Hello everybody. In this video, we will talk about heart failure, which is the end stage of virtually all heart diseases. And especially now, we'll talk about the pathophysiology of the disease. So, my name is Andreas Flammer, I'm a deputy of the heart failure clinic at the University Heart Center of Zurich in the Department of Cardiology. I would like to begin with heart failure. What is actually heart failure? And we can explain this quite simple: that is, if the heart is not able to pump enough blood to meet the body's needs. Heart failure, and I can start with that, we need to look at the risk factors. Smoking, cholesterol, hypertension, diabetes, and this may lead to arteriosclerotic disease, and also left ventricle hypertrophy, as you may know. If you have arteriosclerosis, it's possible that your arteries to the brain may be affected and stroke is a risk. It may be that your renal arteries are affected and you get renal failure. You may get peripheral artery disease or coronary artery disease. So, if you have coronary artery disease, this will eventually lead to myocardial ischemia, coronary thrombosis with a myocardial infarction. So, if you have a myocardial infarction, the blood supply to your organs is stopped, in many cases, stopped completely. This may lead to arrhythmias and sudden cardiac death. But if you survive, it may lead to infarction with a consequence of remodeling, and we will talk about this in a second, dilatation of the ventricles, and at the end, heart failure. So, heart failure is not only a consequence of myocardial infarction, but myocardial infarction is one of the most important contributor. But also valvular heart disease, cardiomyopathyies, hypertensive heart disease, or even arrhythmias, may itself lead to heart failure. If you have heart failure, this predicts a very bad prognosis. You have symptoms and signs of heart failure, you have a high risk of rehospitalization, and you have an especially high risk of dying due to heart failure. If you have myocardial infarction, this will lead to destroyed, it means infarcted myocardium, that means infarcted muscle mass, which will, at the end, lead to impaired ejection fraction. So, that means that the pump function of the heart will be impaired. So, how can we imagine how that develops? You can see here on the left hand side, the image, where we have the initial infarction. The coronary artery is blocked, blood supply to one area of the heart is destroyed, and you can see here that the muscle mass will be destroyed at that point. You have the initial infarct. If not treated, there will be an expansion of the infarct area over hours to days, as you can see here in the middle image, which is bad for your muscle mass. Over days and months, the heart will somehow remodel. It will get thinner, it will get bigger, there will be a dilatation, and pump function will be impaired. This has some consequences, but for that I will go and talk a little bit about normal hemodynamics of the heart. If you look at the left side of the image, there you can see, the heart in the middle, and the left ventricle, called LV, is there. It pumps the blood to the periphery to supply all the organs and the muscles with blood, with oxygen, which is needed. And then the renal system will go back to the right heart, the right heart will pump the blood to the lungs, and the lungs are responsible to get the oxygen back to the blood. And from there, the blood goes to the left ventricle again. So, in case of an infarcted heart and heart failure, most of the time, the left ventricle is affected, as you can see here on the right side of the image. And there you can see, you have the left heart. And if the left heart gets weak, not so much blood can be pumped to the organs, and then you have the blood supply, especially, for example if you do exercise, is not enough, it will lead to fatigue and other symptoms. But that's not the only problem, as you can imagine. There will be also congestion: So, blood coming from the lungs, they just overfill the left ventricle, and it gets congested, as we say, and then the lungs will have too much fluids, which will lead to lung edema, and also, it will lead to dyspnea of the patients. So, this is the major symptom of heart failure, and we will talk about this in the next video. So, if the lung is full of water or fluid, in bad cases, it may also go to the right heart side even, and will lead to edema in the entire body. So, we have some compensatory mechanisms to maintain cardiac output and cardiac strength. Which is, on the one hand, the sympathicus activation, and on the other hand, neurohumoral activation. So, you have to imagine, we have myocardial damage, we have impaired muscle function. So, then, as I just outlined, perfusion results in inadequate oxygen supply, and also in a clot in the kidney, for example, which will lead to activation of the renin-angiotensin aldosterone system. On the other hand, we have some barorezeptors and the pressure in the vessels will go down, which will then suggest to the body to the nervous system, that it has to get activated, so that there is an activation of the sympathicus nervous system. These both are important mechanisms to maintain blood volume, for example in the case of a blood loss in an accident or in other cases. But now, in heart failure, it has unfortunately further deleterious effects on the body: It leads to vasoconstriction, salt retention and to an even more fluid overload. And this is bad for the heart because there is more fluid, and also the afterload, so the work that the heart has to work against will increase, so it further impairs muscle function of the heart. We have some treatment options for heart failure. We talk about this in future videos. On the one hand, there are beta-receptor blockers. They interfere with the sympathicus nerve activation, the power receptors. And we have, on the other hand, medication like ACE inhibitors, angiotensin-rezeptor blockers, and aldosteron antagonist, which will interfere with the activation of the renin angiotensin aldosteron system. We have all the endotrainers and mechanisms, which may help. We have natriuretic peptides and other vasodilatory peptides, which are increased to counteractive these effects. However, those are insufficient. So, I'd like to conclude, that heart failure is the end stage of virtually all cardiac diseases. Myocardial infarction is the most likely cause of heart failure. And we have structural, that means scars, and also functional, meaning reduced contractility changes after, in which altered hemodynamics, and this leads to the typical signs and symptoms of heart failure. Compensatory mechanisms, such as a sympathicus nervous and neurohormonal activation, try to counteract the reduction in cardiac output, however, lead to CCs progression, paradoxically. So, with that, I would like to conclude and thank you very much for your attention.
