Congestive Heart Failure | Clinical Medicine

foreign ERS in this video today we're going to be talking about heart failure this is going to be again within our clinical medicine section if you guys really like this video and this helps you please support us by hitting that like button comment down the comment section and most importantly subscribe also if you guys want some great notes some great illustrations to follow along with go down the description box below check out our link it'll take you to our website we have a lot of great stuff there also if you guys are interested we are

actually developing a course for the US Emily Step 2 and pants that'll cover all of this in great detail go check that out as well and check out the merch we got some great stuff please go to our website check out all this stuff get yourself some swag all right let's start talking a little bit about CHF or heart failure congestive heart failure many different terminologies there we talk about heart failure the first thing we want to talk about is the pathophysiology behind it and really there's a couple different types of heart failure believe it

or not there's left heart failure right heart failure and this weird one called high output failure we're going to talk first about left heart failure which is going to be by far the most common type of heart failure now we talk about left heart failure we want to think about two different types or subtypes if you will of left heart failure there's what's called systolic heart failure and diastolic heart failure now what would cause this patient was a normal heart to start diverting its way into developing systolic heart failure the primary reason why this would

develop is a patient would have a reduction in their contractility so the contractility of the left ventricular myocardium is going down so there's a drop in the contractility so then you have to ask yourself the question what is causing this left ventricular myocardium to not contract what are the disease processes which would lead to this so here we're going to say that this myocardium here this left ventricular myocardium is damaged in some way shape or form and the contractility here is knocked down what's some causes one of the most common causes here by far is

going to be a myocardial infarction if a patient had an MI it's going to cause fibrosis of that tissue do you lose you lose contractility there that's one way another one believe it or not is cardiomyopathies you know which one particularly is very very commonly associated with this one it's called dilated cardiomyopathy because what happens is the the actual ventricles get really really thin and very weak that's another one where the contractility goes down another one could be myocarditis but it's relatively uncommon but we'll put that one down as well so another one could be

myocarditis so inflammation of the myocardium but all of these things would be stimulatory factors that could lead to systolic heart failure where the contractility is just not good if the contractility of the heart is not good particularly left ventricle can it push blood out of the left ventricle and into the aorta very well no and so this is where the issue occurs is that the patient has a hard time being able to pump blood out of the heart so it's a problem with forward flow there's a very important kind of like formula we're not going

to go crazy into it but it helps us determine something called the left ventricular ejection fraction and this is a very important terminology so in this person who has systolic heart failure sometimes what happens is as you drop the contractility as you drop the contractility you drop What's called the left ventricular ejection fraction which is basically the amount of blood that you're able to pump out of the heart right and so when this happens a decrease in left the contractility when that happens that goes down you drop your left ventricular ejection fraction and now it's

hard being able to get blood out of the heart when that happens what we do is we have a very specific terminology whenever the patient has a reduced left ventricular ejection fraction particularly particularly when it's less than 40 percent you know we call that we call that heart failure with a reduced ejection fraction we call this hefref and that's usually when it's less than 40 percent so when the left ventricular ejection fraction is less than 40 we call that hefref which is a another way of describing systolic heart failure but the whole point here that

I want you to understand is can contractilities down the amount of blood getting out of the heart is down so what is that called when the volume of blood that you're supposed to be pumping out of the heart and one minute goes down that's cardiac output so in these patients they will start to experience a drop in there cardiac output which we're going to abbreviate Co and that's the big highlighting Factor here for systolic heart failure or hefref heart failure where the reduced ejection fraction their causes dropping contractility due to these can diseases now when

we come over here to the other flavor of left heart failure diastolic heart failure this is another really really common one the problem here is something different in the sense that it is really hard to get blood out of the heart and there's a couple ways that blood leaves the heart right so we call that like stroke volume the amount of blood that you're kind of getting out of the heart and one heartbeat that's dependent upon preload contractility and what's the last one afterload when the afterload is crazy high in these patients it's hard for

them to get blood out of the heart and that's usually the problem here is that these patients develop a massive increase in their afterload what are diseases that would really kind of increase the afterload and cause these particular types of problems chronic hypertension can't say how common that particular etiology is that is probably going to be by far one of the most common causes so this would be a chronic hypertension we'll put chronic here what's another one you know there's a valve right here right there's a valve right here called the aortic valve aortic semilunar

valve what if that valve is super super stonotic and because it's crazy crazy snotic it's almost hard it's kind of obstructing the forward flow that would also cause a lot of afterload aortic stenosis is another really common cause here so another disease would be called aortic stenosis this is another very very common cause for an increase in afterload it's basically anything that's going to make it harder for the blood to get out of the left ventricle these two things by far are going to be the most common thing that will cause diastolic heart failure now

in systolic heart failure what do you notice about The ventricle Cooper dilated right so let's actually write that over here so this is a very dilated enlarged ventricle what you're going to notice here is that this is super hypertrophied this ventricle is very hypertrophied so you have what's called hypertrophy it's a very thick and large left ventricle we call that left ventricular hypertrophy or sometimes abbreviated LVH now the reason why is think about this if the pressure in the actually aorta is so high that you have to overcome it what what's one way that you

can do that get stronger and thicken up the left ventricle but when you do that when you thicken up this left ventricle and you make it to where you're actually able to generate higher stroke volumes the problem is now is that you decrease the actual space of the left ventricle and now my problem is that I can't get the damn blood into the left ventricle I can't fill it properly and so this issue is a filling issue this was a forward flow issue so what do I notice here in this particular disease process the problem

