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what's up ninja nerds in this video today
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All right, let's start talking a little bit about CHF or heart failure, congestive heart failure, many different terminologies there.
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When we talk about heart failure, the first thing I want to talk about is the pathophysiology behind it.
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And really, there's a couple different types of heart failure believe it
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or not there's left heart failure right heart failure
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and this weird one called high output failure we're going to talk first about left heart failure
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which is going to be by far the most common type of heart failure now we talk about left heart failure
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we want to think about two different types or subtypes
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if you will of left heart failure this is what's called systolic heart failure
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and diastolic heart failure now what would cause
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this patient who has a normal heart to start diverting its way into developing systolic heart failure.
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The primary reason why this would develop is a patient would have a reduction in their contractility.
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So the contractility of the left ventricular myocardium is going down.
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So there's a drop in the contractility.
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So then you have to ask yourself the question, what is causing this left ventricular myocardium to not contract?
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What are the disease processes which would lead to this?
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So here, we're going to say that this myocardium here, this left ventricular myocardium is damaged in some way,
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shape, or form, and the contractility here is knocked down.
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What's some causes?
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One of the most common causes here by far is going to be a myocardial infarction.
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If a patient had an MI, it's going to cause fibrosis of that tissue.
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Do you lose contractility there?
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That's one way.
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Another one, believe it or not, is cardiomyopathies.
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You know which one particularly is very, very commonly associated with this one? it's called dilated cardiomyopathy
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because what happens is that the actual ventricles get really really thin
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and very weak that's another one where the contractility goes down another one could be myocarditis
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but it's relatively uncommon but we'll put that one down as well
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so another one could be myocarditis so inflammation of the myocardium
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but all of these things would be stimulatory factors
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that could lead to systolic heart failure where the contractility is just not good.
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If the contractility of the heart is not good,
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particularly the left ventricle, can it push blood out of the left ventricle and into the aorta very well?
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No. And so this is where the issue occurs, is that the patient has a hard time being able to pump blood out of the heart.
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So it's a problem with forward flow.
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There's a very important kind of like formula.
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We're not going to go crazy into it, but it helps us determine something called the left ventricular ejection fraction.
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And this is a very important terminology.
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So in this person who has systolic heart failure, sometimes what happens is, is as you drop the contractility, as you drop the contractility,
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you drop what's called the left ventricular ejection fraction, which is basically the amount of blood that you're able to pump out of the heart, right?
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And so when this happens, a decrease in left, the contractility, when that happens, that goes down, you drop your left ventricular ejection fraction
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and now it's hard being able to get blood out of the heart when
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that happens what we do is we have a very specific
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terminology whenever the patient has a reduced left ventricular ejection fraction particularly particularly
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when it's less than 40 percent you know we call
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that we call that heart failure with a reduced ejection fraction we call this HEFREF.
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And that's usually when it's less than 40%.
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So when the left ventricular ejection fraction is less than 40%, we call that HEFREF, which is another way of describing systolic heart failure.
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But the whole point here that I want you to understand is contractility is down.
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The amount of blood getting out of the heart is down.
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So what is that called when the volume of blood
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that you're supposed to be pumping out of the heart in one minute goes down?
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That's cardiac output.
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So, in these patients, they will start to experience a drop in their cardiac output, which we're going to abbreviate CO.
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And that's the big highlighting factor here for systolic heart failure or HEFREF, heart failure with a reduced ejection fraction.
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Their cause is drop in contractility due to these diseases.
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Now, when we come over here to the other flavor of left heart failure, diastolic heart failure, this is another really, really common one.
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The problem here is something different in the sense that it is really hard to get blood out of the heart.
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And there's a couple ways that blood leaves the heart, right?
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So we call that like stroke volume, the amount of blood that you're kind of getting out of the heart in one heartbeat.
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That's dependent upon preload, contractility.
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And what's the last one?
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Afterload.
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When the afterload is crazy high in these patients, it's hard for them to get blood out of the heart.
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And that's usually the problem here, is that these patients develop a massive increase in their afterload.
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What are diseases that would really kind of increase the afterload and cause these particular types of problems?
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Chronic hypertension.
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Can't say how common that particular etiology is.
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That is probably going to be by far one of the most common causes.
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So this would be a chronic hypertension.
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We'll put chronic here.
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What's another one? you know there's a valve right here, right?
