Treatment of Congestive Heart Failure (CHF)

[Music] I ninja nerds in this video we're gonna talk about the treatment of heart failure a lot of things to go over let's go ahead and dig into it I'm engineers so when we talk about the treatment of heart failure before we start really diving into that I want to take a quick look very quick at the diagnostics of heart failure if you guys remember in the video where we talked about the pathophysiology we talked about the compensation mechanisms we talked about the symptomatology of heart failure it's primarily a clinical diagnosis you based upon their symptoms if you really want to and they maybe are having like an acute exacerbation their decompensating and you want to figure out the underlying cause or the reason why they're having this heart failure you can order other tests for example one of the things that are commonly done for people with heart failure is they get a chest x-ray what's a chest x-ray gonna show it could show big heart cardiomegaly what's the second thing it could show it could show that if the left heart is failing fluid is backing up until the pulmonary circulation what's that called pulmonary edema and sometimes I can even show fluid in the pleural cavity sometimes people with heart failure can get what's called bilateral pleural effusions that's one thing you can get from heart failure but again it doesn't completely diagnose it it's just something that you can look at based on their symptoms well it's another thing you can do another thing we'll talk about it in the mechanisms here is another one is called BMP brain nature attic peptide it's made by the ventricles one there under extreme stress so when a person has heart failure their muscles under extreme stress all the time so the level of B and P or B and P we have brain nature attic peptide can also help in some way shape or form to determine the likelihood of CHF it's not diagnostic it determines the likelihood of CHF it's more commonly used to determine the effectiveness of treatment we'll explain that a little bit later another thing you do pretty much the gold standard if you really want to determine heart failure is an echo and echocardiogram is gonna tell you a couple things it's gonna tell you whether the heart's basically dilated the ventricles are dilated systolic heart failure it's gonna tell you if they're really stiff and they don't want to relax during diastole diastolic heart failure or it might tell you that they have a wall motion abnormality it's not contracting right maybe they have MMI may be they have cardiomyopathy maybe they have a valvular heart disease but you get the point heart failures primary clinical diagnosis if you really want to I'll write down these things other diagnostic clues for heart failure if you really want to remember is chest x-ray okay that's one second thing if you really want to remember is you can measure the BMP levels the BMP levels are super elevated depending upon if they have heart failure it might be grading them what's called 4400 picograms per milliliter you don't really need to know that though okay third thing is it might also be something like an echo an echocardiogram this might determine whether somebody has again SAS taluk diastolic or some other type of pathology going on okay if you really want to another cause if you guys remember all the causes of heart disease is sometimes ischemic heart disease like a myocardial infarction so sometimes doing what's called a cardiac catheterization can also be done to determine maybe the underlying etiology of heart failure but again primarily clinical diagnosis okay now treating heart failure when we treat heart failure we treat it based upon the severity of the patient the New York Heart Association developed this class or grade system so again New York Heart Association developed a four class system class one says that the patient is having heart failure right but their shortness of breath or their chest pain that they experience is only with extreme exertion so again with extreme exertion the patient develops signs of shortness of breath or chest pain moderate exertion you guys get where I'm going here ready exertion they develop shortness of breath or chest pain mild exertion they develop shortness of breath or chest pain and if it's at rest that's class four that's the most severe whenever they have shortness of breath or a chest being at rest that's another thing that can tell us now when we treat patients we give them medications to treat their heart failure we do it based upon the class system and we'll go over each one and I'll mark what class they're primarily in one thing I want you to remember though is regardless of what their class is you have to treat the underlying disease if the patient has diabetes insulin or diabetic medications or lifestyle management if they have hypertension put them on anti hypertensive medications if they have hyperlipidemia put them on statins if they have an MI cardiac cath or cabbage if it's really that bad right so you get the point it's trying to be able to minimize the risk factors if they have obstructive sleep apnea put them on CPAP if they're obese have them lose weight reduce the risk factors treat the underlying disease and you're gonna help the patient out overall regardless of what their class is second thing these people hold tons of fluid in their body you want to restrict their sodium intake because sodium holds on to water so you restrict salt intake and you restrict water intake particularly two grams of sodium per day less than that or less than two liters of water per day so no matter what treat the underlying disease lifestyle changes and also restrict water and sodium to less than two liters of water less than two grams of sodium per day now the first thing we need