Home
This site is intended for healthcare professionals
Advertisement

Cardiology Session: Heart Failure | Hussam Alkhalifamohamed

Share
Advertisement
Advertisement
 
 
 

Summary

This virtual teaching session covers the anatomy and physiology of the heart, and explores heart failure and its clinical presentation. Join us today for 45 minutes of discussion, followed by a Q&A session, spanning topics from cardiac cycles and heart muscle characteristics to ischemic heart disease and causes of heart sounds. The session will be interactive and is relevant to medical professionals. Your feedback will be valuable, and a certificate of attendance will be emailed to you upon completion.
Generated by MedBot

Description

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.

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

Dr Hussam Alkhalifamohamed from Al Emadi Hospital will be teaching on

Heart Failure:

  • Systolic vs. diastolic heart failure
  • Causes and risk factors
  • Clinical presentation and staging
  • Management (lifestyle, medications, devices)

This is the first of 3 teaching sessions

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

Learning objectives

Learning objectives for this session: 1. Identify the three different types of muscles in the human body 2. Understand the differences between calcium regulation in the skeletal muscle and heart muscle 3. Recognize the components and stages of the cardiac cycle and the heart valve closures which produce associated sounds 4. Describe the cause and location of S1 and S2 heart sounds 5. Analyze the importance of diastolic blood supply and relaxation for contraction of the left ventricle
Generated by MedBot

Speakers

Related content

Similar communities

View all

Similar events and on demand videos

Advertisement
 
 
 
                
                

Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello, everyone. Welcome to me, education. My name is Sue and I'm usually on the support desk. It's really great to have you with us today for our talk and we are joined by um Husam. Now I'm not going to be able to say this name properly. Al I should have, I should have practiced this. Al That's exactly what I was trying to say. We joined my lovely Husan today. Um What we're gonna do is to us about 45 minutes um around heart failure. He's just gonna touch on the subject and hopefully we're going to have more teaching on this later on in subsequent sessions. He's going to talk for about 45 minutes and during this time, I really do need you to pop questions in the chat because I am not medical. So I am not going to be able to come up with any questions for him. And then in the last 15 minutes, we'll have Q and A at the end of the event, there will be a feedback form emailed to you once completed your your attendance certificate will be on your medal account. So now over to the ones All right. Hello everyone. This is uh Hosam Al Khalifa. Mohammed Suda is doctor who now lives in, in Qatar. And I'll be presenting to you as a series session about heart failure. OK? So just uh I hope that everyone is OK, especially those who are affected by war. And so I just, let's just start um fairest of all I want to tell you that uh this session would be merely basic session. OK? So just review uh anatomical and physiological stuff. So to set this stage for the next ones and at any time, just feel free to ask any question. OK, any question or ask if you want me to repeat anything, just just feel free to, to, to ask in the chat. OK? And I will try to address them uh when appropriately. OK. So let's go. Uh I hope this decision to be interactive. So we also, I'll be asking and you can just answer me in the chat box. Don't be afraid, answer any question, answer uh as you feel appropriate if, if you got mistaken. So don't be afraid I'll correct you. OK. So uh we'll start by introduction just uh and physiology, some of the introduction and physiology about the heart and the heart functions and how does the heart operate? And after that, um maybe most likely for the next sessions, we're going to talk about the both pathology and both of physiology of the heart clinical part. Uh How does the heart failure could present and so on and then how to diagnose heart failure and how to manage. And at the very end, we'll have just review questions to review all the topics that we discussed. OK. When does it start? So do you remember just quickly uh how uh what the structure constitutes the heart? How many uh what the structures are inside the heart? Do you remember just write it in the chart box? We have uh we know that we have two ventricles, two atria. OK. And they are valves, they are connective tissues. Yeah. OK. For Jamar to ventricles, to atria and the heart valves. OK. If I ask you, what are the functions of the heart? Yes, exactly. A three ventria involved. And what are the functions of the heart? Ok. You had enveloped, what else? What else? The heart should contract to get blood and should also relax. Don't forget this is an important function of the heart. The heart should be able to contract and relax. OK. So uh to exert these functions for getting blood relaxation is an important part and we, we're going to see why. Ok. Yeah. The rejection of the blood that will give uh the the body, the necessary nutrients including oxygen. Ok. So do you remember the uh we know that we have three different types of uh muscles in the body, smooth muscles, skeletal muscles and heart muscles. What is special about the heart? Muscles. There are several characteristics uh regarding heart muscles makes him special. Yes, they haven't collected discs. OK. What else? Ok. Contractile. OK. What else they have? Also gap junctions? Ok. Gap junctions, the stimulation of one heart muscle can stimulate many other muscles, including maybe all the heart, they have gap junctions. So the electrical stimuli move, move between the muscles, OK. Through the gap junctions. This is very important. OK. And we should do that. Why? Because just the the the impulses originate from one part of the heart and then travels alongside the heart uh to all chambers. So the heart will contract uh in sequences. OK. So the heart muscles, in order to be able to contract and relax, they should receive blood supply through which arteries does. The heart has received blood supply through the coronary arteries. We know that at the very end uh at the very start of the aorta, we have the coronary arteries in May and runs through the heart uh sub distance. OK. And then they supply the heart. The heart supply depends mainly OK. At what mainly OK? At what uh timing all the time or to meet you. So Vena cava gives venous return to the heart. OK. But supply of the heart comes through mainly through the coronary arteries. But supply supply, blood supply mainly depends on what or catch when. Yes, it it it differs slightly between the two ventricles for the left ventricle. Mainly it occurs during dias, ok. Mainly it occurs during diastole. So this is very important for the heart, for the left ventricle to relax, to be able to receive its blood supply. But for the right ventricle, it occurs the resist and diastole. Ok. So uh blood supply comes from coronary arteries and the supply for the left ventricle is mainly through the corrects through the through the. And when when, when you, when you study about like for example, ischemic heart disease, you can see that one of the causes ischemic heart may be