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Hello, everyone and welcome to our Monday meal education. Um We don't have too many viewers at the minute but I'm hoping that will er improve over time and the ones that we do have, you are gonna have a lot of work to do answering who sounds questions. So um this is gonna be interactive what I'm gonna do um and don't be afraid you can ignore me. I am gonna invite you onto the stage if you don't want to come. That's OK. You can come on to the stage, you can just click on er join stage if your mic and cam is off, no one's gonna see you. No one's gonna hear you, ok? But we would love for you to be able to just turn off your microphone, turn on your microphone and answer Hussam question. So if you wish to join us on the stage, you can keep your er camera off but it just means that when hasam asks the question, you can just turn on your mic and answer it or he can ask you to answer it. Alright? You can still put your questions and answers in the chat. Absolutely. But if you wanna join the stage, we would love you on here. Alright. His would definitely love you on here. Um So please join if you want to. If not, that's ok. Um obviously put all your questions and your answers in the chat, your feedback form will be with you in an hour. Perfect. Hi Mohammed. Excellent. Yay. Thank you. Oh, it's good. The feedback will be in your inbox in an hour and just fill out the feedback form. Um We really are interested in future topics that Hussam can teach on. We're thinking about Ec GS and so really, you know, fill out your feedback form, let us know what you're looking for and I'm gonna start looking through the feedback forms this year to see what it is your saying, to see what I can match up with speakers that I know are keen to teach on the platform. So we can start really tailoring the learning to what it is you need. So anyway, without any further ado um I will pass you over and if you get joined stage, come on onto the stage. It's alright. We're all family here. We're like a lovely little group here. All right. So I'm gonna pass you over. Thank you, Sam. Ok. Thank you, sir. Hi, everybody. Thank you for joining again and uh please do join stage. Oh, George, please joint. It's not about answering questions. It's about chatting with you as well to, to just help each other to understand the topic better. OK. Um So this is the last, this is uh uh this was the last slide we stopped on last time. How to go for to diagnose the the uh heart failure, the common steps to learn how to classify. And we talked about different classifications for heart failure. And one of the most important uh one of them is depending on the ejection fraction. So let's go to the last part of heart failure and let's speak about management. You know, all people are waiting for this. So let's go. So uh management of heart failure, we're going to speak about. We're gonna spend a lot of our time talking about the drugs of heart failure and how to manage acute heart failure and chronic heart failure. Ok. And although there are other modalities to, to uh there are some surgeries, there are some uh assisted devices that that could be used to manage heart failure. Usually this is for specific cases or for advanced heart failure, advanced heart failure. And I'm not going to talk about this because these are out of uh our um maybe uh hello. Hello, George. Hello. Uh Can you hear me? Yeah. Thank you for joining again. Yeah, I think I'm lagging a bit. Uh I'll try to my best to not lag while speaking. Ok. Ok. So let's start which drugs do you know that could be used to manage heart failure? Any drug um let's start with like the biggest uh two groups, uh beta blockers and uh diuretics. OK. Diuretics. What else? Uh ace inhibit uh ace uh and Arbs like uh OK. What else from, from other people in the cat, from the cat or anyone can join? So you already mentioned beta blockers diuretics and ace, what else could be used to target the hardest fan in general regardless of its mechanism. It's uh uh how, how unwell to use it, any drug that you, you know? Yes, it's very inactive. So it's good. Captopril. Captopril. What is captopril? No, no, no problem, no problem. We all get the spelling wrong, I guess. Captopril. What's captopril? You? Um excuse I didn't hear the question. Can you repeat, please? One shock said it's cap captopril could be used for heart failure. What is captopril? Uh captopril is uh uh ace? I think it's an ace inhibitor. Ace inhibitor. Yeah. Yeah, it could be as far as uh hypertension as well. But now we are talking about heart failure. It also is used in heart failure. So, captopril, what else? So it's, it belongs to the ace inhibitors. What ace inhibitors. What do you mean by ace? It's a um uh a uh anti uh conversion or anti anti conversing enzyme or something? It's like anti conversing enzyme. Mm Anyone can help your, what's ace? I know. Yeah, like ace is like an uh uh I remember the acronym but the like the words were a bit different angiotensin. Yeah, angiotensin converting, converting inhibitors. Ok. What else? Uh We up to now we said the beta blocker diuretics, ace inhibitors. What else could be used to manage heart failure? And we can replace the ace inhibitors with herbs if the patient suffers from uh uh dry cough. Mhm. What, what do you mean by herbs? Uh uh It's the angiotensin receptor inhibitor I uh or blocker. Yeah, we can replace this with herbs. Uh What else could be used? What else? What are the classes of diuretics that could be used for heart failure? Bye. Uh Well, like I remember the three main groups, the thiazide, the loop diuretics and the, the potassium reserving spironolac. OK. Uh And uh I want someone else other than yours to tell me which one of the diuretics is the most important in the context of heart failure. Yeah. Furosemide is one of Z Yeah. Uh I remember furosemide being like the loop uh uh diuretic which is very important, especially in uh pulmonary edema. OK. OK. But if you have to use all you went one class to manic heart failure in general, what, what would be that