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Cardiology Session: Heart Failure - part 2 | Hussam Alkhalifamohamed

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Summary

This event is for medical professionals interested in continuing their education on cardiology through Sped's fair medical education program. The interactive session will explore metal's vision for healthcare training being available to all, no matter location, wealth or circumstances, and will feature a talk by Hus Sa continuing his talk on heart failure. A special guest for this session, Maram, will share her experience of using Sped's platform to reach out for medical education during a traumatic time in her native Sudan. The session will also feature interactive questions with an emphasis on peptides and the renin-angiotensin system in relation to heart failure. Everyone is invited to join in the conversation, either through typing in the chat or, if you're feeling brave, you can join Sam on stage and answer and ask questions verbally.
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Description

Please Note: As this event is open to all Medical professionals globally, you can access closed captions here

This is our second teaching with Hussam Alkhalifamohamed, this will be interactive with lots of questions and learning. You can find his previous event right here: https://app.medall.org/contents/v-cardiology-session-heart-failure-hussam-alkhalifamohamed

None of the planners for this educational activity have relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

Dr. Alkhalifamohamed, faculty for this educational event, has no relevant financial relationship(s) with ineligible companies to disclose.

Learning objectives

Learning Objectives: 1. Explain the history of Metal Education and its vision to provide healthcare training to all, regardless of location, wealth or circumstances. 2. Identify various peptides that are released or regulated when the heart is stretched, including atrial natriuretic peptide, pro-atrial natriuretic peptide, and renin-angiotensin system. 3. Describe the normal cardiac cycle and heart sounds and the changes that may be seen in pathological conditions. 4. Describe the structure and main functions of the heart and how cardiac muscles contract. 5. Explain the role of the autonomic nervous system in reflexes associated with the cardiovascular system.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello everyone and welcome to our event today. We have Hus Sa who is gonna be continuing his talk on card card and we're gonna do something a little bit different with you. We're gonna make it a little bit more interactive. But before I do this, I would love to tell you a little bit about metal but mainly how metal education where we are now came about. Um Metal has been around for a few years now and it's primarily to help doctors and students with their continued education. Medal's vision is that healthcare training is available to all no matter location, wealth or circumstances. Every one of our healthcare professionals worldwide should have access to good quality learning. So a few years back, we created fair medical education, which is where organizations like the Royal College of Surgeons of England, uh bo A bo ass and many other organizations can host their events through Metal and offer those in a lower middle income country free access to their events. This is all done through the verification scheme and I know that for some people who have fled um a troubled country, this is where some of you got stuck and actually had to reach out to us to me on support and say, hey, I don't have my ID. I fled a country and can you help? And this is where my good friend Rem comes in who has joined me today to cohost. So I would love to ask Marre if she would mind speaking and tell us a, a little bit about herself how she found Medal and, and to let us know uh what was going on in Sudan and how she helped us both med education. It over to you. OK, let me restart. Um So as I was saying, um during the, since April there have been going on that and that we have to leave the country. And because of that as well, there has been a lot of interruptions that happen between education in the country starting from um universities stopping and for us who are actually nearly graduates who have to like stop train and so on. So I was having a lot of free time during that time and I didn't know what to do. So I was looking online for any platform that would offer something right now, especially since due to the fact that most of my colleagues and my doctor and the doctor also to contact them. So I stumbled across the all and I tried to sign up because again, as you mentioned, because of the whole situation with not having all of my papers, not having your email, not having any of these, I was able to verify it. So I basically contacted you and told her about the situation and I explained to her that to be able to access it all. And she was very supportive. So like immediately she helped me out with the verification, explain how to verify. And I shared it on my social media. And so the moment I shared it over there, so many like thousands of people started reaching out to the