tachycardia because tachycardia there is less diastole high. So at least supply to the left ventricle. Ok. And so the heart uh now has the blood. So the heart should contract and and for the heart to contract, it depends on calcium as in the skeletal muscle. But there is a slight difference here between the uh uh excitation relaxation coupling between uh in the heart and the skeletal muscles. Anyone anybody knows the difference between calcium uh calcium uh for contraction in the skeletal muscles and the heart muscles in the myocardial. What's the difference? The heart depends on both intracellular and extracellular calcium. Skeletal muscle depends depends mainly on intracellular calcium, but the heart depends on intracellular and extracellular calcium. So any time there is increase in extracellular calcium that can lead to increase in the contractility of the heart. And we'll see there are many drugs that act through this mechanism by increasing the extracellular calcium levels so that they would increase the contractility of the heart. Ok. Um OK. So let's now go for reviewing cardiac cycle quickly. And um can anybody just uh can you just start by what what occurs in the cardiac cycle? Uh starting from the venous repair? Ok. What kind of car in the cardiac cycle? What are the sequences of cartilage sign? Ok. Penis returns comes through the superior inferior vena cavity to the right atrium. Ok. To the right atrium. At this time, the atria are relaxed and ventricles are contracting atria relax and ventricles contract. Ok. So atria are in the and ventricles are in cysto. OK? And as the blood filters the right atrium from the superior inferior ve the cav and left atrium from the pulmonary pulmonary veins. Ok. So now when the pressure inside the atria exceeds the pressure, uh the threshold um which is the to the valves and now the valves open at that time, the ventricles now in relaxation in the aster. So now the atria is start, it start to uh fill the ventricles with blood. Ok? Fills the ventricle with blood filling occurs mainly passively. But at the end of the uh the filling there is contraction of the atria to complete filling of the ventricles. After that, the the valves, the uh tricuspid and mitral valves close the ventricle start to contract at that moment, they start to contract while all valves are closed. So this is isometric isovolumetric contraction phase. Until the pressure inside the ventricle. It sees the pressure in the in the uh in the valves, uh atrial and pulmonary valves. At this point, the atrial and pulmonary valves open. And since the right ventricle, it gets blood to the to the lungs and left ventricle is get blood to the systemic circulation, the stomach circulation and then at the the valves also close and that result in again, then finish, return to the atria, filling of the ventricles, then injection of blood. Ok. And this sequence of cardiac cycle should occur with you like very regulated, very regulated and um it can, it, it um and this is the movement of the valves, closure and the opening of the valve create the heart sounds, the heart sounds. Ok. So do you remember what, what, what is the cause of the S one or the Ferres heart sound and S two, the second heart sound and r disease, normal or abnormal cell? What causes various heart sound? Nobody can remember that this is very important. Ok. This is very important. Yeah, they are normal sounds, right? They are normal sound. The question is what, what, what is the result of f heart sound? And what is the result of the second sound? The closure of every virus causes? What s one is a result of closure of mitral and tricuspid valves, mitral and tricuspid valves. And they, they, when they are closed this indicates the beginning of ventricular cystoid, the beginning of cystoid. Ok. Because it it occurs after filling of the ventricles by block. Ok. So now the ventricles are ready to get blocked. So this indicates the beginning of cystoid. S one indicates the beginning cys as secondary to closure of mitral and tricuspid valve which occur almost at the same time, almost at the same time. And the best place to appreciate s one to, to cult that S one by cystoscope is at the api what is the api what is the Apis or ABIs beat? Yeah. Ok. It's, it's defined as outermost lower most strongest beat, look outer, most lower, most strongest beat to the heart because this is usually a normal, normal population. It's at the fifth intercostal space, midclavicular line, fi intercostal space, midclavicular line, not lateral, fifth intercostal space, intercostal space, left clavicular line. Ok. So this is S one it as the APY S one then we have S two. And what is the result of S two? The second heart sound? The what is the cause of second heart sound? What about simul valves, closure of, closure of aortic and pulmonary valves, closure of aortic and pulmonary valves which occur at the end of systole and beginning of diastole? Ok. Now, ventricles injected the blood. Now they are ready to receive again, blood again. So this is the start of diastole end of systole. Ok. And because the pressure is the pressure there is a huge difference between the pressure in the right side and left side of the heart means and the aorta and the pulmonary and the lungs also. So it's pulmonary trunk. So the closure doesn't occur at the same time as with what happens with the tricuspid and mitral valve. There is a delay, usually there is a delay in the closure of the pulmonary valves and this creates a normally split of the second heart sound. Normally split of the second heart sound. Not easy to be appreciated, especially for uh for students