to do before we start talking about each drug class is briefly go over the renin-angiotensin-aldosterone ADH axis if you guys remember what do we say was the stimulus for Renan it's basically low perfusion right so if there's decreased perfusion to the kidneys if you guys remember what does that do to the jg cells so you have JG cells in the kidney that respond to that decreased perfusion of blood volume that triggers the JG cells to release an enzyme called renin now if you guys remember the liver also makes a protein called angio tense Inogen and what renin does is is he Cleaves the angiotensinogen into another molecule called angiotensin one now there's an enzyme in the capillary endothelium of the pulmonary vasculature and this enzyme is called angiotensin converting enzyme commonly referred to as ACE what this enzyme does is is it stimulates the conversion of angiotensin 1 into angiotensin 2 what does angiotensin 2 do he does a ton of stuff man this guy is a troublemaker one of the first things that he does is is he binds on to these receptors on your arterioles and induces vasoconstriction now go back to some of the physiology lectures that we've done what does vasoconstriction do if you increase the vasoconstrictive mechanisms you're decreasing the diameter of that lumen if you decrease the diameter of the lumen you increase the resistance of blood moving from this direction to this direction right that's called an increase in the total peripheral resistance remember the formula blood pressure is equal to cardiac output times peripheral resistance if you increase this what else to increase BP now remember why is all of this stuff happening it's because if you guys go back and think for a second if we come back up here to the top what was causing this decreased perfusion a failing heart right so if you go back to this whole thought here when a person had a failing heart right so their heart is basically kaput it's not working it's decreasing it's cardiac output and that decreased cardiac output is leading to decreased perfusion to your tissues your body's trying to compensate for that by increasing the blood pressure because we're trying to try to increase perfusion to the tissues but it's making it worse why here's another thing let's come back here if you increase the total peripheral resistance of the arterioles what does that do to your afterload it increases the afterload and if you guys remember what's after load it's the amount of pressure that your ventricles have to overcome in order to push blood into them into the into the aorta right so for example if I have here the heart if I have an increase after load the pressure inside of the aorta is really really high my ventricles are gonna have to work hard and they're already weak that's not gonna help them okay what else is angiotensin to do he also stimulates your anterior pituitary so you know you have your ant or pituitary within your central nervous system right so here we're gonna draw again this is not what you think it is that's the pituitary gland it stimulates the pituitary gland to make a hormone called ADH up specifically is the post here pituitary ADH comes down to the kidneys and what it does is it works in the kidneys by decreasing the urine output so it decreases urine output and specifically increases water reabsorption if I increase water reabsorption I increase blood volume and technically I increase blood pressure but here's the other issue with this I increase blood volume I increase technically the amount of blood that's going to my ventricles which is called my II D V and when you increase a DV you also increase preload why is that a problem the heart's already weak you're putting more blood into a weak ventricle if it has more and more blood it's not going to be able to continue to keep pumping out the volume that we want that's putting more stress on the heart the next thing angiotensin 2 also does is he also acts on your adrenal gland and tells your adrenal gland to make another hormone which is called aldosterone and if you guys remember aldosterone acts on the kidneys and what it does is is it actually increases sodium and water reabsorption if you increase sodium and water reabsorption you increase blood volume which is designed to increase blood pressure which is the whole issue here but what else is it doing it's increasing my edv increasing my preload and what is that doing to the heart it's stressing the heart even more if you guys can understand how how all of this stuff works guess what drugs are gonna do they're gonna prevent all of this let's go over which one it's the best drug that you start off in a class one so this is the best one that you want to start in class one patients with heart failure is ace inhibitors okay so ACE inhibitors are angiotensin converting enzyme inhibitors what are some of these drugs captopril enalopril lisinopril and even another one called benzo pro okay so benz pro alright so you got all these different medications what are they doing well if you guys remember they're doing what they're inhibiting this enzyme so if I come over here I'm inhibiting this enzyme if I inhibit this enzyme I inhibit angiotensin 2 I decrease the total peripheral resistance I decrease the afterload I decrease the stress on the heart if I decrease angiotensin ii a decreased ADH released on a decreased significant water re-absorption increased blood volume and increased preload less stress on the heart if I decrease angiotensin ii i decrease aldosterone production a decreased sodium and water reabsorption decrease the edv and decrease the preload on the heart and again decreasing that excessive stress on the heart that's why these drugs are one of the best ones other drugs that you can also use if you can't tolerate ACE inhibitors in other words one