this is all due to low cardiac output right I'm having very little blood getting out of the heart but on top of that sometimes it's hard to be able to get blood out of the heart and that backs up into the left atrium and then increase

the pulmonary capillary wedge pressure and causes fluid to back up into the interstitial spaces and this is called pulmonary edema so the patient may also develop pulmonary edema and oftentimes this is very mild and these patients will present with the finding of dyspnea they'll present with the finding of dyspnea okay so with that being said there's a couple findings but oftentimes we use like a little trick to remember this I'm going to kind of put a box around them it's sad syncope angina and dyspnea are the common findings of a left ventricular rifle tract obstruction

worst case scenario is some type of fatal arrhythmia where they go into sudden cardiac arrest all right the last one here for the hypertrophic cardiomyopathy is the murmur this left ventricular tract obstruction can create a problematic murmur meaning whenever you auscultate right whenever you're oscillating and listening to the heart generally we say that like dilated cardiomat but they can have an S4 Hearts I'm sorry S3 heart sound left ventricular Alpha tract obstruction murmurs are very weird when you listen to them it will actually present kind of like a very weird systolic murmur it's kind of

like a whole systolic merman it has a crescendo de Crescendo pattern to it we'll talk about this more in the murmurs lecture but what I want you to know is some kind of differences whenever you're actually reading the vignette you can pick out which one it is so the interesting thing about this particular murmur is I want you to think about two scenarios one when the patient is like very pre-load they have very little preload all right so we're gonna have two scenarios here in this scenario where you see The ventricle is really really small

really really small in this particular scenario what happens is the obstruction gets worse what would be something that would cause the ventricle to be very very small one is they would have a very low preload all right so if they have a very low preload that means they're not going to fill the ventricle very well so it'll be a lot smaller another thing is if you have a decrease in the afterload so if I have a decrease in the afterload what does that mean that means there's less pressure in the order I can push a

ton of blood out that means that there'll be very little blood remaining in the ventricles so a decrease in preload and a decrease in afterload oftentimes will make this obstruction worse and what it'll do is it'll increase the intensity of the murmur now this may seem like okay well what in the heck would actually reduce preload and what would reduce afterload you would reduce preload by doing what maybe if you have the patient kind of like do what you have them stand up and whenever they stand up generally it kind of like actually reduces the

venous return to the heart that would be one mechanism or another one is you can have them valzava and if you Val Zava you kind of like actually help to decrease the venous return in that way as well so these would be mechanisms that would reduce the preload reducing after that we don't have any technical mechanisms but again that would also you can give like a drug called ammo nitrate very short acting and that can also increase the intensity of the murmur but this is the basic concept I want you to understand here all right

and this one super like that kind of like very compacted ventricle that makes the obstruction worse and that's going to intensify the murmur this one The ventricle is big it's a lot bigger and so because of that it reduces the outflow tract obstruction and that's going to make the intensity of the murmur decrease so what will be some particular things that would do this it's the exact opposite it's not hard so it's going to be an increase in preload and an increase in afterload what are things that would increase preload you have them squat down

when you squat you actually squeeze more blood up to the right heart the other thing is afterload if you have them squeeze kind of like hand grips that would also increase the afterload and it would make it what harder for blood to leave the heart so more of it would stay in there these are things that would actually do what decrease the intensity of the murmur that covers hypertrophic obstructive cardiomyopathy so we have the sad features cardiac arrhythmia and the murmur think about whenever it's small ventricle big ventricle and the Maneuvers that you do for

that restrictive cardiomyopathy the least common one let's blow through this puppy here right you have all this kind of like myocardial infiltrative process and this myocardial infiltrative process is going to reduce filling if it reduces filling it's going to lead to a heart failure process and what's going to happen is it's more commonly going to affect the right heart than it does the left heart that's interesting right so it's going to have more kind of like effect on the right heart than it does the left heart so this filling process is actually going to be

inhibited and so because of that the blood will back up here into the inferior vena cava and back up here into the superior vena cava what did we say it would increase the central venous pressure central venous pressure and if you increase the central venous pressure this should be a quick reminder here of all of these we'll blow through these in the Supreme vena cava plumps up the jugular veins you should get jvd if it's in the inferior vena cava it should cause the liver to get plump cause a patomegaly maybe even liver failure plump

up the legs cause pitting edema and plump up the belly due to the portal pressures and cause ascites let's write that down all right my friends so that would cover the right heart failure which is again the primary manifestation of restrictive cardiomyopathy remember dilated can cause both restrictive primarily right heart failure there's one other common feature that really helps us to distinguish patients who have restrictive cardiomyopathy from other types and this is called the Coos Mall sign very very interesting so here we have this infiltrative process in The myocardium right and this infiltrative process in