uh split of the second heart sound, but it's, it's very important to appreciate it with time. Ok. So there is normally split aortic then pulmonary pulmonary component and the best place to appreciate the second heart sound is to in aortic area. One that is just below the uh upper uh sternal border just to the right, that's second intercostal space to the right of the, of the sternum and the second intercostal space to the left of the sternum. That is the pulmonary area. Ok. We're going to mention that again. Ok. So this is the second heart sound, have aortic component and pulmonary component and usually there is split. OK. There is split. Um uh So we have S one that, that indicates the beginning of systole and we have S two that indicates the beginning of diastole. Do we have other heart sounds normally? Oh, is there any other signs or just S one and S two. Right. Yeah, normally there are no other heart sounds but sometimes they cannot care even in normal people, especially there is S3, s3, s3 s3 mostly pathologic but sometimes it can occur in normal population, like especially in young uh athletic patients. But um three is mainly could be um abnormal and what, what can cause S3. Yeah, it's called gala point. It's present S3 or four called gall. But what can uh cause three? Yes and infants also. But what is the cause of sthree? I mean, um the mechanism behind sthree. Yeah, heart failure definitely can, can result in sra but what is the mechanism behind sree and venous congestion can result in what? Yes, there is one, there is ra ra triggering during trier filling. OK. And that usually can result in S3, S3 and S3 usually is a best, best to be appreciated also in the speed. OK. And that can result from many causes, as we said, sometimes physiologic but mainly pathologic causes. As we are going to discuss with heart failure, then you have S four, false heart sound, false, heart sound S3 catch during the S two shortly after SS two. OK. If the resistor, it's usually short thereafter too. And uh then you have S 44 her and for heart sound almost always a pathological sound. OK. It's almost always pathological sound. So, and what is the mechanism behind us? Four, what is the mechanism behind his form. Yes. Usually four indicate a stiff, stiff ventricles. Ok. Stiff ventricles. Ok. Either a stiff left ventricle or a stiff, right ventricle. And usually it's appreciated in the Abbi also just shortly before systole, I'd say at the, that's the end of dias. Ok. Uh, at the end of diastole. So normally you have S one indicates beginning of systole. S two indicates beginning of diastole is if we have S3, that usually as the start of the te shortly after S two and S four, just shortly before SS four, just shortly before S one. OK. S one. So other than the heart sounds, sometimes you can have abnormal heart sounds like some murmurs and this is usually due to tear plants of blood. OK. It's usually tea of blood and murmurs. You may occur within the valvular lesions but sometimes can occur due to other lesions as well. Ok. Up to this point, anyone has any question. Little, feel free to ask any question. OK. OK. Good, good. And 10, can you repeat? S four? Yeah. Sure. OK. S four, we, it s four. It's usually indicates, it usually indicates a, a stiff ventricle could be either one of the ventricles or both of them. Ok. Stiff ventricles. And, but most common pathological cause of S four is, is hypertension. OK. Usually it's hypertension because ventricles have to uh have left ventricle, has to contract again. It high BP in the, in the arterial system, then that's what resulted is the ventricle, but there are many causes of S one and S four usually occurs during diastole shortly before S one. Usually there is S one indicates the beginning of systole S two indicates the beginning of diastole. And then at the end of dias again, S one, this is a normal card cardiac cycle, but when there is S four, that's usually just before S one just before the beginning of cystoid at the end of the OK. Does that address your question, Mohamed? OK. So do you remember about its action potential? Remembers action but then of the heart? Yeah, action potentially leaves the heart. OK. Action potential of the heart has many characteristics, has many characteristics. One of the most important characteristic of the action of the heart that the heart has the ability to generate action potential on its own what's called automaticity, automaticity. OK. Automaticity from automatic side because the heart can generate action potential. So any stimulus, OK. Automaticity. And generally speaking, any part of the heart can generate action potential. OK. Has the ability of automaticity. But if that occurs, this would result in irregular irregular sequence of the heart functions. OK. So everything will be distract. So that's why then the, the second rule is that the control that uh the highest, OK. The highest uh uh rate takes uh takes the action. For example, in general, we have the S A not the rate between six something, some, some somewhere between uh 60 to 100 is usually the one that initiates action potential. OK? The one it has auto but if the, if the S A not is down, then next to a not there, there will be another area that will take the automaticity from this another energy. It is started to generate the action potential and guides the heart in another direction. OK. So, but normally you have not, which is called cardiac pacemaker, cardiac pacemaker because it organizes everything, it starts action potential. So it organizes electrical activity. So the mechanical activity of the heart. OK. So automaticity is the