- Overview of heart failure
- What is heart failure?
- Systolic heart failure pathophysiology
- Diastolic heart failure pathophysiology
- Compensation and decompensation in heart failure
- Symptoms of left sided heart failure
- Symptoms of right sided heart failure
- Heart failure diagnosis
- Heart failure treatment - Early stages
- Heart failure treatment - Late stages
- Heart failure treatment - Devices and surgery
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- Can this material be printed? If so, where? thanks(3 votes)
- Then why does heart failure decompensate with infections? I understand that the infection itself increases the methabolic needs of the organism, but does that have any impact in any of the 3 mecanisms you explained?(2 votes)
- Infection increases demand of blood supply. In a already fully compensated heart failure u can't further increase CO which ultimately results worsening of condition.(1 vote)
- Does that mean that if you don't compensate, everything will be fine (I mean, for the cells etc.)(1 vote)
- Not exactly. It's true that it does cause problems if you compensate, but the reason that you compensate in the first place is to make up for the oxygen loss for your muscle cells. The reason behind compensation is to help the cells, even though it makes things worse. From7:39-7:46. It talks more about the reasons of compensation and how it will lead to decompensation.(3 votes)
- What are the receptors on the heart called?(1 vote)
- The types of sympathetic or adrenergic receptors are alpha, beta 1 and beta 2. Alpha-receptors are located on the arteries. When the alpha receptor is stimulated by epinephrine or norepinephrine, the arteries constrict. This increases the blood pressure and the blood flow returning to the heart.(2 votes)
- In pharmacology book, there is another explanation of the second compensatory mechanism .Here you said that aldosterone and ADH increase the filling capacity. But there it's written that the MAIN effect is increase in afterload -that means the peripheral resistance --> blood pressure and water and salt retention,which after leads to edema. So which is true or both are true?(1 vote)
- do you have a video explaining the different type of receptors on the heart (alpha, beta1, beta2) and their functions?(1 vote)
- I hope it helps, Speed Pharmacology has many good explanations about medications. There are may good videos on Youtube you can watch.
- You mention that the overactivation of the sympathetic nervous system causes a reduction in the number of receptors. How does this worsen heart failure?(1 vote)
- It causes the heart to work harder and in turn can worsen an already battered heart.(1 vote)
- [Voiceover] So what do we mean when we say compensation? Well, let's remember that heart failure, you have this decreased ability to meet your body's demands, right? Well, your heart and body have this way of trying to make up for this decreased ability and increase the blood you supply, and that's called compensation. Because you're compensating for this decreased supply. But in heart failure this can lead to something called decompensation. So eventually you can't compensate anymore and your symptoms start to get worse and heart failure gets worse. So there are a couple main ways we try to compensate. And each of these ways either increase your stroke volume or increase your heart rate. And remember that cardiac output equals stroke volume times heart rate. So if you increase either one of those you're gonna increase your cardiac output. The first thing we're gonna look at is activating your sympathetic nervous system. And this is like your fight or flight response. So, for example, what if you're hiking along in the woods and you see this bear? Your sympathetic nervous system is gonna kick in. And your heart rate's definitely gonna go up and your stroke volume is definitely gonna go up. And so your body is preparing you to either fight or flight, or run away. So when your cardiac output goes down your sympathetic nervous system kicks in. And it uses these receptors on the heart that tell the heart to one, beat or contract harder with more force which increases your stroke volume. And two, to beat faster, which increases your heart rate. But if you use these too much they start to down-regulate. Or decrease in amount. So you know, there's less of them. And less receptors means your heart won't respond as it did before. So think of it like this. What if you're moving? And you call a bunch of your friends over to try to help you move your stuff. And you know, they're glad to come over and help you. And so you move your stuff and then you decide next week, oh, I want to move again. So you call them up again and say "hey, I need some more help". And they're like okay, I guess it's kinda weird, but I'm gonna come help you. And then they come. But then the next week you're like, oh, I'm gonna move again. And then you keep doing this week after week and those friends are gonna start to well one, question why you're moving so much. And two, they're gonna stop maybe answering your phone calls. It's sorta the same thing with your sympathetic nervous system. When you activate it too much it's gonna start helping less and less. So the next big way we can compensate is by increasing this thing called preload. Now preload is defined as this pressure in the ventricles. So in this lower chamber, after it's filled but before it contracts. So during diastole. When it's filled, the walls and the heart muscle cells are all