middle trying to sign up as well. And it was a really large overwhelming in of people who all want. And so afterwards, we decided to take it even a bit further. Um we decided to start this channel for this channel and actually invite other doctors from all over the world, including to these doctors, like to give that as well to the current people and people of Ukraine and anyone else who is and for like anyone who else is affected by. Um so this is currently free platform for also people and all people currently going through the same situation, you can easily find the time and we do have the time actually a lot of it. So we find the help and uh support to actually continue our education and not forget about everything, ok? Because it's actually very difficult at the moment to keep up with medicine and so on. So thank you so much, Sue and thank you doctor Hassam and everyone else who's actually contributing. So really that is how me education came about. We it came about because Mam contacted us. She explained there was an, there was pro that, you know, what was happening in Sudan. And we just felt we have to step up, we have to do something more to help ma we have people as in as speakers, good speakers on our platform. We have contacts, we have the platform. So let's go the next step. And that's when we reached out to consultants who are already using our platform. And Maron reached out er for Sudanese um or anyone, any er doctors or anyone who wanted to teach to get in contact with us so that we could start planning these educational events for doctors and students to come along and uh bolster their er al already what they learned. Um And that's where, that's why we are here today and, and I am so happy that Maram was able to join us and I'm really happy that Hossam has come back for another teaching er event with us today. So I said to you at the beginning, we're going to do something a little bit different with Sam's teaching. If you were here with us last time you'd have seen that it was very interactive and I'm sure your fingers hurt at the end of the talk because he was asking you lots and lots of questions. So this time. What we would love is for you to, to join Sam on the stage uh with your mic camp off, that will be automatic. Um And you can come along and you can answer the questions verbally and you can ask questions verbally. So if you would like to join, I would love for you to type, join in the chat. I'll invite you onto the stage and you can just sit there, watch, watch what's happening. And if your son asks a question that you think I know the answer to that you can just turn your mic off and give him the answer. All right, you can also still use the chat if you want to. Don't feel like you know if you don't want to come on to the stage, that's absolutely fine, but we would love for you to come onto the stage and answer and then we can get a lot more, we can get through a lot more and it'll be a lot quicker. Alright? If if we don't have people saying join, then it's gonna be like school where I actually invite you anyway. So it's entirely up to you. You either put, join in the chat or you get invited onto stage anyway. Alright. With that Cosan, I'm gonna pass over to you. Alright? Ok. Thank you. Thank you maam for the nice welcome for us today. Uh Hello again, it's always a pleasure to be here. Uh so let's go directly to continue our session on heart failure. And please please do join the stage and uh just try to try to be as responsive as possible. Even if you feel like I may know the or I don't know the answer, just try to try to bring it out. Ok, so that all we can learn. OK. So last time I started to talk about heart failure and just we started on the very basic stuff about uh the structure of the heart, the two functions, main functions of the heart, the heart muscles. And and I just brief talking about blood supply and how does the heart muscles contract and how does the heart muscles contract? And also about the cardiac cycle and heart sounds the normal and and some of the abnormal heart sounds. OK. And also have to talk about action potential and how action potential is conducted throughout the heart. And also just we had a touch on the autonomic nervous system and reflexes that could affect the cardiovascular system. And we mentioned plod and after lo and we finished all the homework that I gave to you to, to to to look for peptides that could affect the heart or could be released from when the heart is affected. So who looked for that and can give us some examples of the peptides. Any peptide, any peptide, any peptide could be hormones, could be uh another, another molecules, other molecules. So just feel free Yes, I do. We know that they are made peptides. There's many hormones, many, yeah, feel free to put your arms as a cat or preferably to talk and the restaurant. So OK, we know that there are many peptide. Uh Yes. A MP A MP is one of the examples atrial peptide A MP. And also there is another one just like a MP released from the the atrial pet from its name atrium. So it's from the atria. And also there is another one that secrets from the ventricles called P MP. PNP also. OK. Uh Pre nitro T. So what what does this nitro bips do? And why is