ability to generate action potential. OK. Action potential is generally speaking also is different between the muscles and notes. What are the muscles and what are the not in the heart? What is the difference? What is the difference between muscles? And since the heart? Yes, not just they have the ability to to generate electrical activity. Ok. Muscle has the ability have the ability to generate electrical activity and mechanical activity and uh has the ability to contract as well. OK. This this is the difference. So the nodes starting from this node can create the action potential. Muscles also can create a potentials all through gap tens. OK? Is what is the difference? What is the main difference between nodes and muscle? Someone wrote it wrote it uh previously, there's a difference between the action potential of the nodes and muscle. We'll see that in a minute. What is the main difference between action potential and muscles? Like a like an action potential? Anyone they have a different phases. But in there is a major difference between action potential is the heart and other parts of the body as there is a difference between action potential in the muscles and the ners. So let's see, let's see that. Ok. So here this is the main action potential inside the muscles and this is the main action potential inside sys. OK. So look here inside the muscle, we have this face which is the depolarization phase, the depolarization phase. OK. And this usually is gets through sodium influx, sodium influx. OK. Then here we have initially polarization phase after closure of the sodium influx and opening of other canals. OK. In other uh parts of the body usually just we have the repolarization immediate continuous. But here we have the plateau phase is the plateau phase. What results in plateau phase in the heart? And what is the importance of plat phase? Are you able to hear me? OK. So what result? Don't be afraid to answer please. Anything is wrong. It's OK. Just try to keep it as interactive as possible. OK. What is important? What is, what can cause plateau phase? And what is the result? And what is the importance of the plateau phase? Mhm OK. Is hard to fill in. It's due to calcium influx Yes, it's due to calcium influx. OK. Reflux. So we said that cardiac contraction depends on the calcium. So platt two phase is important for cardiac contraction. OK. For myocyte contractility. OK. So that it can contract to inject the plot. OK? To inject the plot. Yes. OK. So it allows us for a longer period of contraction. Then after plateau phase, we have the repolarization, the re repolarization phase. That's uh because of closure of calcium S and also potassium cannot open that leads to repolarization, repolarization. OK. And then there is uh resting membrane potential by sodium potassium cans as usual and then start again. So we have sodium influx creates depolarization, initial rep phase, very important phase through calcium cans. And then we have the depolarization and resting membrane potential. This in mainly in the muscles, mainly in the muscles. OK. But we have different action potential for slightly different in the no ins the nots is that why like for example, in sn, the rate is higher than the other parts of the body because we have other, we have uh slightly different initiation of action potential through what is called prepotent three potential. OK. Three potential. This regains the potential fast. OK. Through sodium and potassium cans. OK. So sodium and potassium channels called canals. OK. And then after that, we have phase there, depolarization phase, depolarization phase. We don't need plateau phase, correct because this these are the nodes, they don't need to contract So no need for plateau phase. So that immediately repolarization phase, immediately rep phase and then again, ent phase. So just three phases, hypertension, ization ization, that's why the rate is much higher in, in a node. OK. And that's what creates the Hema a pre potential effect. OK. So that is the difference is a potential between muscles and nodes. And this is very important because we can just find some drugs just act on the, on Z nodes, mainly predominant in the nos. And that's why because there is slight difference in action potential between this and and the muscles. This is clear, this is very important. This is the foundation mainly of many drugs in the heart. Any questions on this? OK. OK. So we said the action potential usually origin is or then be conducted through the heart, it's conducted through the conductive system. So just uh let's, let's uh let's uh refresh our, our uh memories. What cons what constitutes a conductive system? What are the parts of the conductive system? This is it not have not OK. But be between not and not. What, what do you have between not and not you have in the pathway then yeah, then we have the, then we have the bundle branch, bundle bundle branch. OK. So in uh the, the action potential is conducted very fast from the SNO to Z every, not through the atria through the. But in the, a note, there is a slight delay in the action potential in the action potential. Because A not, doesn't, doesn't have the same amount of channels like in the S A, not, that's why there is a slight delay. And this is, this is important physiologically because we don't need the atrium ventricles contract. At the same time, we don't need them to contract at the same time, we need slightly so that the atria will be able to fill the ventricles while the ventricles are relaxed. And then the A node conducts the, the action potential to the ventricles. Now, the atria are in ization, things