with diastolic heart failure is that they have a reduction in their filling process so there's a decrease in there left ventricular filling and because I can't fill the ventricles very well that's going to cause a problem now here's the thing they're left ventricular ejection fraction is completely fine it's usually completely preserved so this filling process won't affect the ejection fraction so their left ventricular ejection fraction is usually what we refer to in this case as normal or let's use the term preserved and so that's where we get this term a heart failure with a lowercase

p preserved ejection fraction where if we were to give it a particular number it's at least greater than 40 percent so in these patient populations of diastolic heart failure their filling is reduced because their ventricle is super super hypertrophied that causes their left ventricular ejection fraction to be preserved and they have what's called a half path but here's the question this has a low cardiac output because of low contractility this will also have a low cardiac output you guys know why why this one will have a low cardiac output this will have a low cardiac

output because again think about your physiology guys it's very very important to understand physiology here if I have a decreased filling I'm not going to load my ventricle very well so I have preload is going to drop if my preload drops what happens to my stroke volume that goes down if stroke volume goes down what happens to my cardiac output that goes down so both of these patients will have a low cardiac output but the primary difference here is that this is a preserved EF because they have no problem with the rejection fraction no contractility

problem this one has a reduced ejection fraction because they have a contractility problem dilated ventricle hypertrophy ventricle super high yield can't forget these things understanding the causes high afterload understanding the causes contractility problem okay now we get into something that I think is really really important and I think can often be overlooked when patients develop heart failure because of these issues it can continue to get worse and worse and worse if not treated let me explain why when cardiac output goes down this is going to go back a little bit to your physiology here when

cardiac output goes down what we know is there's always that formula do you guys remember the formula uh for blood pressure the formula for blood pressure is you have this one here that blood pressure is equal to cardiac output times systemic vascular resistance in patients who have heart failure what's the problem here their cardiac output drops and then if you were to say keeping this normal or constant what would happen to their blood pressure that would also drop so then what's the general compensatory mechanism that our body tries to create we'll do this in pink

svr has to go up and so this is usually what ends up happening to the body is the body creates this weird mechanism to try to increase your systemic vascular resistance which causes a lot of problems let's see what that looks like so the reason why you may be like Zach I really don't want to know this this is kind of like foundational stuff it's very helpful for your pharmacology and understanding I promise so here critic output is low normally what this will do is a couple different things you know there's a those Barrel receptors

and bear receptors are located in like your your carotids like right at the bifurcation or the aorta and they sense changes in cardiac output and blood pressure and so what happens is you're going to stimulate these things called Barrow receptors and they're going to go and they're going to activate your sympathetic nervous system when your sympathetic nervous system becomes crazy activated it's thinking to jack up all your epinephrine and norepinephrine release so then what you're going to see is you're going to see a lot of epinephrine and you're going to see a lot of norepinephrine

increasing why is that a problem well the reason why that's a problem is is that these little chemicals here they love to go to the heart and to your vessels and cause some problems they go to the heart and they say hey why don't you speed up the heart rate because if you speed up the heart rate that'll increase the stroke volume hopefully increase the critic output but it's not good for a patient's heart rate to be super high but that's one of the potential compensations is you're going to increase the patient's heart rate oops

sorry guys you're going to increase the heart rate and again this is because it acts on what's called beta 1 receptors this is going to become helpful I promise the other thing is it acts on other types of receptors like alpha-1 receptors on your vasculature and causes it to constrict and if you constrict these vessels what happens to the diameter of them they get smaller what happens to the resistance it goes up so my svr will go up and if that happens on the artery side what's that going to do in my afterload it's going

to go up and so it increases the afterload now you're like that sounds like a terrible thing it is terrible because think about this if a patient has diastolic heart failure and you increase their afterload what are you going to do you're going to worsen their diastolic heart failure because now if their afterloads High what does their body try to do to compensate it hypertrophes and it's going to worsen their already present heart failure so this is going to be it's going to trigger hypertrophy and guess what that's going to do that's going to worsen

their heart failure and they're going to get sicker and their heart failure is going to get worse the other thing it's going to do is it's going to constrict the veins because there's alpha 1 receptors on both the arteries and there's Alpha interceptors on both the veins so it's going to squeeze the veins and try to push a lot of blood back to the heart and that's going to try to increase the preload but then if you increase the preload now the ventricles have to dilate to accommodate for that volume and if the ventricle dilates

what does that sound like systolic heart failure so it's going to worsen the patient's systolic heart failure so this is why it sounds like these things are kind of like a good mechanism to try to increase your svr that's what it's trying to do is increase the svr to increase your blood pressure right but unfortunately it worsens the patient's heart failure and their heart rate another thing if that wasn't enough is this cardiac output is going to stimulate these like weird cells in the kidney called juxtaglomerular cells and these juxtapoor cells are very sensitive to

blood pressure and what they'll do is they'll release a molecule called you guys already know this right ran in all right so it's going to release a molecule called renin now renin will then do what it'll then lead to the formation of angiotensin one Angiotensin one will then lead to the formation of angiotensin two what's the enzyme that stimulates that process Ace don't forget that Angiotensin II can do a couple things but one of those things is it increases aldosterone release from the adrenal gland and it also increases ADH release from the poster pituitary now