of the common symptoms that people can experience is a dry cough or another one called angioedema and that's the case we don't really want to put people on ACE inhibitors so we'll try another drug another drug that's commonly utilized our class is called angiotensin ii receptor blockers we commonly abbreviate this as ARBs okay angiotensin ii receptor blockers some of the big ones that are used are Lazar ten Val's art tan and another one called can desert tan okay obviously Lazar Cana valves are tend to more commonly utilized ones that you'll see what are these drugs doing they're inhibiting angiotensin 2 everywhere that it binds so if I inhibit angiotensin 2 I'm gonna do the same thing that the ACE inhibitors do decrease the ADHD crease the preload decrease the preload and decrease the total peripheral resistance decrease in the after load and the stress on the heart it makes so much sense guys again this is a class 1 drug ok so class ones so far that we've established are going to be ace inhibitors if you can't tolerate an ACE inhibitor ARP next drug that's also utilized it's more of a class 3 drug and we use this in patients who have had myocardial infarctions and we're trying to decrease the remodeling of the heart are called aldosterone antagonists and these drugs are going to be things like spironolactone and another one which is called Epler nun now we use these again what are the reasons why we would use this we use this as a class 3 so again this is a class 3 drug so in other words with my basically with mild exertion they develop shortness of breath and chest pain you'll add this one on the benefit of this drug is two things one is it decreases the remodeling of the heart which is important you don't want a lot of fibrosis of the heart after it's out of myocardial infarction that's one of the benefits and the other one is it's potassium sparing so if someone is already having hypokalemia with their condition you can spare some of the potassium with this drug what does it do it's pretty simple to realize what it does guys right it's going to hibbett aldosterone action if you decrease aldosterone production you decrease sodium water reabsorption decrease the DVD crease the preload decrease the stress on the heart overall effect decreased ventricular myocardium remodeling and potassium sparing diuretic beautiful thing right the next drug class that I want you guys to think about really this is also more of a class three drug you don't really dip into this one until it's like you know the patient is having all these other medications not working and then you'll try this drug there is some evidence that says that it has been able to decrease mortality and morbidity in patients with heart failure again there's not tons of evidence on it they did have a couple trials on I think actually two trials on this drug and it's called entresto before I do the drug I just want to briefly explain what it does remember I told you whenever someone has heart failure the stress on the myocardium that stress on the myocardium causes it to release a specific chemical called brain nature etic peptide BNP BNP does what it's pretty simple actually it opposes all of the actions of angiotensin ii that's cool if I block angiotensin ii what do i do I decrease the vasoconstriction I decrease the total peripheral resistance I decrease the after load and the stress on the heart okay that's gonna help the already pre-existing stress I'm also gonna block its effect on stimulating a boström if I drop out dosterone and drop ADH I pretty much combined decrease the water volume in the blood decrease the sodium volume in the blood I decrease my edv I decreased my preload and I decrease the pre-existing stress on the heart well that's a benefit as well so these this is actually a pretty good drug problem is though there's an enzyme that breaks him down and this enzyme is called Knepper licen Knepper lisen and what this drug does is is he breaks the BNP down so if we give a drug which is BNP yeah it's gonna have some effect but we need something that's actually going to inhibit this thing right here to increase the BMP concentration and we can also increase its activity by adding another drug as well so here's what we do we give an epilation inhibitor we're gonna give a specific type and that's called Tsukuba trail okay so we'll write down here one drug is called Tsukuba trail so Cuba trill another one is called like you have another thing called nazir Thai but we're not gonna worry about that so Cuba Trail is going to be the knepper lisen inhibitor okay so here we'll put down here nefra licen inhibitor but we're gonna add on another drug to even enhance this effect another drug that we add is an a our B so this is common to give what's called Tsukuba trail and another drug called valsartan okay when I give these two together the drug that they give the name is called entresto so sometimes you might hear this and what it's designed to do is have a two effects one is this drug is going to inhibit the knepper licen okay so it's an effort lisent head-but are increasing the BMP concentrations to enhance this effect but also let's even enhance it even more and give Val's our ten so now we're going to drop the angiotensin 2 activity even more can you imagine now how much more effective that's going to be because in people with heart failure this system is super jacked up so if we inhibit angiotensin 2 with this drug and increase the BMP to counteract the angiotensin 2 that's a beautiful drug so again this is something that they use and it has been shown in two trials one of the trials specifically to decrease the mortality and morbidity in patients with severe heart failure alright that's the drugs that I want to talk about relative to renin-angiotensin-aldosterone axis now we're going to do