cross? So, no, I mean from direct excision. Oh There are other people, Marian. Are you able to hear me? Ahmed? Just to check. Are you able to hear me? Are you with N and my other? Yeah, I can hear you. Uh Yeah. I'm, I'm just taking it. The sound is a bit laggy. I think it, I don't know if it's my own problem but I think uh your sound is a bit laggy. Mm. Ok. I wanna check on the other people if they are. Hey guys, are you able to, to, to, to hit me calcium channel blockers? What do you think? You, I think that calcium channel blockers could be used to manage heart failure. Um I remember calcium channel blockers are um uh contraindicated in heart failure. I think. Why do you think so? Why do you think so? Um I think they uh increased the uh well, let me, let me try to remember their mechanism. Uh they are venous uh mainly veins dilators. So they increased the uh they, they reduce the preload. Mhm. Is that something good or bad? Then I failure? I remember that's, I don't know, I think it's uh good but like, II I'm trying to remember there, there was a reason that they were uh that they are in uh intra indicated, but I can't remember exactly the, the why. Ok. Ok. So people are sleeping today sleepy. So there are many, many, many, many classes of drug hands, at least every day, every ones in expanse and many drugs could be used. Uh Most common drugs that could be used is drugs that target train and of the strong system. When we talked about the pathophysiology of heart failure, we mentioned that this system is one of the most active systems with heart fail that can lead to compensation. And the short term and the long term can lead to the uh the vicious cycle that uh that uh leads to decompensation and advancing in heart failure. Ok. Uh So system, every drug that can can, can work here theoretically could be used to heart failure. Many drugs on the autonomic nervous system could be used. The most important. One of them is the beta blockers. OK. But many drugs could be used in atropic drugs. Intro drugs could be used in acute uh and some for chronic heart failure, venodilator, one of the class of drugs that are now increasingly used in heart failure, especially in specific groups. OK. When we have other drugs and from the other drugs that there are two worth mentioning, the sodium will cause cotransporter inhibitors that's first uh used in diabe in diabetic patients, but now also used in uh heart failure patients and corticoid receptor antagonists or potassium sparing diuretics. Also, they are now the first line drug for management of chronic heart failure. So just try to cover pharmacology of this uh fast because uh we don't have time to talk about them in details. I hope you are able to see the detail. These are drugs that target system. OK. And do you know that is converted sin one and Gin one is converted to S two from converting enzyme I think gas two has many effects including vasoconstriction, activation of sy nervous system and uh also in the stimulation of uh aldosterone release. So, one of the ways that we can inhibit the system is to give drugs that could inhibit it is converting enzyme that's converting to sin one is also vasoactive, but it's not potent. And that s two. Um so by inhibiting this enzyme, we could just prevent the vaso restrictions. That means vasodilatation become unopposed. Um we could um inhibit sympathetic activation and also the strong secretion. So, is that how converting enzyme inhibitors could uh could benefit patients of heart failure? Ok. So what are some of the side effects of fungi? Tensin converting enzyme inhibitors like captopril, enalapril and many, many drugs, ramipril and many other drugs. But other side effects from the compression enzyme inhibitors. Headache is not that common. Mhm. Dry cough is like more common. Uh and we can replace them with herbs then cause uh oh there a mechanism of dry cough. And um if I'm not mistaken, they affect the um OK. The converting enzyme works in the lungs and they affect the some kind of enzyme there which causes this dry cough. Uh They mhm What do you say? I don't remember the exact uh biomechanic but it's something about the enzyme in the, in the lungs. Mhm What do you think? Uh so far and why there is strike of and it's nasty and it's troublesome for the patients. This is it stopping the drug and replacing it. As George said the case scenario on 10% of patients usually as a start of the management but theoretically at any point of using the truck. OK. One of the things enzyme inhibitor inhibit sin to s to one of the things that sin to uh not prostaglandins. One of the things that uh the in the inhibition of the enzyme does is that it increase little of Prade prade zinc prade stimulates the cuff receptors and that lead to dry cough, dry cough. Ok, dry cough. So dry cough is usually occurs in around 10% of patients. What are other side effects? That could be caused by things worse? Maybe hypertension, uh hyper hypertension because uh uh it uh causes vasodilation plus, reduces the amount of fluids. Yeah, hypertension usually uh with the start of the medication, that's why usually we start the medication in low dose and and increase the dose to target dose. But habitation can occur at any time. Of course. What else? Yeah. So it doesnt converting enzyme inhibitors inhibit aldosterone secretion. Now, this one of the mechanisms of one of the functions of the A two keep uh sodium and uh and uh secrete the potassium. So we have hyper kalemia and hyponatremia. Yeah, hyponatremia usually do doesn't happen. The body can, can compensate for that, but some patients can develop hyperkalemia and you while the patient on the the uh on the drug you need, you need to follow up his potassium every now and then. Ok, specialize sort of a medication or when the patient has some other condition or other drugs that can also cause hyperkalemia. So, hyperkalemia is very important side effect edema. No, cannot cause edema. No. So what else? What else? And get enzymes like one of the side effects that can be caused by enzyme is a rising creatinine level, rising