The myocardium makes it hard for the ventricles to be able to fill particularly the right remember I told you the right heart is more commonly affected than the left heart and restrictive cardiomyopathy what happens is let's say here you fill the ventricle whenever you actually go through what's called a diastole so this is the process whenever your heart's supposed to be filling with blood what happens is you take a breath in when you normally Inspire it should actually drop the intrathoracic pressure and suck blood into the right heart so naturally blood should help to move

right here but what's the disease process in restrictive cardiomyopathy reduce filling if you reduce filling it won't be able to do that and what happens is the blood will actually stay in this kind of Cava and cause it to plump up even during the inspiratory process which is super weird so we say in KU small sign there is a paradoxical it shouldn't happen a paradoxical increase in the jugular venous pressure during what inspiration there is a paradoxical increase in the jugular venous pressure during inspiration and why because it's restricting the filling process it's a hard

myocardium and it won't allow The myocardium to stretch during inspiration that's a key feature so at this point we've covered the cardiomyopathies we got down these complications let's figure out how to diagnose them hypertrophic obstructive cardiomyopathy is really important you have to be able to identify this murmur and know how to evaluate it what to do to change the murmur's intensity be it decreasing or increasing so look for that classic Crescendo de Crescendo murmur you see how it rises up Rises down between systole usually the left sternal border you may hear an S4 heart sound

you may hear that systolic anterior motion of the mitral valve Sam which causes the mitral regurgitation big thing here is I want you to know what increases the intensity of the murmur so if I do this and I have the patient try to valzava or stand what this does is this reduces the amount of blood flow coming into the heart if I reduce the amount of blood flow coming into the heart this will then cause the what happens is if there's less blood flow the septal hypertrophy will kind of increase and then it'll bulge into

the actual uh the outflow attract here more look see how it's kind of like bulging out more that's the problem so again you reduce the patient's preload you don't stretch out that LV as much and you increase the outflow tract obstruction same concept here if I decrease the afterload now the pressure in the aorta is actually going to be lower it's going to be easier for blood to leave the actual left ventricle that leaves less blood in the actual left ventricle and if there's less blood left in the left ventricle then you decrease the stretch

and you increase the awful attract obstruction so it's either again you're not filling it enough because you're not loading it or you're causing a lot to leave and then leaving very little left that's the concept so you decrease venous return and decrease after load that will increase the intensity of the murmur now do the opposite here you decrease the murmur intensity it's going to be the exact opposite scenario you're going to increase the venous return squat or lay down flat or lift their legs up what that does is it increases their preload fills their left

ventricle more stretches out that actual bulge here look at the Bulge it's not there as much because you're stretching it out and that decreases the lvoto if you increase the afterload you make depression they order higher you squeeze hand grips it makes less blood leave The ventricle if you leave less blood leaving The ventricle it stretches the vent left ventricle out more and relieves that outflow tract obstruction and that decreases the murmur intensity so remember decreasing venous return decrease afterload increases the murmur increase venous return increase afterload decreases the murmur intensity that's super key to

remember all right we got an idea now of the different types of cardiomyopathy the car the causes the pathophysiology the issues we even know how to evaluate the HCM murmur how do we approach these all now in differentiation if you see biventricular failure if you see S3 what do you think about dilated cardiomyopathy if you see right heart failure too small sign restrictive cardiomyopathy you see sad symptoms syncope angina dyspnea you hear a holocystolic murmur which is the lvoto with the different changes in murmur intensity increasing with decreasing venous return and increase afterload and then