with all of this being said what's the overall effect of all of this I'll show you Angiotensin II works on your vessels you get a lot of Angiotensin II receptors on your your vessels so here let's say we have what's called a Angiotensin II receptor here in your vessels guess what it does squeezes the heck out of them what'd that do svr goes up because that's the compensatory mechanism if svr goes up then what happens to your afterlook that goes up what happens if you have diastolic heart failure you worsen the hypertrophy patient's getting sicker

that's not helpful what happens if you do the preload you're going to cause more blood to get returned to the actual heart preload goes up but in a patient who has systolic heart failure what is it going to do it's going to dilate their heart even more and worsen it so you guys get the concept here is that this is another potential problematic issue that can worsen the patient's heart failure and that's why we have drugs that we'll talk about a little bit later that I'm going to kind of preemptively kind of covering here that

this will help to treat because we just don't want to have these high angiotensin two levels the high sympathetic nervous system activity and just to complete this concept aldosterone ADH will be higher and you know what this does this increases your reabsorption now the patient's reabsorbing lots of sodium and water and if you reabsorb sodium and water what is that going to do it's going to cause the patient to retain a lot of this fluid and they're going to start developing edema they'll have more preload so the hot ventricles will have to dilate more but

one of the problems that you'll see here is they'll start developing a lot of Edema because of this so this is the concept that I really really want you guys to be able to understand here with this nasty disease process there's one more thing which is actually super cool though so this system here is called the renin angiotensinaldastrin system right you know whatever your heart your critic output is really really low another really interesting thing that happens is is that your heart whenever it's like really low cardiac output the hearts actually kind of get filled

with blood and so they can release this molecule in response to a lot of stretch so let's say that the heart is really really being stretched it's being stretched a lot when the heart is being stretched a lot it makes a molecule called atrial natureuretic peptide and it makes a lot of it and the whole point of increasing this atrial nitritic peptide is it wants to go and inhibit the hope is that it inhibits Angiotensin II and if I inhibit Angiotensin II I prevent this whole disastrous process from occurring well that's cool I would really

like drugs that increase amp then I would really like drugs that decrease Angiotensin II block aldosterone and block the sympathetic nervous system and that's we'll talk about in the treatment section but this is what I want you guys to understand about left heart failure now let's quickly go through right heart failure and high output failure bye my friend so now we got to talk about right heart failure so we talk about the left heart failure the right heart failure is actually a lot easier when we talk about right heart failures the same kind of concept

we take this normal heart and we jack it up to cause systolic heart failure now when we talk about this it's again you're dropping what the contractility so what generally drops contractility on that right heart well in the left heart the most common cause was an MI guess what it would be here in mi okay so generally a right ventricular Mi is going to be the most common cause generally of this systolic right heart failure so you're dropping the contractility here and that's leading to the formation of the systolic heart failure now again what you're

going to notice is that this puppy's going to start be getting super dilated all right so what you're going to notice is this dilated type of right ventricle now another concept here with this dilated right ventricle here is that your right ventricle the contractility is reduced right so this whole right ventricle let's say is really really messed up because it's messed up it's going to have a hard time being able to pump blood out into the pulmonary artery right so it's going to have a hard time with forward flow so what you'll notice out of

these patients is that they're going to have a low right ventricular cardiac output right because of the contractility and so because of that they're going to have this low contractility this is going to lead to a decrease in their right ventricular ejection fraction now we don't generally give these you know as we compared prior the heart failure with the reduced ejection fraction that's primarily only consistent with left heart failure but again you can think about it in this particular way but again a reduction in contractility will lead to a reduction in the right ventricular ejection

fraction and the problem is that these patients are going to have a hard time generating a good cardiac output out of the right ventricle and so that's the concept here it's pretty straightforward something is decreasing contractility because you infarcted the right ventricle in the other aspect over here you have something increasing the afterload right so if I have something increasing the afterload in the example for left ventricle it was hypertension it was aortic stenosis for this one it's anything that increases I'm going to put a little parentheses here anything that increases the pulmonary vascular resistance

so for the art systemic circulation was called systemic vascular resistance that was hypertension oreatics aortic stenosis and this thing it's anything that causes pulmonary hypertension so we say this is pulmonary hyper tension and there is different types we'll talk about this in poem when we go over pulmonary hypertension but there's type 1 which is idiopathic type 2 which is due to left heart failure type 3 due to some type of like lung disease like COPD or interstitial lung disease Type 4 due to some type of chronic pulmonary emboli and then type 5 is there's usually

something like sarcoidosis like something compressing the pulmonary vascular but this is the concept I want you to understand pulmonary hypertension for right heart failure systemic hypertension for left heart failure for that diastolic type now what do you notice here about this right ventricle is thick right so they have some hypertrophy generally of that right ventricle so we could say a right ventricular hypertrophy and this is usually because that ventricle is going to have to thicken to be able to accommodate the high pressure of the pulmonary vasculature that's the only way it can do it and

so because of that it's going to have a hard time being able to fill with blood so the problem with this situation here is the same concept they have a reduction and right ventricular filling which caused them to have a again a normal ejection fraction they don't have a problem with their ejection fraction so they have a normal right ventricular ejection fracture so again decreased filling process but normal right ventricular ejection fraction that's the big kind of thing that I want you guys to understand here now again remember both of these are going to have