they are secreted? I doing a little um they're secreted as a reflex when the heart is stretched. So the atrium is stretched, the A is secreted. OK. Yeah, exactly, exactly. And that could happen in, in, in many conditions. One of them when it happened due to heart failure due to heart failure. OK. So what do they do? What do they do? A PM PM? Their functions are very similar. Um They have, they, they have an II I that effect they, they come as a mechanism to flush out the fluid that I build because of the heart failure. So they have a di in Yes, thank you from its name na na tic peptides. So they do not, they try to get rid from the sodium. So and sodium is always followed by water so that they might get rid of the fluids that are accumulated in the body uh in, in conditions like heart failure? Ok. So these are one of the examples of the peptides. What else do we have? What else do we have? We have many, many, many plans. There are main players and there are also other players as well. We also have, have you ever heard about rain? Rain? Yes, rare. And what does ras stand for stress? What the stress stand for renin angiotensin system? A system is a very important system in many cardiovascular conditions. This system is implicated. OK. So it's, it's very, it's very important system uh uh to maintain uh physiological and hemodynamic status but uh also during some pathological conditions. OK. And what, how does the system work for system? How does it work? Anybody knows when there is heart failure, there is uh a low flow flow to the kidneys. Yes. With the secretion which will act on the angiotensin again, which are in the circulation and converted by the angiotensin converting enzyme to angiotensin two. It then act uh on the, on the kidneys and the to this thing. OK. OK. Yeah, just you are talking about heart failure here. We mean on you are right. But we what we when men first and the physiological status on just normal day to day living. So re get a strong system. It started with dr release from glom apparatus into the kidneys and renin has many stimuli. For example, as mentioned, low blood flow to the kidneys. Ok. And los of deliver it to the kidneys that will stimulate renin secretion also, don't forget renin could be stimulated from sympathetic stimulation through beta one receptors through beta one receptors. You should remember that through beta one receptors. Ok. And where a stimulator is secreted and acts on, on a on a peptide released from the liver That angiotensin again, angiotensin again. OK. Angiotensin again is then converted by renin to angiotensin. One angiotensin one is an active peptide but has a weak activity. Ok. So that's what angiotensin one is circulated until it reaches the, the lung. So it's converted through angiotensin converting enzyme to angiotensin. I and angiotensin two, I has many, many effects, many, many effects including it's a very potent vasoconstrictor causing vasoconstriction. OK throughout the body. So it increases the BP. Uh it also increases uh aldosterone secretion. Al Theron is one of the is one of the uh molecules that want to retain sodium inside the body. So, sodium will be followed by water. OK? And that in some conditions might lead to, to swelling in some areas. Ok? And or ox gets rid from potassium. Ok. So it secrets potassium and that is some conditions might lead to hyperkalemia. Also angiotensin. One of the things that angiotensin can, could do is increase sympathetic stimulation and what does sympathetic stimulation do to the to the re it could increase the rein secret. OK. So the, so the acts as positive feedback uh for each other. OK. So that renin angio strong system is a very important system. And we have a lot of a, we have a lot of uh peptides and systems that act in the heart including including the uh epinephrine or epinephrine, including many other uh hormones and peptides. OK. So just ren a strong system is very important regarding the heart pa. OK. Uh in order to understand anything about cardiology in clinical parts, you need to have, you need to have uh a basic understanding, at least basic understanding of the history and examination of the heart, how to take history because this is how you are going to approach the patients and, and you know that the patients might have heart failure and how to do the examination and what you could you expect from the examination? Ok. So we'll then I talk about how does the, how do, how do patients present and the clinic in the clinical presentation part? OK. But now we're going to talk about some things about the examination of the heart. OK. Just in the next slides. OK. So this is the action potential we talked about last time and um we we we could read the action potential of the heart through ECG 12 leads ECG OK. And anyone who was able to remember the ECG components and run us through them electrocardiography. So we have many, as you see, we have many things like P QR S. What does these things that stand for? Anyone? Don't be afraid. I know that A CT sometimes could be a nightmare for, for, for students but don't be afraid. Yeah. All you need the basic stuff. Yeah. P is atrial depolarization. B is atrial depolarization and we know that this disease comes mainly from