is we're going to transition into other drugs that affect the sympathetic nervous system alright so the next thing we're gonna do with this heart failure treatment is talk about the sympathetic effect on how heart failure isn't well because remember heart failure and ramps up two systems renin-angiotensin-aldosterone ADH axis and the sympathetic nervous system to compensate for the decreased perfusion or the decreased cardiac output so if you guys go go back remember we said that whenever there is decreased cardiac output what does that do it stimulates specific receptors remember you have here and you have your carotid system right you have those specific nice little beautiful receptors here in the carotid sinus and the aortic sinus and whenever they're stimulated by decreased blood flow what do they do they activate your sympathetic nervous system you should put that ignore system response to this in a couple of different ways one of the ways here is it's going to try to increase your heart rate so it has these fibers here that come out and try to release norepinephrine onto the beta 1 receptors on the SA node and the beta 1 receptors on the contractile myocardium remember the effect of this if you increase the release of norepinephrine and increase the heart rate what does that do you increase heart rate that increases the what cardiac output and that increases the blood pressure well what else does it do to the patient unfortunately you increase the heart rate you don't give the the ventricles a proper amount of time to really relax and also to contract and eject enough blood out and again so whenever someone is having a tachy rate maybe they're tacky okay you know you in other words you're trying to increase the heart rate you're not giving the ventricles enough time to really get their blood flow get their oxygen and so that's stressing them so again as you increase the heart rate you decrease the oxygen delivery to the myocardium because remember when does the myocardium get its oxygen supply during diastole well if you're tacking away here your diastolic periods gonna be a little bit shorter so now the ventricular myocardium isn't going to be getting the amount of oxygen at once in that small amount of time it's gonna end up having a higher demand and not enough supply that can make it worse so we want to slow that down a little bit and we'll talk about drugs that we use that for another thing is you release norepinephrine onto the beta 1 receptors what's that going to do that's going to increase contractility if you increase contractility you increase your cardiac output if you increase cardiac output you increase blood pressure what else do you do when you caused the myocardium to have to contract so much you consume large amounts of oxygen now the myocardium needs more blood flow and it's not capable of being able to pump as much blood as you need to deliver the oxygen demand okay so with these two situations you increase the oxygen demand and you just don't have enough supply and that stresses the heart another thing is what else do these fibers do you guys remember that they are also beta 1 receptors here on the renal arterioles right and what does that do it also triggers the renin release but it's also going to cause vasoconstriction right so if it causes vasoconstriction of the renal vessels as well as other vessels that's going to do what it's going to increase the total peripheral resistance that's gonna increase your blood pressure but on the other aspect of it increases the afterload and if you increase afterload what do you do you increase the stress on the heart so let's give drugs that can block these different things okay what are some of the in remember this receptor here I'm not talking about the JG cells we already discussed those yes the sympathetic nervous system can't act on the beta 1 receptors on the JG cells of the kidney and cause written release I'm talking about the alpha 1 receptors multiple different arterioles on the body and whenever that Veysel constricts it increases the total peripheral resistance increasing afterload okay now if we give drugs like beta blockers these are your classed class 1 okay so these are going to be ones that you're gonna give to the patients whenever you start them off okay so first line you can try an ACE inhibitor or ARB if they can't tolerate it and a beta blocker big thing can't forget this you need to remember this let me put it here in orange never use beta blockers they're contraindicated in decompensated heart failure you never give these never give beta blockers when they're decompensated they're not able to generate enough cardiac output I'll explain why in just a second what are some of these beta blockers that we use so beta blockers that are commonly used there two main types one is called metoprolol and the other one is called car Vader law okay so you got metoprolol and car vada law they work by having a negative Crona tropic action decreasing heart rate negative inotropic action decreasing contractility and they also cause vasoconstriction to increase total peripheral resistance in afterload okay yes this aspect of it will be good and car Vader law is really the only one that has this mixed activity carbonyl all has alpha and beta activity metoprolol a beta activity so that's important to remember taupey law is more cardio selective car beta law is a little bit less selective nonetheless these drugs you give them because they decrease after load they inhibit the renin-angiotensin-aldosterone axis as well remember what else do they do just for the heck of it so you guys have it remember they also act on the kidney and if you guys remember the act on the GG cells and when they act on the GG cells that triggers the release of Rendon so I don't want you guys to forget that