a reduction in right ventricular cardiac output it's just again the mechanism behind them developing this all right that covers this one for right heart failure the pathophysiology and the causes what about this weird one there's this weird entity called high output heart failure and generally high output heart failure is particularly only consistent with generally left so the left heart and what I want to do quickly is talk about this one so for the most part what you've noticed is that when we talk about left heart failure before is that there was a low cardiac output

and then would you talk about right heart failure there's a low cardiac output there's this weird entity in the world where this is called a high cardiac output heart failure like what that seems odd it is weird but here's let me let me kind of explain why this happens and this patient here we see that their vessels are super dilated so they have extremely super vasodilated blood vessels so what you'll notice here out of these patients is they have a massive vasodilation all right and when you vasodilate vessels that's a big ding we'll talk about

what causes this but this is massive vasodilation right so there is massive vasodilation here the question that you have to ask yourself is what's causing these vessels to become super super dilated and there's a bunch of different things one reason is very common is sepsis sepsis will cause massive vasodilation another one which is an odd one is when you have thymine deficiencies such as berry berry this will for some reason cause massive vasodilation thyrotoxicosis so when patient has thyroid storm this can also cause massive acetylation other kind of interesting things could be things like AV

fistulas as well as severe and I mean really really severe anemia these are particular things that in these diseases but I would say sepsis being kind of one of the most common ones these will cause massive vasodilation when you massively visually dilate these vessels what happens to the systemic vascular resistance now soccer's huge resistance has got to be low so now there's systemic vascular resistance is crazy crazy low now go back to that formula what was the formula called for everything with low or how output heart failure we said that we have blood pressure is

equal to cardiac output time systemic vascular resistance and all the ones that we talked about cardiac output was low which dropped the blood pressure now in this disease process the systemic vascular resistance is low which will cause the blood pressure to be low what has to compensate the cardiac output and that's why we call this high output heart failure so then what happens is when your systemic vascular resistance drops what it does is it creates a reflex kind of situation here so what it does it'll drop the blood pressure So the patient's blood pressure may

drop when you drop the patient's blood pressure what that's going to do is it's going to activate the sympathetic nervous system and the renin angiotensinaldosterone system and that is going to increase the sympathetic nervous system now look at this if I increase the sympathetic nervous system that's then going to go in work on the heart and when it goes and works on the heart it's going to work on a bunch of different components here one is you have your SE node your AV node your bundles of hiss and bundle branches that's all going to be

activated and your heart rate is going to try to go up because it's going to hopefully try to increase your cardiac output and you're going to contract your heart like a son of a gun so then on top of that you're going to try to cause the heart to really really contract in the stroke volume will go up and both of these are going to be an attempt to try to push as much blood possible out of the heart so what you'll notice here is that these patients will have a massive increase in their heart

rate and a massive increase in their stroke volume but here's what's really odd you would think okay these guys are pumping and I mean pumping blood out of their heart into the coronary I mean into the systemic circulation so the cardiac output has to be high enough right it's got to be good enough to be able to meet the actual tissue demands it's not and that's where the problem here in the cycle occurs this disease causes vasodilation leads to this whole process tries to increase the cardiac output but no matter what it's not enough to

meet the body's demands and so what happens here is it's not enough and that's the issue so you see how we talk about heart failure it's the inability to perfuse the tissues and meet their demands that would be a definition then so high output heart failures the cardiac output's high but it's not high enough to overcome this massive vasodilatory effect to meet the tissue's oxygen demands and that is heart failure so so far we've gone over left heart failure low output right heart failure low output and the Rarity of high output heart failure now let's

go over what are the complications of a patient developing heart failure all right my friends so now if a patient has left heart failure whether that's diastolic or systolic heart failure or right heart failure whether it's systolic or diastolic heart failure we have to understand the particular complications that can arise when a patient has left heart failure one of the big things that you'll see with these patients is features of pulmonary congestion so either way the patient's cardiac output stinks they're not able to not get enough blood out of their left ventricle so what happens

is because they have a cardiac output that is being reduced if you will in other words and these patients it's hard to get the blood out of the heart because of why because they have a reduced cardiac output now because of that if the blood can't get out of the heart where is it going to go it's going to start backing up into the left atrium when it backs up into the left atrium it goes into all of these like cute little pulmonary veins here you see it starts moving into the pulmonary veins and then

what happens is it starts kind of like congesting these pulmonary veins intensely now when the pulmonary veins start coming very very filled with all of this Blood the pressure in those go up and we specifically use a terminology here called pulmonary capillary wedge pressure so we'll use that on both of these here and this will go up and the pulmonary capillary wedge pressure is a measure of left heart pressures so if the left heart pressure is high the pulmonary capillary wedge pressures will also be high when that happens the pressure in the pulmonary capillaries rise

enough that guess what starts leaking out of these actual vasculature fluid so you're going to have fluid leaking out of this vasculature and into the interstitial spaces and into the alveoli so now this alveoli is going to become filled with fluid you're going to develop some edema here in the interstitial spaces and now these patients have pulmonary edema and so this is one of the potential complications is they get a little bit of pulmonary edema now why is that bad when you have pulmonary edema some patients can present a couple different ways one is they