the S A not B is atrial depolarization. OK. QR S is ventricular depolarization. Yeah, ventricular depolarization looks. How narrow does this QRS look? OK. Because if it's one that's, that indicates there might be some abnormality and QF is ventricul repolarization. So atrial depolarization, ventricul ventricle rep where is atrial repolarization. Yes and done by PR S. It appears like in uh more or less, it's the same uh QR S. Uh so it's hidden by the QR S component. So also we have PR interval, this is the time it takes for for the action potential to, to drop it from A no until it reaches the every node. OK. Pr inter through the interatrial pathways, we have the ST segment ST segment from the start of S to the T to the T wave and this is time. So it takes for the uh action potential to travel through the ventricles. And then we have the QT interval that all the whole action potential for the ventricles from start of the Q to the end of T OK. And all of these are important. All of these are important. Then you have the 12 lead ECG through the 12 lead, six chest leads, OK? And three limb leads and three margin leads. So this 12 lead ECG is uh is record record. The E is protected from different parts of the heart. OK. So different areas. So just remember the ECG because it's important in the and see, OK. And you may have cardiovascular conditions including heart failure and it it might help you to diagnose heart failure and it might help you to to have a clue about the about the cause of the heart failure as well. Ok. So the the ultimate function of the heart is to give the body with the with the uh is pro provide it's providing body with the with the blood, right? So in form of cardiac output, what is cardiac output? It's the amount of blood pumped out of the heart each minute. Now the blood dumped out each minute, each minute. Ok. This is very important and usually uh this amount, how much is this amount? Usually about five liters is around five liters, around five liters. Ok. So the heart has to pump around five liters more or less uh each minute. Ok. And what are the determinants of uh uh cardiac output that how how can I go in? Yeah, heart rate and stroke volume, heart rate and a stroke volume. What is his drug amount of pump out of the blood. Each its cardiac beat, its contraction. Yes, each each beat. That's why it's, it's uh heart rate is time stroke volume because the stroke volume is amount pumped by the heart, each beat, each beat. Uh multiplies out your heart rate. That is the rate at each minute. That gives you the cardiac output. Ok. That gives you the cardiac output. So the heart rate and stroke volume. So anything that could affect heart rate, the stroke volume could affect the aortic output as well as well. What could affect the heart rate? What might affect the heart rate physiologically? What do you mean out? What by physiologically you are right? Just explain to us, please. Yeah, high temperature, your temperature, sleep exercise. Yes. Ok. Yeah. Sympathetic and the autonomic component, sympathetic and parasympathetic. So heart tempera increases heart rate, low temperature decreases heart rate, exercise increases heart rate, sleep, for example, decreased heart rate at rest. Uh sympathetic innervation increases or decreases heart rate. What are the effects of sympathetic, am very sympathetic? What is the heart rate? The heart? I measured them last time. Yes. Increases heart rate. Where is mm it decreases heart rate. Ok. Anemia. Yeah, it affects the heart rate and it because it increases the workload and anemia can lead to a specific type of heart failure. We're going to talk about that next time. Ok. And so the physiological omm what else could affect the heart Ok, let, let's, uh, uh, go to stroke volume. What could affect the stroke volume? Yeah, a shock affects the heart rate but it, it is not like that affect it, reflexive effect. It's a compensatory mechanism. Yeah, but you're right at the end it affects the heart rate. Yeah, frankly speaking. So, uh, stroke volume. What could affect the stroke volume? Yes, that, are you aware of that? Ok. Preload and afterload, please. Uh, Yeah, so preload is about the amount, sorry. Uh So the more blood that's in the heart, the more blood that's going to be pumped out, that's for the preload. Um an afterload is about the amount of resistance against the the yeah, the resistance that the blood has to pump against. Ok. Ok. So any anybody just has like my mom said, what my mom said is correct but just we need to do minor correction to what she said or minor addition. Anyone anyone could uh yeah, the they preloaded the amount of the the clot in the heart before the contraction before the cyto uh it means basically the load of the heart before it get contract uh pumped out of out of out of the heart. So it's called the load, the load of the blood in the heart before the contraction. Other one we can, we can call it in in diastolic volume. Ok. Ok. That's exactly what said suggest in different words. Anyone anyone could correct. Correct that. Yeah, they, what they said is correct. But we need the better trend for that. Anyone. Is it preloaded the amount of a stretch for the heart muscles before systole the amount of a stretch? So