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There's a valve right here called the aortic valve, the aortic semilunar valve.
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What if that valve is super, super stenotic?
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And because it's crazy, crazy stenotic, it's almost hard.
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It's kind of obstructing the forward flow.
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That would also cause a lot of afterload.
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Aortic stenosis is another really common cause here.
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So another disease would be called aortic stenosis.
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This is another very, very common cause for an increase an afterload it's basically anything
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that's going to make
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it harder for the blood to get out of the left
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ventricle these two things by far are going to be the most common thing
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that will cause diastolic heart failure now in systolic heart failure what do you notice about the ventricle
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super dilated right so let's actually write that over here so this is a very
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dilated enlarged ventricle what you're going to notice here is
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that this is super hypertrophied this ventricle is very hypertrophied
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so you have what's called hypertrophy it's a very thick
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and large left ventricle we call that left ventricular hypertrophy
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or sometimes abbreviated LVH now the reason why is think about this
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if the pressure in the actual aorta is so high
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that you have to overcome it what what's the one way
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that you can do that get stronger and thicken up the left ventricle.
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But when you do that, when you thicken up this left ventricle and you make it to where you're actually able to generate higher stroke volumes,
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the problem is now is that you decrease the actual space of the left ventricle.
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And now my problem is that I can't get the deadened blood into the left ventricle.
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I can't fill it properly.
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And so this issue is a filling issue.
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This was a forward flow issue.
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So what do I notice here in this particular disease process?
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The problem with diastolic heart failure is that they have a reduction in their filling process.
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So there's a decrease in their left ventricular filling.
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And because I can't fill the ventricles very well, that's going to cause a problem.
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Now here's the thing.
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Their left ventricular ejection fraction is completely fine.
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It's usually completely preserved.
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So this filling process won't affect their ejection fraction.
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So their left ventricular ejection fraction is usually what we refer to in this case as normal.
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Or let's use the term preserved.
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And so that's where we get this term a heart failure with a lowercase p preserved ejection fraction,
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where if we were to give it a particular number, it's at least greater than 40%.
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So in these patient populations who have diastolic heart failure, their filling is reduced because their ventricles super,
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super hypertrophied that causes their left ventricular ejection fraction to be preserved.
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And they have what's called a half -pef.
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But here's the question.
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This has a low cardiac output because of low contractility.
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This will also have a low cardiac output.
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Do you guys know why?
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Why this won't have a low cardiac output?
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This will have a low cardiac output because, again, think about your physiology, guys.
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It's very, very important to understand physiology here.
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If I have a decreased filling, I'm not going to load my ventricle very well.
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So my preload's going to drop.
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If my preload drops, what happens to my stroke volume?
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That goes down.
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If stroke volume goes down, what happens to my cardiac output?
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That goes down.
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So both of these patients will have a low cardiac output,
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but the primary difference here is that this is a preserved EF because they have no problem with their ejection fraction, no contractility problem.
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This one has a reduced ejection fraction because they have a contractility problem.
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Dilated ventricle, hypertrophied ventricle, super high yield, can't forget these things.
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Understanding the causes of afterload, understand the cause of this contractility problem.
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Okay, now we get into something that I think is really, really important and I think can often be overlooked.
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When patients develop heart failure because of these issues, it can continue to get worse.
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and worse and worse if not treated.
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Let me explain why.
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When cardiac output goes down, this is gonna go back a little bit to your physiology here.
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When cardiac output goes down, what we know is there's always that formula.
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Do you guys remember the formula for blood pressure?
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The formula for blood pressure is you have this one here.
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that blood pressure is equal to cardiac output times systemic vascular resistance.
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In patients who have heart failure, what's the problem here?
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Their cardiac output drops.
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And then if you were to say keeping this normal or constant, what would happen to their blood pressure?
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That would also drop.
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So then what's the general compensatory mechanism that our body tries to create?
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We'll do this in pink.
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SVR has to go up.
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And so this is usually what ends up happening to the body,
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is the body creates this weird mechanism to try to increase your systemic vascular resistance
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which causes a lot of problems let's see what that looks like
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so the reason why you may be like zach
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i really don't want to know this this is kind of like foundational stuff it's very helpful for your
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pharmacology and understanding i promise
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so here cardiac output's low normally what this will do is a couple different things
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you know there's uh those baroreceptors and baroreceptors are located in like your carotids, like right at the bifurcation or at the aorta,
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and they sense changes in cardiac output and blood pressure.