particularly present with what's called dyspnea now dyspnea it may just be a generalized Disney this may be with exertion this may be at rest and that depends upon the severity of their CHF but another very interesting presentation is that whenever these patients lie flat the fluid tends to kind of like kind of separate out into multiple parts of the lungs normally they'll be in the dependent inferior portions but as you lay flat this edema can become worse and spread throughout multiple alveoli and this can worsen their actual shortness of breath when they're laying flat and

so there's two terminologies one is called proximal nocturnal dyspnea this is whenever they're at their sleep and they're laying flat they're super short of breath or just in general maybe they're not sleeping they're laying down flat or laying on a recliner and they have some shortness of breath there it's the same concept it's called orthopnia These are big big common features that we see with pulmonary edema one is just dyspnea whether it be exertion or rest or the other one is when they're laying flat proximal nocturnal dyspnea orthopnia another potential problem here is that whenever

these patients let's say they really really have a massive reduction so let's say that their cardiac output massively reduces maybe for whatever reason common triggers for patients to develop what's called acute decompensated heart failure is they have an MI or they have a massive tachyarrhythmia or they stop taking their their medications they're supposed to be taking and what this does is this massively drops the cardiac output massively increases the pulmonary capillary wedge pressure and worsens their pulmonary edema like terribly and sometimes this pulmonary edema can be severe I'm talking severe pulmonary edema and this is

something that we would generally see when a patient has what's called acute decompensated heart failure and what happens is is this fluid will really start kind of like like all over multiple different alveoli and interstitial spaces will become filled with fluid and this can cause a massive VQ mismatch when you fill up multiple alveoli with fluid that causes a VQ mismatch decrease in ventilation normal perfusion there's a mismatch and that leads to hypoxemia so watch out for a VQ mismatch here and what will happen is the patient's spo2 will be very low and they can

exhibit features of what's called hypoxia the other thing is that this fluid that leaks into the interstitial spaces when it actually does leak there sometimes it may just cause the patient to have generalized dyspnea or increased work of breathing so they may be working hard to breathe or they may have a higher respiratory rate so that's another kind of thing that you want to watch out for is watch out for an increased work of breathing or an increased respiratory rate so these are some of the big findings that you want to watch out for so

again watch out for a stimulation of VQ mismatch because of all of these alveoli being filled with fluid and then hypoxia so watch their O2 sat to see if they have desaturations this is super super common in left heart failure so big things to look out for is go to the patient see if they have any respiratory distress or hypoxia on their O2 saturation ask them if you have any shortness of breath at rest exertion or they're laying down flatter when they're sleeping the other thing get your stethoscope that you paid so much money for

and go and listen and see if you hear any rails or crackles all of these are potential signs of pulmonary edema this is very common in left heart failure the scariest complication that I say that you would potentially see in a patient who has left heart failures cardiogenic shock and this is definitely the scariest one generally again a very common trigger here that can happen is an MI a massive tachy arrhythmia or you stop taking your medications these are very very common triggers now again same concept the patient has a massive drop in their cardiac

output if you drop their cardiac output you're not going to be getting enough blood flow out of their heart when you don't get enough blood flow out of the heart particularly enough volume you drop that cardiac output what happens to their perfusion oh that's stinky that systemic perfusion goes down so not only whenever you have a low cardiac output do you have a hard time getting blood out of the heart and it backs up into the lungs but you have a hard time getting it out of the heart and delivering it to multiple tissues when

you have a decrease in systemic perfusion the problem with this is that your body kind of says okay perfusion is kind of stinky right now the credit that's because the cardiac output is really low you know what the body tries to do is it says okay what I'm going to do is if the cardiac output is low what's that formula BP is equal to cardiac output times the systemic vascular resistance let's write that out so BP is equal to cardiac output times the systemic vascular resistance and these patients who are in cardiogenic shock this is

low causing this to be low what has to compensate my friends svr and this will shoot through the roof and when svr goes up it's clamps down on your vessels squeezes them and now you have very little blood flow going to your extremities you know what this is going to do this is going to cause these patients to have very cold or pale extremities another really really terrifying sign here is they have like modeling this is really really kind of scary it's where they have this weird kind of discoloration usually at the knees and that's

a very sign of that's a very poor sign of perfusion and this is usually because you're clamping down on those vessels to compensate another thing is that when you have decreased systemic perfusion not only do you create this reflexive vasoconstriction but you also get organ malperfusion right if I have organ malperfusion oh man that ain't good because now I'm not perfusing various tissues what are some of these tissues that actually become effective because of an increase in more organ malperfusion one is the brain the brain is super sensitive to blood pressure the coronary circulation which

supplies The myocardium of the heart well it's going to make things a lot worse it becomes very susceptible the kidneys become susceptible and the git would probably be the last one of the line but it's also super susceptible if I don't perfuse the actual brain you know then I can develop encephalopathy and this is probably going to be one of the most common causes sometimes if the actual mouth perfusion is severe enough it's possible it could cause a TIA CVA all right that's another thing you want to watch out for the other thing is that

if you don't profuse the actual myocardium well enough it may cause a myocardial infarction so you may see things like an n stand me or a stemi potentially so these are things that I think are really really important to remember the other thing is it may stimulate son of a gum it may stimulate injury to the kidneys this is called an Aki there is a very common terminology that you may hear here when patients have very severe left heart failure and they don't perfuse their kidneys very well because of decreased systemic perfusion but also their