creatinine level. It a almost all patients has some slight insignificant rise. But you need to follow up at the start of the of the uh of the use of medication frequently to mean to ensure that there is no kidney damage. It's just, it's uh it's just a benign rise in the creatinine. Ok. So we should, we should be aware of the dry cough. We should be aware of the hypotension of course, of the hyperkalemia and the kidney injury that could be caused by against the copper enzyme inhibitors. So what's the difference between ace inhibitors and Arbs and Keta receptor blockers? Uh ARS blocks like the uh angiotensin uh receptors directly uh without like affecting the uh converting enzyme. Uh-huh and what no dry cough. So this mainly deals with the dry cough. Yeah. Uh it's not also uh precaine also can cause angioedema. It's rare but it's very serious by the way. And uh so uh Arabs go directly for the receptors, lead lutenin two unf affected So, angiotensin two can degrade it pre and that will lead to decreased level of uh decrease the incidence of dry cough and edema. Ok. So that's why it started. Like patients usually start with a inhibitor. But if they develop dry cough and the orange edema are shifted to Arabs. Ok. They shifted to Arabs. Um most of the uh other side effects and uh drug and uh angioedema are shared between us and Arabs. OK. So let's go for the third class of drugs called angiotensin receptor. Nipro inhibitors. Nipro what is naprosine? What's nipple? These two groups, I actually the last two groups, I never heard of them. No, the last thing is side effects. Don't worry. The last group is uh uh Nipro inhibitors. Lycine is uh is an enzyme that, that uh degrades. Um many of the vasoactive uh vasoactive molecules in the body, including angiotensin, including praina, including uh nitro peptides and many other inhibitors. Ok. So we give inhibitors that leaves the vasoactive metabolized and affected, that would try sprain levels. And one of the one of the one of the effects of these vasodilatation. So, but with nerosin inhibitors, we have rising sin too as well. That's why we combine it with angiotensin receptor blocker. That's why it's called angiotensin receptor and resin inhibitors. So, it's two drugs used as one and this class of drugs showed to have uh have significant improvement in mortality and morbidity in patients with heart failure and now as they are commonly used in a first line for patients with heart failure. So this is very important and it, the good news is it has way less incidents of dr of and edema as compared to ace inhibitors. Ok. So angiotensin and there is just one class of drugs called Sacro, Sacro, ok? Just one of the drug that NLY inhibitors. So these are drugs for the system. You should know all of the three, all of the three are very important. You should know they can be used for heart failure and other cardiovascular conditions as well. Any question on on this class of drugs? Yeah, I did not uh uh comprehend like the mechanism of uh lysine. Exactly. OK. Neprolyzin. If you can, if you can see the left side of the slide, uh the bottom one, OK. There is nerosin that act on basal active metabolites. OK? And can act on angiotensin. Two can act on Praina and many other ones. So from the vasoactive metabolites, we have prekinin and retic peptides that promotes vasodilatation and uresis. And and these fun, these uh functions are important to target for patients with heart failure. So the patient has vasodil that means less preload and less afterload, right? And that would uh decrease the heart cardiac work out if there is not, that means low. So low serum sodium and one of the things that you need to ensure for patients heart failure that they have low body low sodium intake. So, OK. So these effects are beneficial in heart failure. But the problem is that mm Lily also degrades sin too. So if we inhibit neprolyzin, we would have beneficial effects from vasodilators and not agents. But we can also have delicious effects from angio tense symptoms. That's why it's combined with angiotensin receptor blocker. OK? Like sartan like any, any indigens. Ok. So now we have the both we have the beneficial effects and we will prevent the uh the harmful effect of indigens. Ok. What do you mean by? I also perform inhibition action. What do you mean? I didn't get the co naprosine is the enzyme that sets, that's produced by the body. The drugs is called naprosine inhibitor inhibits this enzyme. Ok. Did I answer you? Ok. Ok. Maybe one day I can do all uh cardio cardio pharmacology because this needs uh to be discussed in more details. Then we have the drugs that can be is that uh target autonomic nervous system, sympathetic nervous system specifically. And to know about the sympathetic nervous system, we need to know about the receptors. Of course. So we have alpha and beta receptors, alpha receptors is very important. It's, it's found in the blood vessels, most of the blood vessels in the body and they ca they can causing vasoconstriction. Ok. Then you have fa is just regulated receptors, then you have beta one and it's found in the heart. And they can increase heart rate, contractility and conductivity. And then beta two receptor is found in some of the blood vessels caused by dilatation. Ok. And also found in the lungs cause broncho broncho dilatation. Ok. And uh alpha two inhibitors, severe release, beta one, increased uh beta one also increased release of OK, and increased libo and beta two increased like A. So the the the effect is increase in blood glucose levels as well. Ok. So there are many drugs that could be used including beta one agonist. Ok. But the most important drugs that's used in management of heart failure is the beta blockers. Why do we use beta blockers in management of heart failure? It's called result in heart failure. That mean failure of the heart to eject the blood. Yeah. And we need more uh contractility. Beta blocker decreases contractility. Why should we use beta blockers? And they improve morbidity and mortality. Patient is heart failure. Anyone knows anyone can guess