stretched out because it's like filling up a water balloon. So you put the water in it and then the water causes that balloon to expand, right? So the more you fill in, the higher this pressure or preload. So as you keep filling, the walls stretch more and more and we get higher pressures or preload. To do this, to fill more, to get more blood in those ventricles your body releases these specific hormones like antidiuretic hormone, or we call it ADH sometimes, or aldosterone, to increase this filling volume. So if the ventricles used to have about 100 milliliters at the end of diastole, now maybe they have a little more, like 115 milliliters. This extra little bit might not seem like a lot, it's like one tablespoon, but it's enough to stretch the heart chamber and muscles just a little more. So that's great, but why does increasing the preload, or filling pressure, increase the force of contraction, and so your stroke volume? Well, think of it like stretching a rubber band. The more you stretch the rubber band the more force it'll snap back with, right? Okay, so there's a lot going on here, right? So let's go one step at a time. So as you fill the ventricles with more blood it stretches those muscles out, right? And just like the rubber band did, when you stretch it out it contracts, or it snaps back with more force. And when it contracts with more force, you get more stroke volume, you get more blood ejected. And so this guy named Frank-Starling saw this and kind of decided to cut corners and create this law that says, as you increase your pressure or your preload, you also increase your stroke volume. And that's the Frank-Starling law. Sweet, so increasing preload increases stroke volume and therefore, your cardiac output, and is one way we can compensate. But again, like over activation of the sympathetic nervous system, this is a real delicate balance. So these muscles now contract with more force, right? But that means that they use up more energy to do that. And therefore, they need more blood. And if there's no additional blood flow coming to the heart muscle cells, they can begin to die off. So let's get back to that first analogy where that guy's moving all the time. But this time maybe he decides, oh, I'm gonna pay my friends to help. And so all the sudden they all come running back and then they help him move in and they kinda support his weekly moves. But then all of a sudden he starts moving every other day, and he's not increasing their pay. Well, they start to get overworked, and without more money, they're gonna leave, right? It's kinda the same thing with our muscles cells. They're contracting harder and they're working harder. So they need more oxygen and more blood, but they're not getting that so they start to die off. So we just saw that when you contract harder you eject more blood. Well, besides increasing preload, there's one more way we can do that. And that's gaining muscle, that's bulking up. This is also called myocardial hypertrophy, where your heart gains muscle mass. And when it gains muscle it contracts harder because it's stronger. So to try to make up for this decrease in stroke volume or this death of cardiomyocytes, or heart muscle cells, these surviving cardiomyocytes become elongated and they grow. And this causes the heart muscle as a whole to get larger. So you get this enlarged heart muscle. So it's like the ones that don't die are like whoa, I gotta start bulking up so I can take over for these guys that aren't contracting anymore. And these bulked up muscle cells contract harder, they eject more blood and they increase cardiac output. Perfect. But as we know, this usually comes at a cost, right? Well, more work means more oxygen and more blood supply. But with heart failure we know that that's not an option. And so without an increased supply these bulked up cells get overworked and then they start to die off. Not only that, if the heart muscle gets too big the chambers start to get smaller and so there's less blood that can fill in the chambers. So those were the three modes of compensation. You can activate your sympathetic nervous system. You can increase your preload. Or you can gain muscle, which is called myocardial hypertrophy. And so for each of these, our goal is to increase cardiac output. By either heart rate or stroke volume. But like we saw, when you use any of these too much it leads to unintended consequences. And eventually heart failure gets worse. And this is what we call decompensation. So when you overuse the sympathetic nervous system your receptors start to go away. And you end up with a lowered response. When you increase preload, you muscle cells stretch and then contract harder, but this costs more oxygen and then eventually leads to cell death. Similarly with hypertrophy, these bigger muscles also use more oxygen. And without that the cells die. So not only that, these three can often feed back on each other. Like the death of muscle cells from an increased preload might result in hypertrophy, because those remaining cells start to bulk up. And this increases cell death even more. And then as the heart weakens from this it might stimulate the sympathetic nervous system to try and beat harder and faster, which further progresses heart failure. Most of the time it's really difficult to pinpoint which one was the initial culprit. But the major takeaway should be that compensation, regardless of its intentions, is often a major contributor to worsening heart failure and eventually decompensation.