cvps are really high so it's hard to get blood out of the kidney they can develop kind of something called cardiorenal syndrome very common trigger of Aki so don't forget that one and the last one is they may cause acute mesenteric ischemia this is another really really big one or ischemic colitis and this is another big trigger so you're going to want to watch out for any kind of like bowel ischemia and abdominal pain the last thing that's always a feature of systemic perfusion that's being very very poor is your tissues whenever there's very little

oxygens being delivered to the tissues so here this tissue is supposed to be getting oxygen if it's getting very very little oxygen they do not like that and what they do is they trigger the production of a molecule that's usually a sign of poor perfusion you guys know what that's called lactic acid but lactic acid gets broken down into lactate and so you want to watch out for this because one of the things that this will do is this will really cause the pH to drop and it'll trigger an acidosis so watch out for acidoses

that can occur in the setting of cardiogenic shock so again when a patient has heart failure it can kind of look a little bit different the patient may have chronic CHF where their primary symptom may just be dyspnea peroxism nocturnal dyspnea orthopnia but if they develop an acute decompensated heart failure from those triggers Mi tachyarrhea is medication non-compliance they can develop severe pulmonary edema hypoxia respiratory distress and most patients who have chronic CHF they may just have minimal decreased systemic perfusion and the way that they compensate is an increase in systemic vascular resistance so they

may have cold kind of pale modeled extremities but whenever it's really bad to where there is an acute decompensated heart failure due to an MI tachyarrhythmias medication non-compliance now they don't perfuse multiple organs and they can develop things like encephalopathy Mi Aki and acute mesenteric ischemia and lactic acidosis these are big things to think about my friends all right we come to the last one here patient has right heart failure all right so the patient is Right heart failure was because they had something wrong with the contractility or the high after the pulmonary hypertension this

one's super easy thank goodness whenever the right heart is Damaged what happens is again the whole concept here is that it's either you can't fill it or you can't get blood out of it right so that's either one of those Concepts you can't get blood in or you can't get blood out of it when that happens what happens is the pressure in the right heart increases and we use a terminology to really describe that and that's called your central venous pressure so your central venous pressure becomes very high when your central venous pressure is high

what happens is the blood is is kind of a measure of the blood backing up into your superior vena cava and blood backing up into your inferior vena cava and what this will do is this will kind of present in two different ways that you want to try to look for one is it'll present with a patient having a lot of jugular venous distension so they'll have a plump jugular vein and the other one is they'll have some edema of their lower extremities usually what's called pitting edema so when you press on it it kind

of really dips in and gives this kind of deformity there this is super common in right heart failure another common presentation again regardless of the type whether it's problem filling or problem getting out the concept is the same is that you have a very high central venous pressure when your central venous pressure is high the blood is going to back up into the inferior vena cava and what it does is it causes one particular problem which leads to hepatic congestion so you know the liver I'm kind of zooming in on a basic model of the

liver let's say this is a liver cell this is an artery this is the hepatic veins which empty into the IVC and this is a biliary duct whenever this hepatic vein is congested and it can't get blood to go up it congests in the liver and causes the liver to become injured and damaged and you know what this could potentially present as this could cause a patient to develop liver failure more specifically I would say you see this more commonly as a serotic kind of presentation but you can see this as a potential trigger of

liver failure because of the increased hepatic congestion all right the other thing that it can do is it can increase your portal pressure so what happens is your hepatic veins what happens it can actually cause this to really cause the portal pressure within the venous circulation the hepatic portal circulation to become very very high so if you increase your portal pressure what this does is this causes the hydrostatic pressure in the portal veins and the peritoneal capillaries to be super high and leak fluid into the abdomen and when you leak this fluid into the abdomen

what do we call this type of fluid that leaks into the abdomen ascites and so that's another very very common presentation here is ascites so watch out if a patient develops liver failure and they have a history of right heart failure think about that if they have ascites and they have a history of right heart failure think about that and again if they have very plump jugular veins and pitting edema think about a right heart failure and the last one it's not commonly thought of but it can happen left heart failure we talked about cardiogenic

shock right heart failure can also get cardiogenic shock so think about this this concept is super interesting in this situation here you're having let's say blood difficulty this is more common in the systolic types where the right ventricle is super dilated in this situation you have problem getting blood out of the right heart and because of that now this right ventricle has a hard time if it becomes super dilated maybe it can't fill properly or it just can't get blood out of the heart when that happens because you can't get blood out of the heart

the right ventricle dilates even more so if it's dilated before it dilates more all right so now this sucker is huge so whenever this happens you can't get blood out of the heart it's going to stimulate the right ventricle to dilate even more when the right ventricle dilates more the next thing it does is is it causes the septum to Bow over into the left ventricle and now look at the space of the left ventricle it's smaller so then it causes it's called a septal shift so a septal shift and we'll say that this septal

shift is occurring from right to left from the right side to the left side what that does is it makes it hard for the left ventricle to fill with blood because now it's much smaller if it can't fill with blood what happens to the left ventricular cardiac output it drops so now you have a septal shift and that's going to cause a decrease in the left ventricular filling if you decrease the left ventricular filling that is going to then do what that is going to decrease the left ventricular cardiac output and if you decrease the

left ventricular cardiac output oh son of a gun that can potentially lead to systemic malperfusion and then if we go on further cardio genic shock so this is a pretty scary one I'm actually usually we don't see this one too often right heart failure causing cardiogenic shock but when you do it's pretty terrifying because it's a really really bad one but this is another potential one that I want you to think about but you really primarily only see this one with right ventricular Mi as the particular etiology here not so much the pulmonary hypertension causes