it's not necessary to get the answer correct. Uh Like what's the specific question? Uh it, why they increase mortality? Uh Why they have me reduced mortality or is it be because uh why they increased contractility? Why is they, why is beta blockers are used in heart treatment? Why do you use it heart failure? Because they increase contractility mainly and uh the blockers increases contractility. I mean, no, no. Uh with uh why you uh no, I mean for reducing the tachycardia because like uh we need to inhibit uh like we need to protect against uh what do you call it? Uh arrhythmias. Uh mhm. But we still will decrease contractility on that. Theoretically means that to be decreased. But like we need to, we do need the longer uh uh diastole for the heart. Um We call for the heart to uh to have enough uh blood for itself just like the uh the, the heart gets his blood during diastole. Mhm. So, I mean uh uh far did it in the right way, it's just anti ischemic ef effect. Mhm. Ok. So inhibit the system, they kind of lowers the pressure injection from the BP, anti ischemic effect, right? For uh has some anti ischemic effects, but we are talking about heart failure regardless of the course um you know, increase the they increased the left uh um the left ventricle end of the volume. So we have uh we can have uh like a bigger amount of uh with the reduced uh ejection fracture, we can have a higher amount of blood uh being ejected with increasing the end of the ole uh volume. Ok. Ok. So beta blockers did, did they block the effects of the sympathetic nervous system on the heart? They decreased heart rate, they decreased contractility. That's why when we use it at first, they might aggravate the symptoms of the heart failure because of the acute decrease of cardiac output. Ok. That's why when you use it at first use it cautiously maybe in low doses and build up the doses. But on the long term that if the the the chronic activation of sympathetic nervous system of the heart is one of the factors that leads to cardiac remodeling. Remember cardiac remotor. So on the long term, beta blockers decrease the rate of cardiac remotor. Ok. Also they have some effects on the afterload and preload, they decrease afterload and in the long term and all of these effects are very beneficial in heart failure. So that's why beta blockers acutely can aggravate heart failure. But chronic, chronically, they improve the heart failure, symptoms, improve the mor morbidity and mortality for patients with heart failure. That's why they are used. Ok. Do you get it? Yeah. Yup, of course. In addition to what you said, they uh they prevent the cardiac arrhythmias. Ok. And if patients has ischemic heart disease, that's additional uh additional benefits for a uh so as they improve the systolic and diastolic functions of the heart, they prove the in uh long term they improve the heart, the heart but sounds counter. But yeah, that's what they do. So we can use any beta blockers, any beta blocker we can use in heart fail or just there are a few there for heart failure for heart, we have three drugs, three beta blockers that show improvement in mortality and morbidity that can be used. What are they, I think one is, um, it could be Bisoprolol, um, or is it, is it, is it, what is the, what are the other two? Do you agree? York is a, is a pro, uh, I actually, uh huh. I sh you, yeah, the, the other one is, I think they use on them, uh, and the dosage will be on the higher side, which is CVAD, huh? Carvedilol. Ok. What else? What is the the? Mhm I kind of remember all the drugs ending with a hill. But yeah, all this all this most of the class. OK. So Bisoprolol, carvedilol and metoprolol, metoprolol. These are the three drugs that could be used in heart training. Bisoprolol and metoprolol are selective beta one, selective beta blocker. Carvedilol is slightly different. It's nonselective, it blocks alpha one, beta one and beta two and has also additional effects other than in the system related related to free radicals accumulation in patients of heart failure. That's why it's very beneficial. Bottom line with these three drugs can be used. Metoprolol br or carvedilol and some, some um data about uh lidol also can be used. But now just remember metoprolol is a product Carol. These are the three drugs that commonly used in patients with heart failure. And as we said, we start with, with a small dose and we build up. So if patient presented today with acute heart failure symptoms, when should we start the beta blockers, when should we start a bit of blockers. So patient presented today, admitted to the CCU and now symptoms controlled patient improved and uh as you know, start to think about uh mhm. And usually is that uh you are right. But uh we need some specific details. At least, at least it's, it's case dependent, but at least you wait for 24 hours, at least 24 hours, maybe slight longer, but just do it for 24 hours and then start with the smallest as possible four beta blocker. OK. There are many side effects. There are many contraindications of beta blockers. But if there is one thing to remember about beta blocker, and you should tell every patient who is using beta blockers, don't stop beta blocker abruptly, don't stop beta blockers abruptly. If, if you have to, if the patient has to stop beta blocker regardless of the cause, the patient should stop it gradually over 4 to 6 weeks. OK. If they stop abruptly, that could result in ischemic heart disease or cardiac arrhythmia because of any post in the stimulation to the heart. OK. Please remember this. Please remember this. Don't stop beta blockers properly that could kill the patient. OK. Any question, the beta blockers. Yeah. Yes. Yes. OK. Broncho spas usually cases because of the stimulation of beta two receptors in the lungs. OK. Theoretically speaking, be selective beta one agents like bis and metoprolol should not result in Bronchus spas. OK. Especially when used in the doses. But still some patients have bronchospasm from, from this, from these drugs. So if you are going to use selective Beta, one, use