if, if there is increased venous return, for example, that stretches the heart more, right? So yeah, when you have more blood, that means more stress, that means more uh strong contraction and more strong volume. So preload is the amount of stretch. That's the amount of the blood blood is one of the things that affect the stretch that affects the preload. Yeah. Uh ok. And if you mean the preload, yeah, preload is the amount of the stretch of the heart before the system. So one of the things or one of the main determinant of the preload is the venous repair, the venous repair as venous return increases the stretch increases, contraction becomes a strong gut and then we have more stroke volume. Ok. So it's a amount of stretch that could be affected by the blood or other other things as well. So one of the things that affects the preload is the blood is the venous return is the blood amount of the blood. Yes, I agree, but it's not just the amount of blood, it's the amount of the stretch. Ok. So that's the pillar after all. Yeah, you all got it correct. That is um the resistance again, the ventricles, mainly the left ventricle should contract to, to to to to get rid, to inject the plot. So that's after load in increasing preload means increasing stroke volume and increasing afterload means decreasing stroke volume, decreasing stroke volume. Ok. So this the main, these the main uh uh factors that affect the stroke volume, preload and afterload. In addition to other factors as well. For example, also autonomic nervous system could affect this uh stroke volume by increasing or decreasing contractivity. Ok? Anything that increases contractility is called the positive inotropic, build positive inotropic. Ok. And anything that could decrease contractivity means negative inotropic. For example, exercise increases contractility through different mechanisms. OK? Through different mechanisms and that leads to increased contraction and increased uh stroke quality. OK? And for example, sleep, it decreases contractivity. So many things that could affect the stroke quality but in the main things are preload and afterload. OK? And this is why it's here, it's a control uh cardiac output is controlled through different mechanisms. Neurohormonal control. OK? Through the nervous system, mainly through the autonomic nervous system. Ok. And sympathetic, increased cardiac output and parasympathetic decreases cardiac output through different hormones, which hormones other than epinephrine and norepinephrine. Ok. Although they act mainly as neurotransmitters but also can act as hormones. But other hormones can affect the cardiac output, increasing or decreasing cardiac output. Dopamine. Yes, dopamine, dopamine, dopamine increase or the car increases. Crazy. Do you know through which receptors do you know her receptors? Dopamine increases cardiac output by increasing contraction through be one receptors through be receptors. Ok. Thyroxine, thyroid hormones, thyroid hormones, increase cardiac output by increasing increasing sensitivity of uh upregulation of beta receptors in the heart thyroxine. Ok. That's good. Then we have preload and after we discuss that and then last thing we have the Frank Starling mechanism. Anyone remembers this Frank Starling mechanism that discovered by Frank and later on uh confirm this by Starling. That's a good question. What is the normal range of stroke volume? I ask any blood knows who us. Yeah, the normal, we are speaking like the normal range. Yeah, roughly around 50 to 152 100. OK. Yeah. So what is Frank startling me against it is said that energy contraction is direct in proportion to the initial links of the muscle fiber of the heart. OK. So when when you have increase in preload means increasing the the stretch of the fiber. So the fiber of the bio side get uh more length. So the energy of contraction will increase. Yeah, exactly. This pravastatin uh links mainly the venous repair which affects the preload to the cardiac output. So if you have more venous return, that means that that's just the the the ones that I explained earlier on when you have more venous return. This means you have, this means you have uh more stress, it means you have stronger contraction, which means you have higher cardiac output. OK. So that is for a mechanism. Ok. So um there was a question up say about or systolic and diastolic pressure. Ok. Systolic and diastolic pressure are affected directly by the cardiac output. Systolic pressure. The cardiac output is the main determinant of systolic BP. Ok. Increasing cardiac output, increase in systolic BP and decreasing cardiac output, decreased systolic pressure. Uh The self pressure mainly depends on the depends on the blood vessels. Ok, especially on the diameter of the blood vessels, the peripheral vascular resistance. Ok. So decrease or increase in pressure. Yeah, it can affect the heart indirectly by the power receptor uh reflexes. OK. But the main effect says the systolic BP is mainly affected by the cardiac output. OK. So any question, how about here be this is very important slide because the fair thing on the heart failure is decreased cardiac output is decreasing cardiac output. So any question you should know it, especially