decreasing murmur intensity with increased venous return right and decrease afterload then you think about HCM now once you have these the way that you can truly differentiate them is an echocardiogram an echocardiogram will give you an idea is their big dilated ventricles and is there a reduction in contractility systolic dysfunction that suggests dilated cardiomyopath if you go looking for the a b Triple C D causes is there an lvoto septal hypertrophy is there diastolic dysfunction does this look like HCM lastly is their biatrine enlargement preserved ejection fraction but diastolic dysfunction because the ventricles are super

rigid you think about RCM now you want to be able to differentiate restrictive cardiomyopathy from constrictive pericarditis on your exam they will try to mess with you on this what you want to look for in comparing these side by side is physical exam they will both have a kusmal sign one of the big differences though is constricted pericardites which we'll talk about later has what's called a pericardial knock restrictive cardiomyopathy does not echocardiogram constricted pericardites will have a thick pericardium a septal bounce and a abrupt reduction of ventricular filling but the equine restrictive cardiomyopathy should

be biotron enlargement and diastolic dysfunction the next thing is cardiac CT or MRI it'll show a thick pericardium but for restrictive a normal pericardium and last thing here sometimes they can do a cardiac catheterization and they can look at the actual in diastolic pressures and what you'll notice is without getting too crazy is that I want you to think about this constricted pancreatitis involves the entire pericardium restrictive cardiomyopathy usually hits the muscle and so it usually it loves to hit the septum too the septum moves a little bit with the ventricular filling process but if

the septum is thick it won't be able to move as much and change the end diastolic pressures so what happens is there's concordance of in diastolic pressures because the septum is not moving and restrictive cardiomyopathy and constrictive pericarditis there's discordance because that septum can move and if it moves it can alter the end diastolic pressures in both of the ventricles that's the concept to understand between these two just a quick chart for you guys to think about when you're actually having the exam and you have to try to differentiate between these two all right we

got a diagnostic approach how do we treat these it's so straightforward dilated restrictive cardiomyopathy will present like heart failure and so you treat them like heart failure which we again understand is what reducing the sympathetic nervous system activity I do that with beta blockers and sglt2 Inhibitors I reduce their Razz activity and I can use things like ACE inhibitors arbs or I can use AR Andis and aldosterone antagonists I can increase their BMP activity which would be via Arnis and I could decrease venous congestion symptoms through things like diuretics or restricting sodium and fluid intake

all right but here's the big one that you'll probably tested on more when it comes to the cardiomyopathy for treatment it's hypertrophic here's what I want you to think about we treat these patients by trying to reduce the lvoto and you have to go back to the murmurs which one decreased the murmur intensity is it things that you want to do I want to increase Venus return because it stretches out the left ventricle and flattens the septal hypertrophy keep these patients hydrated avoid any diuretics and avoid excessive exercises that really dehydrates them okay that's really

key the other thing is I need to increase afterload because it keeps more blood present in the actual left ventricle which will stretch out the LV and stretch out that septal hypertrophy so in this scenario I have to avoid vasodilators don't give them ACE inhibitors ARB is hydralazine amlodipine anything like that because it can actually cause their obstruction to be worse which seems odd right the other thing is I have to decrease contractility when you cause the ventricles to contract it'll actually bring the septum inwards into the outflow tract and obstruct it more things that

decrease contractility is beta blockers and calcium channel blockers that's going to be key but you know what else avoiding vigorous and crazy exercises oftentimes so what they'll present in the actual clinical vignette is a young child who's playing sports they end up having a sinkable event or they have a cardiac arrhythmia and they want to go back and play football or do whatever sport they can you can't because what happens is they can get dehydrated reducing their venous return and they increase their afterload usually with exertion and they increase the contractility all of these things

can worsen their murmur intensity worsen their lvoto and then put them into a deadly cardiac arrhythmia with that being said if a patient does develop a cardiac arrhythmia you do not want them to develop another one and so oftentimes what we will do is is we will implant in what's called an aicd which will help to be able to detect them being in an abnormal Rhythm and shock them back out of it lastly if the patient is refractory to all of these methods what we can sometimes do is is we can cut the actual outflow

tract obstruction you can do something called a myectomy where you literally are my Academia which you cut out that actual disease portion or you actually use a catheter and you take and you run some alcohol through that catheter and into this area and you ablate the actual area there that's the ways that we can do this but that covers cardiomyopathy all right my friends I hope you guys enjoyed that I hope it made sense I really hope that it helped and as always until next time [Music]