as well and if you guys remember that triggers a whole reign in angiotensin aldosterone axis and again if you guys want these are beta 1 receptors okay but you inhibit the renin-angiotensin you decrease the chrono tropic action decrease the inotropic action this decreases the oxygen demand slows down the heart rate decreased the contractility to allow for the myocardium to relax a little bit and you inhibit the afterload to continue to decrease the stress on the heart these are the drugs that you use never a decompensated heart failure can't stress that enough other drugs that also affect the contractility of the heart are called digoxin okay this is a class 4 really you don't kind of go to this one until the patient has pretty much tried everything and nothing else is working so a class 4 drug that you can try here is called digoxin okay so digoxin is pretty much - your last line here that you're going to go with medications one thing I want to add in here because what dioxin is is it actually increase contractility it's a positive inotrope but also a negative chrono tropes we also use it an afib it also can block the AV node another drug that you can give but specifically when a person is actually having a decompensated heart failure is dobutamine why do I say that if someone is heart is failing so much that they're not able to generate enough cardiac output so significant that their blood pressure drops super super low what do they call that shock whenever their blood pressure is were like refractory to any type of thing and it's super super low and it's just not able to do what it needs and compensate and try to increase the blood pressure the best it can and it's still low that's called cardiogenic shock heart failure is a very common cause of cardiogenic shock especially if they D compensate so a drug that we can give to patients if they super decompensate and we need to increase their pressure is w to me okay so what you remember it's primarily for decompensated heart failure next thing that we'll talk about here is going to be your diuretics these are technically considered to be class two so these are your class two drugs okay so diuretics there's two types that I want you guys to remember the main one that's utilized is your loop diuretics the main one that I want you guys to remember is called furosemide or commonly known as lasix okay the other one is going to be your thiazide diuretics and these can be two types that I want you guys remember hydrochlorothiazide and another one is called Mottola zone I specifically want you guys to remember this one all right so class two what I want you to remember about diuretics specifically is you use them whenever someone is basically not responding as well as you want to with an ACE inhibitor or an ARB and a beta blocker or another situation where they're having a lot of fluid in their body so they have peripheral edema they have ascites they have jvd they have pulmonary edema then we want to pull all that excess fluid off that's when we'll give these drugs so again you can give it as class two but another thing I want you to remember is as you can also use this drug whenever there is significant edema and you want to pull fluid whether it's pulmonary edema or peripheral edema okay and if it's causing them to become symptomatic you definitely want to give these drugs how do they work very very simply all I want you to remember here and it's really really simple the loop diuretics act on the loop how do they do that I want you to remember I'm going to put D here for the DX it inhibits a specific transporter called the sodium potassium to chloride co-transporter do you need to know that not really what I want you to know is if it inhibits this it doesn't allow for that sodium potassium and chloride to go out so now sodium potassium and chloride build up here what does sodium do it brings with it water so now I'm gonna pull out maybe 25% of whatever they filter so whatever gets filtered out of this the glomerular filtration rate whatever that is 25% of that I'm actually going to urinate out and if I pull all of that fluid out that's gonna help me so I'm gonna increase their urine output and by pulling off all that excess fluid what do I do that decreases their edv that decreases the preload and that decreases stress on the heart okay the other one are going to be your thiazide diuretics your thiazide diuretics are going to inhibit this sodium chloride transporter in the distal convoluted tubules if I inhibit sodium chloride reabsorption in the distal convoluted tubules and at this point it might only be you know 10 to 15 percent of the GFR that's less than 25 but again if I have some of this I'm gonna cause less sodium chloride to be reabsorbed that's gonna build up what's going to follow with it water and because of that I'm gonna get an increased urine output that's going to cause a decrease in the total blood volume decrease in the EDV decrease in the preload decreasing the stress on the heart okay as well as getting rid of all this excess fluid causing their symptoms like pulmonary or peripheral edema okay now before I move on to these next two drugs I want you to remember what's the primary one that you give well it depends on the GFR but pretty much people are getting loop diuretics you start at 20 milligrams generally and if you need to you can increase okay but some tricks that can be taught is without having to increase the dosage of your loop diuretic sometimes you can add another drug on called Mottola zone so maybe I could do 20 milligrams of lasix and add on Mottola zone of thighs that they're at it to pull off a little bit more fluid okay without having to increase the dosage of my diuretic all right so this next drug is called hydralazine hydralazine is a pretty cool drug it's well tolerated