about the control, you should know that. Ok. OK. So just let's talk about the examination of the heart exam if the heart is is uh we cannot cover all of it right now, but we cover the most important points so that we can understand when we talk about the pa and the features of the heart failure. OK. Whenever you start examination of the heart, please start with after the general look of of course. OK. Constipation just start with the pulse. OK? Start with a pulse and it the B you need to comment on many things including great a great ay, OK. Just start with pulse and then you need to measure the BP, of course, and measure the GV P. The GP, that's the venous pressure. OK. That is the jugular venous pressure. So we start on the radial part, the pulse, then the uh near the elbow to measure the BP and then JVP in jugular venous pressure. OK. Then go to Precordium. That is the chest, go to the precordium. That is the cardiac part of the chest. OK. The pericordium, we have many steps to do. Starting from palpation up to cult. OK. Up to cult. So let's just get immediately called a for auscultation. What do you want to listen to a cult? What do you want to listen to presence of memories before that? Right? But before that, this order is important. Yeah. Yes. Yes. Try, try, try again. No problem. The rhythm of the heart. The reason we uh we comment about the rhythm of the heart just when we palpate the P OK? But when we ate, first thing is to listen for the normal heart sounds. S one and S two, you might listen in any order but when any comment about the car in order, OK. S one and S two. Are they normal? Are they abnormal? Are they present or absent? OK. Also makes, makes difference. And then if there is any added heart sounds N S3 or NS four N S3 or NS four, that's important. And after that, we comment about the murmurs if there is any murmur. So for example, normal S one, normal S two, no added sounds, no murmurs or for example, absent S one normal S two presence of S3. And then for example, we have the systolic murmur for exam. OK. So yes, when you comment, comment like that S one S two sounds if there are other sounds, you mentioned 344. OK? And then the M pre of me. Ok. So usually the consultation is the last part of the examination but not to the last part of the cardiovascular examination after that according to the responses. But uh you need to go to check for in the lower lymph to check for the peripheral pulses as well and and the lower limb edema in the lower limb edema. Ok? And also you need to do some abdominal examination not to the whole abdomen. You need to check for the liver maybe because there is he an increase in liver and you want to see if there is any, any esti, OK. So again, pulse blood pressure, yeah, and the back as well for anak that is when you have edema that pushes the back as well. Be pressure, BP p then per Corum all the steps up to the cult to listen for the heart sounds and murmurs, then the abdomen for a sinus and liver, then you have to go to the lower limbs and also don't forget about the back. OK. So for example, for example, if you have heart failure, we might find according to the, according to the cause of heart failure. But in any case, you can find low pulse, low pulse volume, for example, OK. BP might differ but you can find some something about low BP as well. OK. D AVP, you can find increased DVT, you can feel pressure from in or because even the right ventricles cannot push the, the blood OK to the lungs. And then, um, you can find some, some uh, uh, s find especially S3 and, or S four. OK. You can find some murmurs either because they could be the cause or secondary to the stretch of the heart and then subsequently the valves as well. Ok? You can find some anti, you can find, find some lower lymphedema. Ok. So, so that's why this all steps are very important and this just as part of the cardiac examination, just part, not part of the cardiac exam. So that's why we're gonna also, we're gonna comment on the bowels, the blood pressures, the and so on. OK. Any question here. Yeah, it's, you should, you should, of course, you should bump it for speed, for any replacement. Yeah, you're right. That might even give you a clue about the possible causes. Any question here. Don't be afraid to ask any question, please, even if it's on the previous slides. Ok. Ok. So let's go for path physiology class is a hu remember all the points we just discussed, Jose, they will, they will help us in the upcoming discussion. So before we start, what do you think? The both certainly is the heart failure could be what could happen fair and what could happen subsequently? What could uh what could contribute to heart failure and what could happen from the heart failure? Yes. Anything that you think could is related to but just bring it out. Don't be a ok. Can you, can you explain that please? No. Ok. And heart is unable to pump to maintain his organ. Like if if there is a a long time hypertension or anything affecting the blood vessel, I mean, affecting the afterward the path of the surgery start with the ventricle with when it start to hypertrophy. So left ventricle hypertrophy is one of the path pathophysiology factors of the heart failure. Then you have to