are relaxed and then the ventricles are contract. OK? This is very important because every node doesn't contain the same canals. OK? There is a delay and delay is that this delay allows for the, for the filling of the ventricles. OK? For the filling of the ventricles, the ventricle should be relax at that time when the you are contracting and the device vers. OK. So this is very important this a node delay. OK. Um So this is a conductive systems. Um The normal rate of the sr usually it's 100 100 beat per minute. But due to action of autonomic nervous system that might, that, that can modulate the the heart functions. OK. Usually the rate is slower than that. Usually uh 67 is in most, in most uh uh persons. OK. So what are the parts of A NS? Do you remember autonomic nervous system for autonomic nervous system. So what other parts of the cyst? We have sympathetic nervous system and parasympathetic nervous system, right, sympathetic nervous system and parasympathetic nervous system. And they in general act to oppose each other. Vagus nerve is giving uh gives the parasympathetic supply. Ok. Parasympathetic supply. But we have sympathetic and parasympathetic nervous system and um the the nervous system helps to regulate the heart functions. Ok. And modulates the heart functions and the physiological states. So, ner system generally speaking, increasing heart rate through action in a ode increases cardiac contractility and increased cardiac conductivity through the conductive system. Ok. Heart rate conductivity and contractility, disease, sympathetic nervous system through which receptors do you remember through its receptors? What what sympathetic nervous system receptors we find inside the myocardium. No alpha receptors are sympathetic receptors that mainly found in signs of blood vessels. Ok. The alpha receptor chore receptors are parasympathetic receptors. Mainly our be re receptors. Yeah, beta receptors, which beta receptors, we have three beta receptors inside our body. Three times which beta receptors. I know beta one receptors. Ok. Mainly inside the heart. You have beta one receptors. Ok. Beta one receptors and parasympathetic decreases heart rate through a mainly through action in the S A not but also affects other parts, decreased conductivity and has a mild effect on the contractility, decreased contractivity as well. Ok. Mild effect on the contractivity through which receptors, parasympathetic throm receptors, throm receptors. OK, thro receptors. So we have sympathetic receptors, increase heart rate conductivity and contractivity, parasympathetic receptors. Thro muca decreases heart rate conductivity and a slight effect on contractility sary receptors. Ok. And then autonomic nervous system usually acts on with uh by refex by reflexes. It uh tries to adjust any change in the, in the physiological state of the body. Ok. For example, if there is decrease in BP due to any cause, for example, due to hemorrhage or loss of fluids. Ok. Uh what was the sympathetic receptor again, re are and be receptors in the heart? You have beta one receptors in the heart. In the blood vessels, you have alpha receptors. Ok. Uh See for example, if you have decrease in blood in, in, in, in in uh BP due to any cause. Now the heart will try to adjust that increase in BP through increasing heart rate and contractility and that would increase cardiac output. Ok. That would increase cardiac output. So to enable uh that might lead to adjustment of decrease in BP. Ok. This acts reflexes areflexic uh has an afferent pathway e pathway and central in the system. And in this regard, we have power receptors, chemo receptors. If you remember from the physiology, ok. Power receptors and chemo receptors. Since the changes in the BP, oxygenation CO2 levels and hydrogen levels and that would trigger either an increase or decrease in sympathetic or sympathetic. Ok. Do you understand the concept of the reflexes? Or I need to, I need to explain it more autonomic nervous system is very important and many drugs. So uh for cardiovascular disorders act to augment or to decrease the autonomic nervous system effects on the heart. Ok. Uh So this is the autonomic nervous system. We said in the contractivity depends one of the factors that contractility depends on the depends on is the is the calcium. Also, there are many things that can increase or decrease contractility. For example, do you remember preload and after load? What's OK? Or the pri locked? So here filling of atrium affects plot but it is not pret it affects plot. Yes, exactly, exactly. It's a stretch of the muscles prior to contraction, usually during the a stretch of the muscles. Ok? Stretches the muscles. It depends on many factors. For example, venous return. If we have more venous return, that means we have more stretch of the muscles. That means more stimulation to the muscles. So more stretch means stronger contraction, stronger contraction. Ok. Muscle is relaxed but stretched. That means more robust contraction when it occurs. So, increasing preload, for example, by increasing venous return, increasing filling of the atria, this results in more stretch of the muscles, increased preload as that increased contraction and increases cardiac output as well. Ok. This preload. So what is after lot, what's after that? Yeah. OK. The pressure again is switch, the ventricles should inject the plot the pressure again to switch the ventricles, which it should inject the plu, for example, for left ventricle should inject the blood against the aortic pressure. And if it's high, that mean higher after load, that mean lower ability of the ventricles