all right my friends that covers the issues or complications if you will of heart failure it's a pretty disastrous thing if it gets really really bad what I want to do now is I want to take you through how to diagnose heart failure first thing is get a chest x-ray this will help you because if they have cardiomegaly that's somewhat helpful do they have pleural effusions pulmonary edema and curly B lines that's all suggestive of left heart failure for the most part now with that being said if a patient has these findings that doesn't Define

or determine that they have heart failure I want to combine oh they have pulmonary edema pleural effusions is their left heart not doing a good job well one way I could say if their heart is not doing a good job is I can check BMP this is not a good test though it's usually used in the emergency department to kind of quickly exclude a CHF exacerbation because if BNP levels are really low then you can say Okay their Disney is probably not from a CHF exacerbation if it is really high then you can't rule that

out the better test as an echocardiogram because it's going to look directly at the heart and it's going to look to say hey what's the rejection fraction is it less than 40 percent their left ventricle doesn't look like it's moving at all that's systolic heart failure or does it look like the left ventricle is Contracting and pumping but it's not filling properly oh that's diastolic heart failure in combination with the chest x-ray that can be very beneficial also do your physical exam if you don't see anything on the chest x-ray look at the jvd look

at the legs look at the abdomen to look to see if they have any features of systemic congestion and combine that with their Echo after you've done that you should be able to determine is it right versus left that's pretty straightforward now the most definitively diagnostic test to determine if the patient is in acute left heart failure or in left heart failure in general is to do a right heart catheterization also referred to as a swan guns catheter you take a catheter you run it down the IJ you run it into the pulmonary into the

right atrium into the pulmonary artery and up into these like pulmonary artery capillary areas inflate the balloon and then measure the pressures I told you that the pulmonary capillary wedge pressure if it's really high that's very suggestive of failure of the left heart and if it's greater than 18 millimeters of mercury that's a very suggestive number of left heart failure so if a patient has elevated B and P levels and Echo and a pulmonary capillar wedge pressure greater than 18 in combination with a chest x-ray suggestive of pulmonary edema I can really be confident in

them having left heart failure now with that being said if a patient has acute left heart failure it's important to go through their medication list and look to see what their heart rate is and look to see if they have any valvular disturbances but one of the big ones that I have to do is get an EKG and also consider a left heart cath if I think they're having an MI because that's going to find the occlusion and then treat that and that might be the thing that knocks them out of this acute heart failure

potentially all right how do we treat heart failure this is a really really important topic when I treat them I specifically went into this for a reason I want to reduce sympathetic nervous system activity reduce Razz activity and increase amp activity and if you remember increasing amp activity did what decrease Razz so my goal is to decrease sympathetic increase decrease sympathetic and decrease Razz how do I do that well if I decrease my sympathetic nervous system I have to use things like beta blockers and sglt2 Inhibitors so metoprolol Carvedilol or impact of losing usually these

sglt2 Inhibitors are very very important patients with diabetes but if they have cardiovascular disease it's also beneficial and what happens is they reduce the sympathetic nervous system that reduces the heart rate and that also reduces the systemic vascular resistance I don't constrict the veins I don't constrict the arteries as much I don't reduce I don't actually cause changes in preload and afterload and I don't cause ventricular remodeling that improves ventricular function that's mortality beneficial right there the other thing is that sglt2 Inhibitors also cause aquauresis they Cause you to pee out of tons of water

and so that can help with a lot of the edema if the patient is edematus the next concept is I want to reduce Razz activity so the reason why is one of our low cardiac output again we said increased sympathetic and low credit output activate renin so renin leads to eventually Angiotensin II but if I give them a drug called an Ace inhibitor that blocks Angiotensin 1 from being converted into Angiotensin II if I also give them a drug like an AR and I that increases amp it prevents amp from being degraded if amp builds

up it shuts down Angiotensin II and then if I also give an ARB our blocks Angiotensin II from binding to receptors all three of these drugs will help to decrease Angiotensin II if I decrease Angiotensin 2 I reduce the constrictions of the arteries in the veins and I have reduced ventricular modeling and that's a mortality benefit another thing is Angiotensin II if there's less of it there's less aldosterone and also ADH but particularly aldosterone because now there's less sodium and water retention if I don't retain as much sodium in water I don't have as much

edema but I also don't have as much preload and I don't cause ventricular remodeling that's where aldosterone antagonists would be really really beneficial in shutting down aldosterone production this is the concept and these are the drugs that we have to incorporate in patients who have heart failure because they have mortality reducing benefits okay that's a part of our guideline directed medical therapy other things that we can add on with guideline directed medical therapy is Alternatives so if patients African-American they can't tolerate an ace inhibit or an ARB hydralazine and isosorbide nitrate is a good combo

to add because they're good vasodilators the other one is an alternative to a beta blocker if they're maxed on a beta blocker and they are a normal sinus rhythm I have a braiding can be considered if you want to help them to get rid of a lot of the sodium and water retention you can make them pee it out by giving them diuretics Loop Diuretics and thiazide diuretics and then the next thing is if a patient has the need for device therapy so what I mean by this is if a patient has heart failure especially