as in of the hy uh of the hypertrophy or to any other cause like if it is uh according to the cause, I mean like if this is any other factor all along the sudden hypertrophy, then the low cardiac output, the ur system nor neurohormonal mechanisms all affect the pa of the heart failure. Ok. Ok. There are many answers. Let me check for that. Ok. And heart pump increase demand that the heart can compensate structural function. Ok. Pretty good answers. So what could cause heart failure? What is the most common cause of heart failure? It is the most common cause of heart failure. Generally speaking, arrhythmias, arrhythmias could cause heart failure, but usually there are, there are consequences of heart failure. Ischemic heart disease, hypertension. Ok. What else could cause heart failure? What is that for stomach anemia, valvular heart disease, CKD, heart resting rhythm, smoking, decreased blood drug like hemorrhage. Ok. Congenital heart disease. Ok. Ok. Thank you for sharing. So, heart failure because it's, it's, it's like a common, it's like a common pathway except the defects. Yeah, it's like a common pathway for many cardiovascular conditions. So it's, it's one of the major causes of morbidity and mortality worldwide. What is morbidity and what is mortality? It is morbidity and that is mortality. Yeah, morbidity related more to, to, to, to, to when the disease like affecting quality of life and so on. Ok. And including the admission to the hospitals. Ok. And mortality related to death. Ok. More related to death. So the heart failure could affect the morbidity and mortality of the patient. Ok. Increasing morbidity and mortality and its major cause of uh of uh it's decreased morbidity and increased mortality. So, and worldwide, this is the most common cause of death. Ok. Most common cause of death, heart failure. And unfortunately all the statistics suggest that heart failure will be increasing with the ear, with the ears. Ok. Uh, unless there are many interventions are put on place. So, and unfortunately, there are like these, there are certain racial and ethnic groups, ok. Uh, are more susceptible to, to, to have worse morbidity and mortality from the heart failure. Uh, a group. Ok. And including low, uh, groups with low socioeconomic status and other groups as well. Unfortunately, and that also just add to the complexity of the disease. OK. So we said heart failure is the fairest thing to regardless of the cause. Generally speaking, because there are exceptions, generally speaking, the fairest thing to have heart failure that the heart fails to do its functions, heart fail, failure of the heart to do its functions. What are the function of the heart to contract or relax? And these two functions uh are organized to to have all this for the body to have optimum cardiac output. So when one of these or two of these functions is affected, then they will be decreasing cardiac output, decreasing cardiac output, decreasing cardiac output, then decreases blood supply to the peripheral organs. So these peripheral organs now need to, to do something about that in order to, to have its blood supply. OK. They will protest against that. Is that what will lead to subsequent steps in the heart failure? OK. So let's see. Let's go here. OK. So when there is heart failure, there is just cardiac output. So how, how do the peripheral organs by neurohormonal activation. Many, many, many mechanisms will be active in order just to compensate for decreased cardiac output. OK? Including MP nervous system, strong system and other, many other systems as well. Many other systems as well. OK. So this is a fair thing. Reduce cardiac output, decreased peripheral uh blood supply and Neoral activation, neur hormonal activation. And we all know that they could be, the failure could be from the right side, from the left side or both sides of the heart or both sides of the heart. OK. So, and there the classification now clinically less uh less. Now it's being less used than before the left, right sided heart failure. But the pa of hiss discussion is good. So what is the difference between left and right sided heart failure much? What is the difference between right and left side of heart? Right? In terms of anything clo symptoms, anything? What are the differences? Sure. OK. This heart and the lungs are affected uh heart failure. But OK. Yes. OK. Left side of the heart, the left side of the heart is unable to get blood to the systemic circulation. Ok. So, and then the blood has to build back to the lungs. Ok. It has to build back to the lungs. And this when now that we have more like uh a fluid accumulation in the lung and that might lead to pulmonary edema, pleural effusion and pulmonary. Ok. So, this, the left side of the heart cannot block the stomach circulation. Now, there is back pressure of the blood to the to the lungs. This is the left side, this is left sided, heart failure, ok. A right sided heart failure when the heart cannot push the blood to the to the pulmonary circulation. Now, the there is the back pressure to the stomach circulation to the venous circulation. Ok? From coming from inferior aci peri vena cava. And mostly it will go through inferior vena cava because of the gravity. So it, it