it cautiously in patients with asthma or COPD or any bronchospastic condition. Ok. And uh some patients need just to, to, to, to change the medication because bronchospasm could be could, could be, could be occur frequently and even with the small doses. So if patient presents bronchospasm, you manage it as any acute bronchospastic condition in the emergency or if patient is stable, you give uh bronchodilator and you discuss changing the medication with with the patient. Uh is yeah, does carvedilol uh cause uh bronchospasm as well like any beta blocker can, you can cause uh bronchospasm even if it's even if it's a little bit. But like carvedilol has a higher risk than uh selective beta one. It's not well studied. I'm sure. Oh yeah. But theoretically speaking, it should. Yeah. OK. Another question. OK. So let's go. Then we have diuretics, diuretics. One of the common class used in patients with heart failure. OK. Including loop diuretics, thiazide diuretic and potassium sparing diuretics. Um So loop diuretics act on which part of the Nephron the or at least remember the, the the target. What do they inhibit the diuretics act on the ascending limb of family. If you remember from the, in after the, we have the proximal tibu, then descending part of the loop, then ascending part of the loop. Then the distal comp as the ducts. OK. And the renal be so ascending lo of he contains sodium potassium, two chloride canal, sodium potassium to chloride cotransporter. And these are inhibited by loop diuretics, loop diuretics including furosemide and other agents. OK. And then we have thiazide diuretics act on is convoluted tubules inhibit sodium chloride transporter, sodium chloride transport. Then we have the potassium sparing there. It takes of collecting but their either act on um aldosterone receptors or sodium potassium uh exchange. OK. Sodium uh indirectly inhibits so the potassium scan. So this potassium sparing diuretics. So why do we use diuretics? Why do you use loops? Why do you use the eyes? Genetics? Um They reduce the uh fluid uh the they reduce fluids in the body which which helps with the edema that uh might uh be caused by the heart failure. That's like the first symptom. Then uh we it also helps by reducing the preload. Ok. OK. They, they may, they are mainly used for patients with volume overload. Yeah, volume overload to relieve the symptoms. And most commonly for patients with pulmonary edema. Ok. For patients, this looks on side are these drugs has do these drugs have any effect on mortality? Morbidity? We wanna talk about heart failure, medications. We wanna know which one targets the mortality, which one targets morbidity and which one target both so can affect the diuretics don't affect mor mortality. I think all of them. Uh No, I mean, uh specifically the loop. I think the loop tics don't affect the loops and thiazide, the loops and thiazide, they just improve the morbidity, not the mortality, not the mortality. Ok. They have no effect on the mortality and some data showed it it might slightly, it might slightly increase the mortality, some of that. Ok. So loops lobe usually we use loops and if patients need augmentation, we we increase with thiazide loops can be used uh parenterally in IV form in patients with acute heart failure, acute volume overload or uh tablets for uh chronic management in patients with chronic volume overload. Uh So it looks on the right then we have potassium sparing the reflex mainly we are talking about Minero corticoid receptor antagonists, cortical receptors antagonists, which drug from antagonists. You know, there are two drugs so far. Uh I only remember spironolactone, spironolactone. Uh-huh spironone. Yeah, usually we start with spiron actone is when it started. And then we have Mione. Also, there's a difference between the spironolactone and mione. Mione doesn't have the some of the side effects that spironolactone have. Ok. So spironolactone and are there are corticoid receptor or do they have any effect on mortality morbidity as far as they lower the mortality? They improve the mortality especially spironolactone. Why do you think? So, what's the difference between spironolactone loops? And that lead to this is improvement in mortality? Um To my understanding, I think spiral lactone um release this um I think it, it it helps in reducing the progression of the disease. Um So yeah, it's not very well understood. But um the most likely there are some receptors for, for aldosterone on the heart itself and these receptors have some part on the remodeling process that occur in the heart. So, by inhibiting these receptors, you would inhibit theoretically and inhibit the progression of remodeling that how spirolactone can can improve the mortality in patients with heart failure? Ok. Usually how I how do I link them? Like any drugs that can affect the system, most likely would affect the mortality starting from converting enzyme inhibitors. Arabs, uh lysine inhibitors beta blockers also can affect the uh the system and then we have the spironolactone itself. So m drug that affect this pathway most likely would improve the mortality. Ok. So this is how you can remember. So what are the side effects of spironolactone that we should be aware of? Um hyperkalemia? That's like the main thing because it's uh potassium sparing, it's potassium sparing, it antagonizes aldosterone so that it can result in hyperkalaemia, especially in patients are using Ac or Arbs or uh Lyin inhibitors because these patients are already at risk to develop hyperkalaemia. Ok. And also in patients with some sort of uh kidney kidney disease also can. So take care if patients using spironone, you need to me, you need to monitor the potassium. What other side effects tissue county. Yup, gynecomasty males and what in females can cause men irregularities in females. And we should be aware because, yeah, because it could be, um, it needs to, for the drug to be changed. That's why there's a difference between myelo and Spiron spironone can cause hyperkalemia. But unusually do doesn't cause uh g cause Spiron