left heart failure it stretches out the left ventricle and kind of causes left bundle branch blocks and then that alters the synchrony of the ventricles if I give them what's called a CRT cardiac resynchronization therapy it'll make sure that the ventricles are Contracting kind of in Tandem and improve potentially the left ventricular ejection fraction I should definitely be instituting that in patients with an lvef less than 35 percent in an lbb B all right that's a CRT if a patient has a left ventricular ejection fraction less than 35 percent and they have ventricular arrhythmias they

need to get an aicd this will shock them if they go into vtac or into v-fib and prevent them from going into cardiac arrest the next thing is if a patient is on all these medications they have device therapy their left ventricular ejection fractions less than 25 percent they're not looking good and they look like they're going to need a transplant sometimes we will play something called an lvat a left ventricular assist device which will take blood from their left ventricle and shunt in a different direction into the aorta to give that left ventricle some

time to rest now and patients who are in cardiogenic shock all right they're systemic perfusion stinks I want to have one primary goal which is to increase systemic perfusion so increasing systemic perfusion is very beneficial in patients who are in cardiogenic shock so what could I do ionotropes or mechanical circulatory support one way I can do that is I give them things like dobutamine or melanoma these are commonly used in acute decompensated heart failure cardiogenic shock the benefit of these is that they reduce afterload and increase contractility which combined increased cardiac output the downside is

that evidence has shown no reduction in mortality the other drug is digoxin this is an oral and IV drug so you can take this outpatient you can't take these outpatient this you can give to the patient and it's been shown to increase contractility and decrease AV node conduction so it's good in atrial fibrillation as well it is not shown to reduce mortality but it may reduce the actual hospitalizations so there's a potential benefit to digoxin and increasing perfusion especially in patients with cardiogenic shock and even as an outpatient continuing that drug if the patient is

failing these inotropes and they're continuing to decompensate and showing signs of potential failure then we go to device therapy and there's two ways that we could go here an intraoric balloon pump has been shown to at least preserve coronary perfusion so this sucker deflates during systole to get blood to go forward and then it actually inflates during diastole so here during diastole it inflates and it keeps the pressure all here and they order really high and what that does is guess what comes right off the aorta here the coronary arteries so if the pressure is

high in the order during diastole it's going to improve coronary perfusion and improve myocardial contractility and that's the benefit of this most times patients who end up on cardiogenic shock refractory to a lot of medications such as dobedamine mil Renown androtic balloon pumps may require something called VA ECMO this is called venal arterial extracorportal membrane oxygenation we take a catheter we run it into one of their veins we run it out of the vein and into a pump from there we run it through an oxygenator and then we put it in a catheter that runs

right into their artery these are Big stinking catheters and they are designed to be able to help to maintain a decent amount of flow and augment the cardiac output and also oxygenate the blood so this is a potential beneficial therapy that could be used as a patient refractory cardiogenic shock the other thing I think that's important to remember in a patient who's in cardiogenic shock or having any signs of cardiogenic pulmonary edema is what's called BiPAP using diuretics to help to get rid of some of the sodium and water which will help to reduce some

of that actual pulmonary edema but BiPAP has been shown to potentially increased answer thoracic pressure and that will help to reduce right ventricular preload so you don't have as much blood going to the right heart and you don't have as much blood going out of the right heart so now less blood is going through the pulmonary circulation and going to the left heart if there's left blood less blood going that way that's going to have less blood leaking out into the pulmonary interstitium less pulmonary edema the other concept is it drops your left ventricular afterload

so the pressure in the orders drops so it's easier to get blood out of the left ventricle into the aorta so you have less blood coming to the left heart and you have more blood going out of the left heart that's going to improve your cardiac output and reduce pulmonary edema but more particularly reduce pulmonary edema and that's one of the benefits of this drug in patients who are in acute heart failure or potentially cardiogenic shock all right I know this is a lot let's go through this in a systematic approach a patient comes in

they have heart failure you've changed their modifiable risk factors after that you start them on an Ace inhibitor or an ARB all right plus a beta blocker they're still symptomatic give them diuretics to reduce venous congestion whether systemic or pulmonary they're still symptomatic add-on aldosterone antagonist and an sglt2 inhibitor they're still symptomatic and they're potentially unable to tolerate an Ace inhibitor in ARB well switch them switch to an AR and I if possible so an Angiotensin receptor neprolysin inhibitor so this would be things where you put them on like succubutril um valzartan so these are

very good drugs that have been shown to be very beneficial the other thing is if they can't do that one or if they're African-American consider hydralazine and isosorbide nitrate it actually has a mortality benefit if the patients are symptomatic on all these therapies and in normal sinus rhythm maxed out on a beta blocker give them either braiding if the patient has a left ventricular ejection fraction less than 35 percent and a left bundle branch block or a QRS greater than 120 give them cardiac resynchronization therapy if despite all of these measures they remain symptomatic try

to increase their perfusion usually inotropes would be the next step here so digoxin would probably be the one that you'd want to continue outpatient if they're an overt cardiogenic shock male Renown or dobutamine and then from there if you have to Mechanical circulatory support if they're an overt cardiogenic shock intriotic Bloom pumps via ECMO hopefully they recover and then the thing that you would need to put them on to bridge them to a transplant is an lvad and hopefully they would get a cardiac transplant and improve all right my friends that covers heart failure I

hope it made sense I hope that you guys enjoyed it and as always until next time [Music] thank you