all accumulates in the peripheral limbs on, on the abdominal organ and the proton and in the liver as well because we know that uh the most of the blood coming from low from the low side of the body goes through the liver. Ok. So it's not, it goes back to the liver that might lead to some edema in the peripheral organs and also the lower lips as well. Ok. So, and the most common cause of right-sided heart failure is left-sided, heart failure, left side of heart because the BP to the lungs, then from the lungs to pul the trunk, from pul trunk to the right side of the body. Ok, right side of the body. And ultimately, both of them can lead to congestive heart failure. So it can start as left, then it affects the right side can start as right and it the heart. Ok. So this is one way to look at the heart failure. There is another way we said function of the heart uh to contract and relax. So also the failure of the heart could be due to failure of the contraction mechanisms or failures of the relaxation mechanisms. So, when we have failure of contraction mechanism, this is called systolic heart failure. That is because your system is the heart should contract when there is failure of relaxation mechanism, which is called diastolic heart failure. Cause here we, we have uh issues with relaxation. Ok. We have issues of relaxation. So it could be systolic. For example, if you have MI I OK. And my in fracture that leads to necrosis of the muscles and that of these muscles and then the muscles now cannot contract because they are dead. They are dead, that leads to systolic heart failure. For example, if you have a condition called restrictive cardiomyopathy, that restricts the heart from relaxation, that might lead to the heart failure. So could start the could be systolic or diastolic systolic or diastolic. Anyway, that would increase end diastolic volume in diastolic volume. That is the volume at the end of diastole because now the heart, the there would be no enough injection of the venous return to the heart, not enough filling of the heart by the venous return. So it will be back pressure to the venous circulation in diastolic volume increase, that would increase in diastolic pressure as well, OK, in diastolic pressure as well. So that also might increase venous pressure. Ok? So from the heart to the veins, the heart to the veins, ok. Impairing venous repair. So just for the sake of time, let's just stop here for today. If you have any question, drop it in the chat or just shoot it out through the microphone and it, I remember uh Doctor Edie, please do copies these questions and in after two sessions, maybe we're gonna talk about the management of heart failure. So feel free after that. If you have any questions not addressed, just feel free to ask them again. Ok? And I see, I see that you said you don't have any Twitter, any social media, so OK, no problem. We'll discuss, we'll try to cover this next time. Ok? Just also put them on at the start of the Yes. OK. It's up to you. Thank you very much. So if anyone like how Sam said, if anyone's got any questions, pop them in the chat, I will just keep chatting for a moment. Um Just to let you put any questions in the chat. Um So what's gonna happen next if you're new to medal is that your feedback form will come into your email, you'll fill that out and you'll get your attendance certificate on your medal account. We would really appreciate if you did fill out your feedback form. Um This is just one way that we can show our appreciation to Sam and help him, um, just improve his teaching. Er, because that's something that all teachers want to do is improve and make sure that they're hitting the right level of teaching. So if you can be really constructive and give, give him some feedback, we would really, really appreciate it. Anyway, I can see that Hala has put something in the chat box. Yeah. Can we have an session? Yeah, just let's finish the heart fail first. And after that, we'll see. Perfect. That was easy done. He wasn't, it might be a regular um speaker on the platform. So if nobody else has any questions, like I said, your feedback form will be in your inbox, please please do fill it out. There's a space there as well that you can put um further topics within heart failure uh within cardiology, you can put further topics in there. So if you could do pop other things that you want to learn, if Sam can, then um I'm sure he will give us some more teaching sessions. Um If that's it, then we will. And also just anything between the sessions, just shoot me a question on Twitter. I'll be more than happy to, to answer it. Perfect. Even if it's not related to the heart failure. OK. No problem. So I can ask you, what are you having for dinner? That kind of question. Yeah. No. Yeah, no problem. We can discuss with Pakistan six. All right. So many thanks everyone. It was lovely to have you. It was lovely to have Mar on with us as well today. Um Like I said, if it wasn't for her medical education probably would not be here. So we are extremely grateful to Maram as I'm as sure as I'm sure a lot of you are as well. So um take care everyone and we'll see you at our next event. Right.

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