noun can affect the hormonal levels of and other hormones. Any, any question. There are many other diuretics but they have, they, they are not used in our chair. Yeah. Any question on diuretics. OK. Then we have vasodilators, vasodilators. OK. Vasodilators vas dilators could affect the arterial system. Mainly the arterioles could affect the venous system. OK? And uh and there are some classes but what class of arterial dilators, you know, like actin the vascular system result in arterial vascular system resulting. Uh I remem I like uh besides the nitrates because you have the uh I remember uh hydrALAZINE which we use with pregnant uh woman hidralazin is that that we talk when we were talking about hypertension, but now I'm talking about heart failure. Ok. Well, for heart failure, we we can uh maybe use uh nitrates. Hydrazine is not used. Yeah, we can use hydrALAZINE it. I mean uh II think hydrALAZINE causes uh uh art uh arterio is an arterial dilator. Uh hydrALAZINE, arterial. I know it can act on the s nitrates on the uh veins nitrate. So when we cause arterial dilators by hydrALAZINE. What will be the effect? Uh Well, uh arterial dilators will cause uh uh hypertension which uh we already like have most of the of other drugs that causing it. So it's like a very high risk for uh yeah, in patient, no intensive patient, we cannot use them like patients, heart failure but not intensive. Not hypertensive cannot use hydrALAZINE. Oh for patients with hyper uh uh heart failure and they're normotensive. We might the nitrates. Ok. Arterial dilators results in arterial part of the circulation to dilate and that will result in decrease after low decrease after low. Ok. Veno dilators result in dilatation of the veins and venules and that will result in decreasing the pre in preload and both effects decreasing pre and decrease after they are good on patients heart failure. So both are beneficial and both are uh both, both are can improve the mortality and especially when you combine to combine both effects, increase preload and load and and and and and afterwards. So we use them combined just in patients hypertension, heart failure, not we can use them in patients heart failure, even normal tensive patient. But of course, we need to monitor the BP. If patients start to become hypertensive, we need to stop or decrease the dose. Ok. Decrease the dose. Another thing to keep in mind they result in vilation and that now it depends on the dos and the response of the patient. It possibly can cause hypertension. But that doesn't mean all the patients will have hypertension. Ok. So we should keep in mind if there is arterio uh v uh vasodilation. One of the mechanisms that the heart would try to increase heart rate and contractility that is not good in patients with heart failure. That's why these agents usually are used with patients taking beta blocker. Ok. So to prevent that compensatory uh tachycardia, but usually there is combined in patients heart failure and they improve mortality, especially especially in plaque patients, African or African Americans, especially improved mortal patients for unknown reason. Ok. In your mortal is best specifically on these patients. I will see that later on. So VASS are very important and usually used in patient who have you still have the symptoms on the optimum therapy for patients who are intolerant to other drugs like uh Ac or Arabs. And we need to address the preload and after loft. So that's how by the Ac and Arabs they decrease preload and after loft. That's the uh both. So that's why we, when we use these drugs, we combine them to, to decrease the period and after that as well. Ok. But they can cause hypertension and we should take care of that. Ok. Any questions so far. So we have any drops, any drops. Ok. And most commonly used INRS is dialysis digoxin and we are just going to touch it. Digoxin is used in patients with chronic heart failure, especially in patients with heart failure and atrial fibrillation. And digoxin doesn't improve mortality. And some data shows that it, it uh it, it, it uh it uh could increase the mortality because heart failure. Uh but digoxin improves the symptoms and uh and morbidity. So it decreases the admission from heart failure. So it should be used with caution beca and digoxin has many side effects, has many drug, drug and drug disease interactions. And you should should, you should use it cautiously because it has also low therapeutic index. Ok. So to use it just for the uh when it's necessary to use digoxin, the smallest possible dose for the shortest period of shortest possible period of time. That's digoxin. But we cannot because if you want to speak about digoxin in details, we need more, we need a lot of time. Ok. Then we have beta one agonists and phosphodiesterase inhibitors. These two drugs are used in patients with acute heart failure with acute heart failure who receive diuretics and it still have this uh still have the symptoms and they just increase the cardio contractility and they can increase it the they improve the symptoms, but you shouldn't use them for chronic treatment. Uh because they in chronically, they have uh they can uh can, can uh result in arrhythmias, the arrhythmias and that usually uh can, can uh increase the mortality of patients with heart failure. Ok. Has anyone heard about ivabradine ivabradine. Yeah. II think I remember the strongest. What is varo um, I don't remember the exact mechanism but I remember it affects the uh sinoatrial node and reduces um uh uh the heartbeats. Mhm. How it, how the e and been cause this effect? Yeah, I don't remember the exact mechanism but I think it's uh uh it affects some kind of uh electrolyte channel. OK. What canal, the action potential on the, on the sa or the best maker uh is diff is different than the action slightly different in action potential. It just has what is called preload. OK. Preload. And that what creates the automaticity in the sa knot? And this is mainly because of some kinds. One of them is what is called if can what is it called funny canals, funny canals. OK. It's