especially in african-american patients and one of the beautiful things about this drug is it's also safe in pregnancy so it's also it's commonly used as a medication one of the first time medications and pregnancy one of the downsides of it is that you have to take it three times a day potentially now hydralazine works by acting on the arterial smooth muscle right and what it does is it relaxes the arterial smooth muscle very quick like a little quick and dirty reason why hydralazine works on these smooth muscle cells by increasing nitric oxide concentration increased nitric oxide into the smooth muscle cell it basically activates a particular enzyme called Guan allow cyclase when you activate this enzyme that converts what's called gtp into cyclic GMP and through specific protein kinase regulation this promotes the inhibition of calcium entry and if calcium doesn't enter into the cell it's not going to be able to contract so what does that result in relaxation so it promotes relaxation of the smooth muscle cells so that's how hydralazine works okay now again to make a little side note here you don't usually use these drugs as first-line they're more your class three hydralazine as well as the other drug over here which is called Isis or bide die nitrate now these drugs right here really the only time that you would use Isis or by die nitrate or high drowsing we talked about hydrazine is commonly used in pregnancy but usually in the treatment of heart failure you would primarily use these drugs when ACE inhibitors aren't tolerated then you go to ARBs if ARBs aren't tolerated then you go to these two drugs here okay you go to hydralazine and or Isis or my die nitrate I so sort by the nitrate does the same exact thing overarching view is that this is also going to inhibit the vascular smooth muscle but primarily on the venules and the mechanism of action is the same it's going to lead to increased nitric oxide production and actually help to promote relaxation of the smooth muscle the overarching difference though is if you act on the arterial side and you promote relaxation of this muscle what does that do it helps to be able to decrease total peripheral resistance right because you decrease the bay's of constrictive mechanisms so the pressure proximal to this is going to drop if you do that you do two things you drop pressure as well as decrease the afterload which is that increased stress on the heart that's a beautiful thing with Isis or by dye nitrate what do you do will you actually promote relaxation of this muscle right and what that's gonna do is if you relax this there's not going to be as much blood the force of blood is not going to be pushed through the venous system up to the right side of the heart so there's a decreased right heart venous return if there's a decrease on the right side of the heart venous return what's going to happen to the end diastolic volume you're gonna drop the in diastolic volume what does that do that drops the preload on an already weak heart which decreases the stress of that weakened heart so these are the medications that you would Oh two and a class three type of situation particularly whenever ace inhibitors are ARBs have failed or you want to use this and someone who's pregnant and someone who has decompensated heart failure the quick easy way to remember the treatment this is kind of a mnemonic that they commonly use is l m n o P so what does this mean L stands for lasix that's a fancy word for saying furosemide and what is furosemide we already talked about this he's a diuretic so he's gonna help to reduce a lot of the edema particularly pulmonary edema which can happen in patients with congestive heart failure particularly left-sided another one is pain right so you got to control some of the pain that they might have whether that be from the leg swelling whether it be chest pain you can treat them with morphine may be anywhere from 2 to 5 milligrams the other thing is nitrates which includes hydralazine Isis or by dye nitrate to help to drop the actual afterload as well and help to relieve some potential chest pain ischemic chest pain the other one is oxygen and I can't stress how important this is whenever someone actually develops decompensated heart failure fluid can back up into the lungs and make it very difficult to breathe so one of the best things to do is to start the patient on maybe BiPAP or CPAP and if necessary or even just high flow nasal cannula to get them as much oxygen that you possibly can in that respiratory struggle especially when someone goes into what's called flash pulmonary edema the last thing is position position them in a way that you're not fluid overloading them and making it difficult to breathe which is in a supine position you don't want them supine have them sit up have them at an incline to allow for unfortunately the fluid to go down with gravity which can cause some edema but it's gonna decrease the stress on the actual lungs okay I engineers are in this video we talked about the treatment of heart failure it was a brief overview of a lot of these medications just overall mechanism of action and particularly which ones you use in a sequential order in patients with heart failure I hope this video made se if it did guys hit that like button comment down the comment section and please subscribe also down in the description box we'll have links to our Facebook page rien and even our Instagram account go check those out as always an engineer until next time [Music]

Channel: Ninja Nerd Lectures

Views: 119,869

Rating: 4.975122 out of 5

Keywords: Congestive Heart Failure, CHF, CHF treatment, treatment of congestive heart failure, treatment of CHF, ninja nerd science, ninja nerd medicine

Id: cpTeSV5l5EI

Length: 38min 35sec (2315 seconds)

Published: Wed Mar 25 2020