to contract because higher pressure. Ok. High pressure. So increasing after load would decrease contractility and would decrease cardiac output and vice versa. If after load decreases, contractility would increase and that would increase cardiac output as well. Ok. So it's preload and afterload. Very important. OK? And we see that many conditions are just one or two of them and many drugs act through one of two or two of them. OK. Pre after lunch, increase afterload because there is a higher pressure against, against the ventricle. Ok. So the contractivity wouldn't adjust for that one cause. Uh at least there is increase preload as well but just increase in after look in isolation, that mean higher pressure again, increase the ventricle should contract. So the ventricles cannot, cannot um cannot overcome that pressure. That means why there is decreased contractivity relatively to increase. And after look. Ok. Relatively. So that's why we would decrease the cardiac output as well. For example, normally the ventricles should contract between uh again the 100 millimeter merry, but now the ventricles should contract again, is 200 millimeter merry. It is a double, almost the same, right. So that's why we decrease in contract results in decreasing contractility. Uh Many factors also can affect the the contractility, including preload and afterload, including start. We're going to discuss that. Uh next time this is all are important. OK. And we in the body, we have many peptides that are secreted. Either a mainly response to any changes or the secretion can, can spark the changes, for example. Um there are many peptides secreted from the heart in response to stresses, but many peptides secretes outside of the heart that can affect the heart as well. Do you know any example of any DIPT that might be secreted in the body might affect the heart or secreted in response to uh uh conditions affecting the heart? OK. Tic DIPT. Yeah, this is important. What is AMP? He di Yeah, it yeah, regular salt water balance A MP. And also we have P MP. A secret secreted from the and PM is secreted from moa secreted from my. OK. So this this will be your homework for today to read about the peptides that can affect or secret it a response to heart conditions. OK. And at least the most important one of them especially PMP. OK. And next time we're going to start our talk with this one peptides. Just let's review a few things before we go, I guess. Ok, this is for next time. OK. Do you have any questions about anything we talked about today? Any questions? OK. Uh please go review the physiology of the heart, this is very important. So to make your life easier to understand heart failure, please review the physiology. Ok. And any case uh uh before our next uh session, if you have any question, don't be, don't hesitate to reach me. You can reach me on Twitter. Just write the same name as it appears. Khalifa Mohammed. This, this long name. OK. And you'll find and just reach out to me. Ok? I'll be happy to answer and address your concerns. Ok? It's brilliant. If that's us done, if anyone wants to ask any questions, I can actually get you on the um on the stage with us if you want to come and ask a question because I know you've been typing away there. I don't think I've ever seen the chat so interactive, so well done everyone for asking questions and getting back to you and it's been brilliant. So if anybody does want to join us on stage to um ask a question directly instead of using their typing fingers, then you do actually need to put join, join or join me or something in the, in the chat and then we can get you uh on the stage. Um If not, I'm just gonna, well, I'm just gonna let you know that um you will get a feedback form in your email er inbox after you've completed that you will then get your attendance certificate on medal. There are other events, other events coming up er, and you are more than welcome to attend those two. And I know that Isam will be er, doing some other events for us as well and we'll get them on the platform as soon as we've got some dates sorted out, please do user feedback. Um And if Sam would be grateful to have any feedback that you want in there, he, you know, this is one way that you can really appreciate the speakers that are joining the platform and giving all their time. So, oh, we have a question. Who's um good job? We chatted long enough. Um What resources do you recommend for cardiology as medical students or medicine in general? Yeah. OK. Uh That's a good question and it depends on, on what, what's your target. If for example, you want to go deep in the, in the discipline. Uh You can choose a large resources like Debit and Kumar. But if you want just for thing for, for college, for exams, you can choose uh select the more concise ones like uh um like the Oxford Oxford series. That's very good. That's very good. OK. And then for review sessions, I would recommend pretest for review things. Just pretest done. You'll be fine if and please also uh go back to Bama for review of pathology. It's, it's really helpful. OK. You can use the book or you can use the also the videos. OK. Does, does that address your question? Yes, it did, does anyone else have any questions? If not, we will um say goodbye. This is recorded. So, um I will edit it and I will put it up as catch up. You'll find it on the Med Education Organization on metal as well as lots of other events that catch up as well as all of the events to come. Ok, so it was really lovely to have you. Thank you for your attendance and thank you all for the opportunity and hope to see you uh maybe next week. Ok.