it, it, it uh it leads to uh you know, current of sodium and potassium, sodium and potassium. And that leads to propagation of action potential automatically for the sino atrial node. So what does aperidine do? It just inhibit this canal canal if canal? OK. And that would decrease the SA node firing and that would result in decreased heart rate, just decrease heart rate without affecting the contractivity of the heart. OK. So, and that's really beneficial when used in correct patients. So which patients we should use a for which patients we should use varo uh maybe severe uh left ventricle and uh heart failure. Mm Nope. For patient. Yes, I should. I think it's, um, we, uh, it's contraindicated for, uh, um, either chronic or acute. I don't know. I think it's indicated only in the situations where there's long term chronic failure. But for acute is, it can be contraindicated in pregnancies and stuff like that. So, in pregnancy I'm not sure in acute heart failure is not used. It's not, it's not beneficial in acute heart failure as far as I know uh when we can use it, it's for chronic heart failure. Mm Yeah, that's what I said. Yeah. Yeah. In patients who are taking beta blockers but it's still their heart rate is more than 70 beat per minute. Ok? 70 BPM. So still that means the beta blockers cannot control the heart rate well or patients who are intolerant to beta blockers, for example, asthmatic patients or patients who are having a bronchospasm from beta blockers or some diabetic patients. Ok. Uh and in terms of the ejection fraction, um should it be less than either 30 or 3540 or something like that? Uh to be indicated for no the indication when uh just when there is high heart rate, despite the beta blockers or patients are into the beta blockers for ejection fraction, less than 35 is usually the advanced heart failure in that like specific group uh to manage it. Ok. Thank you. Ok. Uh what's like the um uh heart rate uh limit that we start using uh I more than 7070. So patient with optimum beta blocker still have high heart rate or patient with beta blockers and we need to control the heart rate. So we use, if patients have the asthma, maybe patients with asthma who are contraindicated for uh beta blockers, we can use uh yes, we can use a after using the other agents and still patients have high heart rate, but you should be aware of that. It shouldn't be used in patients with atrial fibrillation because atrial fibrillation, the firing inaction potentially starts below the sa not, not from the sa not. And by further inhibiting this, you know, you might precipitate acute attack of atrial fibrillation, you might augment atrial fibrillation. Ok. Any question on you. Ok. So next, last drug we talk about is nesiritide. What is nesiritide? Glyceride is a recombinant? Beta retic peptide BMP. Ok. So it has the same effect as BMP. That's sis sis and um as far as I remember, it's only used as parenteral agent as I viv agent. Ok. And it's used in patients with acutely convul with heart failure after using the first line medications. That's the diuretics. One of the one of the options can use neide. Uh so an AIS will result in could result in improvement of the symptoms these patients. Ok. And it's, it's, it's um it's not, it's like a, a new agent, not that old, but I guess it's quite expensive. Ok. Any question you see in the, in the left side after using ivabradine that there is slowing of the heart rate, is slowing of action potential as the heart rate, it's a blue and the pink. Ok. The other times that there are many, many, many drugs that could be used in heart failure, but these are the most important ones. Yeah. Any question on the medications. So, can we take additional 10 minutes or maybe 15 minutes? That for questions, Hussam. Just general questions. Yep. If anyone wants to come on to the stage, although you're all very reluctant, um, if you want to come on to the stage, you can, or you can put your question in the chat, we don't mind either way. Just we want lots and lots of questions. Yeah, I guess we need sessions on cardio pharmacology. Ok. Um, yes, I, and that's, uh, cardio pharmacology is a weak link actually because it's because of the drug interactions. So we're quite cautious about um, how the drug interactions are gonna work in relation to, um, especially the acute uh chronic failure. So that was one of the anxiety. So if you could do cardiom separately, that would be handy. Ok. Yeah, because like, uh, it's kind of complicated uh to connect all the dots. Uh Also I have a, a question. Why don't, uh is it like contraindicated to give, uh, ace inhibitors for uncompensated heart failure? No, no, just you need to take care of patients presented with heart fail and uh hypertension. Other than that, you start as soon as possible as soon as possible. Mm Usually on the first day that patient present with heart failure, there are uh some, some uh ways like some physicians prefer to start with uh with uh 11 drug and then add on the other drug. And but many physicians prefer to start all drugs on uh on the smallest dose possible, like start with one of the angiotensin medro corticoid. So glucose and so on and then uh build up on the on the dose. But usually for all medications start as soon as possible. Just you need to be extra cautious with beta blockers and stuff but other medications are ok. Yeah. Um II have a question about like maybe previous sessions I think they were explained but uh I wasn't there, sadly. Um um I have a question about like uh the types of uh heart failure. Uh what's usually the most used uh like I've seen so many clinical uh and uh other uh schools have different uh typings to heart failure and classifications, which is like the most common one used. Yeah, for a clinically useful one, especially for management. You need to classify heart failure based on ejection fraction and knee classification, ejection fraction and classifications. These are the most important from clinical part of clinical point of view. OK. And that we'll see we'll just, we'll talk about how to manage