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Diastolic heart failure pathophysiology

Video transcript

so diastolic heart failure is similar to systolic heart failure in that the heart doesn't pump enough blood to meet the body's demands okay but how is it different well if you look at diastolic that kind of clues us into how it's different and if we remember that diastole is that phase in the cardiac cycle where the heart's just filling with blood so the heart's all relaxed in Bloods filling into the ventricles and that's called diastole so diastolic failure means that the heart's not filling with enough blood and so if you just compare the two if you just eyeball them you'll notice how much less room there is with diastolic failure and if we bring back our most favorite analogy ever the water bottles if you squeeze the healthy one water ejects out that's great okay but with diastolic failure what if the bottle is not filled with as much water and you squeeze it obviously less water's going to be ejected because there's less in there in the first place it's the same thing with the heart so if there's less blood in the heart in the first place it's going to have a lot harder time meeting the body's demands and ejecting as much blood so less filled means less ejected also remember how the systolic heart failure had a lower ejection fraction which is that fraction of blood ejected with each beat and that's because you know there's about the same amount or possibly even more filled into the ventricles with systolic failure but there's less ejected so naturally you'd have a lower ejection fraction makes sense okay but since diastolic heart failure has both filled and ejected lower so both are lower sometimes your ejection fraction can be the same as with a healthy heart and we would call that a preserved ejection fraction okay that seems a little confusing right well let's do an example and show how that might happen okay so recall that rejection fraction is equal to your volume ejected which you could also call your stroke volume divided by the total blood filled which we can also call end diastolic volume because it's the volume at the end of diastole okay so say your stroke volume is 70 milliliters say your end diastolic volume is 120 milliliters this would be considered you know quote-unquote healthy 70 divided by 120 equals 58% okay that's within a normal range cool what if stroke volume is equal to forty six milliliters because of heart failure it's a lot lower it's pumping less blood but your end diastolic volume is also lower it's 80 milliliters 46 divided by 80 is still 58 percent technically in a normal range so clearly the stroke volume and the blood being pumped out is lower but that's kind of covered up by your end diastolic volume being lower too but just because that ejection fraction is preserved that doesn't mean you know we're out of the woods it's still heart failure but how does this diastolic heart failure get to look so much different than systolic failure well there's pretty much two ways the first way is hypertrophy which essentially means like growth of muscle and when we're going to talk about that word we mean ventricular muscle growth and when these grow they take up more space and since there's more space being taken up by the muscles that means there's less space to fill right and secondly is that these muscles these growing muscles get stiffer not stretch as much when they relax even though they're growing there are these dead muscle cells in here - because it's heart failure and that's a main component is death of muscle cells so these dead muscle cells leave this fibrotic scar tissue and this fibrotic tissue is like a bunch of connective tissue and that connective tissue has a lot lower compliance and basically compliance is the ability for the ventricle or for any tissue to passively stretch and expand during filling and this is super important for the heart because more stretch more compliance means that it can fill more it could get more blood think of like filling a water balloon when you put water into it what happens well it gets bigger it expands but this is like passive the water is forcing it to get bigger now think about filling up one of those like glass flasks from chemistry class yeah I'm gonna be really extreme here just to make a point but what's going to happen when you fill it up it's just it's not going to get bigger it's not going to change shape it's just going to fill up all the way and then start to overflow and spill all over that's because it's a lot less compliant it's probably like one of the least compliant things we can think of and it's the same with a heart with a bunch of fibrous connective tissue it can't relax and it can't passively expand and it can't fill completely so that's what's going on with diastolic heart failure but how does it get like that and how do we get these enlarged and stiffened muscles well just like systolic failure it's a secondary disease which means that this growth and stiffening is caused by some kind of underlying disease that's been there before and the big one that we tend to understand the most is chronic hypertension or high blood pressure so when the pressure in your blood vessels goes up they become harder to pump against harder to pump into this is kind of like blowing into a straw versus like a big tube which one do you things can be harder to blow air through it's probably the smaller one right well it's sort of like that for the heart except the heart has to pump blood through these narrowed vessels and this is way more difficult to do so what is your heart do well it bulks up it gains muscle and it gets bigger so it can pump against these higher pressures now both diet and diabetes can both contribute to higher blood pressure and hypertension and those are definitely big risks ders for hypertension and therefore diastolic heart failure and the second underlying disease is a or text enosis and stenosis from the systolic heart failure video we know is a narrowed valve and specifically we're going to talk about this valve right here this a or DIC valve and then that valve goes out from the left ventricle and pumps into an artery called AAA aorta so similar to hypertension it's a lot harder to pump blood through this narrow it opening as opposed to you know a valve that's opening all the way and what happens well the heart muscle again bulks up and gains muscles so it can try to pump harder through this smaller valve now this is a little tricky though right because we remember that this can also lead to systolic failure so what gives well unfortunately a lot of the mechanisms behind why in one case it might lead to this growth of muscles like in diastolic heart failure or it might lead to this serious weakening of the muscles like in systolic heart failure are pretty complex and honestly a lot of these mechanisms are unknown in still big areas of research and next up you have cardiomyopathies which mean heart muscle diseases and sometimes these can be a little general but for diastolic heart failure in particular there's two that we're going to focus on and the first one is hypertrophic cardiomyopathy which we can kind of figure out by the name hypertrophic or hypertrophy means muscle growth and so this cardiomyopathy causes muscle growth and this is often without an obvious cause the second is restrictive cardiomyopathy which causes stiffer and more rigid muscles and this restricts the ventricles from expanding and these two cardiomyopathies kind of hit the nail on the head right because with diastolic heart failure you have either stiffer muscles or enlarged muscles finally there are some other causes and risk factors like old age and coronary artery disease even but like I said before some of these cross paths with systolic failure and again a lot of the mechanisms behind that are largely unknown especially as to why one might lead to systolic failure and one might lead to diastolic failure these are still big areas of research so with diastolic heart failure the heart muscles either get bigger they get stiffened or both when this happens less blood fills into the ventricles and the heart can't passively expand as much and therefore can't relax completely so ultimately you end up with this cycle that leads to worsening heart failure so you start with some underlying disease like hypertension or stenosis that makes it a lot harder to pump blood to the body to try and make it easier the heart muscles increase in size and they get bigger they bulk up but these bigger muscles do more work so they need more oxygen but with heart failure you know you can't supply more oxygen so this leads to cell death and that cell death causes this fibrosis in this stiffening of the heart muscle tissue and then that feeds back into a lower blood supply making it even harder to pump blood you could also have other diseases like hypertrophic cardiomyopathy that directly affects muscle size or restrictive cardiomyopathy that directly affects stiffening and this cycle progresses and heart failure gets worse