heart failure is reduce injection fraction and other other uh ha other types of heart failure depending on addiction fraction. OK? But there are many ways you're right to classify heart failure. Yeah, because like uh I was uh revising my lectures and I've seen like the types of heart failure. So it was classified into left ventricle, right ventricle, bi ventricle. Then uh yeah. And then there's high out uh high output heart failure, which was a bit confusing just for, for your clinical uh party. Remember the ejection fraction and the knee classification video and cardio facility. Hm I'll try to remember. I don't nothing on my mind right now. Ok. So let's go for acute heart failure. You will have to manage heart heart failure. Uh You need to put the patient on cardiac med 45 degrees bed. Keep the patient aright. That will help with that the blood. Ok. And of course you need to address ABC S. Maybe patient has some breathing difficulties. Maybe the patients is uh most patients are hypo hypoxic. So you need to give oxygen. Maybe the patient has hypotension. You need to address that as well and many patients end up needing CPAP, CPAP. Ok. Positive pressure, ventilation, positive pressure, inflation. And uh of course you need most patients need to be admitted to the CC and attach the monitors and attach the monitors. Ok? To, to look for ECG to look for uh BP, heart rate and all all the vitals, ok, saturation. So that that is the monitors and just from the monitors, you could have a a clue about the cause. So many patients or almost all patients acute heart failure, you need to start with nitrates and there is a mild loop diuretics plus minus nitrates, loop diuretics plus minus nitrates. So, diuretics will relieve the congestion and should improve the symptoms and that will relieve, result in decreasing the the preload that also should improve the uh lead to heart to pump uh stronger and improve the cardiac output. So, if patient still have symptoms, you can use IRS either beta one agonists or uh you can use fosse inhibitors. And some patients also can use digoxin as well or ide uh if it's, if it's available. Ok. And if patient is still symptomatic, you need to go for a device called intraaortic balloon pump, intraaortic pump. And this is invasive and needs uh needs a expert. Uh expect someone expert to, to, to give intraortic B. Um So this usually is a sequence of managing patients with acute heart failure, uh the vital disease and give loop diuretics in addition to s and if patients have still have dyspnea, you can give uh morphine that can improve the dynia, but don't use morphine unless it's necessary unless the patient has still has dyspnea despite all these medications because morphine doesn't morphine cause uh um it doesn't morphine inhibits uh the breathing. Uh Yeah, that's why you need to be cautious with morphine because it can stop the respiratory depression and also it can cause hypertension. That's why you need to be careful. Uh Why do we even give morphine? It's uh it improves it, it improves the dizziness. Oh, yeah. What's like the mechanism? I don't, I don't. Ok. Any question in acute heart failure. Uh Doctor, could you, could you repeat that? Actually? Um morphine inhibits um morphine can inhibit Respi can cause respiratory depression. And that would further results in further hypoxia and can also result in hypertension, hypotension. You said hypotension, hypertension? Thank you. OK. Another question. OK. I think I was hoping to f to end this today, but I guess you need time to revise all our three talked about. So let's stop here. Next time we speak about management of chronic heart failure and I can prepare for you some questions in some cases. Um uh Can we use uh beta blockers for uh acute heart failure? No, of course not. Of course not. One of the contraindications of beta blockers is acute heart failure and advanced heart rate. OK. Yeah. So ef uh under 35 what uh advanced heart failure is like uh ejection fraction under 35. Uh There is uh there are some definitions of advanced heart failure because because them last next time, but it's stage D if you just go to the previous sessions, you find the one of the classification is stage ABCD. Stage D is a trans heart failure. OK. And it needs a specialized, like uh uh card speciali cardial, specialized in heart failure to, to plus. Ok. Ok. Deep breath, respiratory respiratory dyspnea sometimes. And then that beta blockers can also exacerbate the symptoms. Right. Yeah, beta blockers can uh because patients acute heart failure has a lower, lower cardiac output and beta blocker can further decrease the output. It's it's it's quite the opposite in patients, acute heart failure, you can use in the drops to increase the cardiac output to increase cardiac contract in the cardiac output. But you cannot use negative in the tropic agents in patients that acute heart failure. Yeah, it makes sense. Yeah. Yeah. And also uh you remember the first one said calcium channel blockers can be used in heart failure. Actually, no calcium channel blockers. You have two types, cardioselective calcium channel blockers. They are negative in topics. They cannot be used in heart failure. Ok. It's contraindicated in heart failure and they are a vascular selective uh uh calcium channel blockers. They have no benefit in patients with heart failure. They might have benefit in patients with hypertension, patients with ischemic heart disease, but they are not beneficient in patients heart training. Ok. Another question. Ok, just um please go over the cardio pharmacology again. Any questions? Just shoot it to me on the Twitter or ran and next time we wrap up the, the topic. Perfect. So, one more topic on this one and then we're gonna move into some other topics. All right, Hussam has kindly said he will, uh, cover some other topics for us. So as always fill out your feedback form which will be in your inbox and your attendance certificate will be on your medal account once you've done that and we will see you at our next event. Ok, everyone take care. Have a good one. Good luck. Hi.