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And so what happens is you're going to stimulate these things called baroreceptors,
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and they're going to go and they're going to activate your sympathetic nervous system.
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When your sympathetic nervous system becomes crazy activated, it's then going to jack up all your epinephrine and norepinephrine release.
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So then what you're going to see is you're going to see a lot of epinephrine
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and you're going to see a lot of norepinephrine increasing.
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Why is that a problem?
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Well, the reason why that's a problem is, is that these little chemicals here,
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they love to go to the heart and to your vessels and cause some problems.
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They go to the heart and they say, hey, why don't you speed up the heart rate?
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Because if you speed up the heart rate, that'll increase the stroke volume, hopefully increase the critic output.
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But it's not good for a patient's heart rate to be super high,
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but that's one of the potential compensations is you're going to increase the patient's heart rate oops sorry guys
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you're going to increase the heart rate and again this is
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because it acts on what's called beta 1 receptors
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this is going to become helpful
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i promise the other thing is it acts on other types of receptors like alpha 1 receptors on your vasculature
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and causes it to constrict and if you constrict these vessels what happens to the diameter of them they get smaller
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What happens to the resistance?
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It goes up.
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So my SVR will go up.
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And if that happens on the artery side, what's that going to do to my afterload?
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It's going to go up.
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And so it increases the afterload.
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Now you're like, that sounds like a terrible thing.
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It is terrible.
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Because think about this.
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If a patient has diastolic heart failure and you increase their afterload, what are you going to do?
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You're going to worsen their diastolic heart failure because now if their afterload is high, what does their body try to do to compensate?
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It hypertrophies and it's going to worsen their already present heart failure.
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So this is going to be, it's going to trigger hypertrophy.
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And guess what that's going to do?
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That's going to worsen their heart failure and they're going to get sicker and their heart failure is going to get worse.
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The other thing it's going to do is it's going to constrict the veins
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because there's alpha -1 receptors on both the arteries and there's alpha one receptors on both the veins.
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So it's going to squeeze the veins and try to push a lot of blood back to the heart.
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And that's going to try to increase the preload.
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But then if you increase the preload, now the ventricles have to dilate to accommodate for that volume.
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And if the ventricle dilates, what does that sound like?
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Systolic heart failure.
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So it's going to worsen the patient's systolic heart failure.
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So this is why it sounds like
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These things are kind of like a good mechanism to try to increase your SVR.
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That's what it's trying to do, is increase the SVR to increase your blood pressure, right?
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But unfortunately, it worsens the patient's heart failure and their heart rate.
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Another thing, if that wasn't enough, is this cardiac output is going to stimulate these like weird cells in the kidney called juxtaglomerular cells.
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And these juxtaglomerular cells are very sensitive to blood pressure.
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And what they'll do is they'll release a molecule called, you guys already know this, right?
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Renin.
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Alright, so it's going to release a molecule called renin.
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Now, renin will then do what?
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It'll then lead to the formation of angiotensin 1.
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Angiotensin 1 will then lead to the formation of angiotensin 2.
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What's the enzyme that stimulates that process?
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ACE, don't forget that.
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Angiotensin II can do a couple things, but one of those things is it increases aldosterone release from the adrenal gland,
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and it also increases ADH release from the posterior pituitary.
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Now, with all of this being said, what's the overall effect of all of this?
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I'll show you.
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Angiotensin II works on your vessels.
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You got a lot of angiotensin II receptors on your vessels.
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So here, let's say we have what's called a angiotensin II receptor here in your vessels.
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Guess what it does?
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Squeezes the heck out of them.
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What'd that do?
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SVR goes up, because that's the compensatory mechanism.
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If SVR goes up, then what happens to your afterload?
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That goes up.
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What happens if you have diastolic heart failure?
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You worsen the hypertrophy.
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Patient's getting sicker, that's not helpful.
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What happens if you do to the preload?
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You're going to cause more blood to get returned to the actual heart.
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Pre -level goes up.
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But in a patient who has systolic heart failure, what is that going to do?
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It's going to dilate their heart even more and worsen it.
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So you guys get the concept here is that this is another potential problematic issue that can worsen the patient's heart failure.
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And that's why we have drugs that we'll talk about a little bit later
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that I'm going to kind of preemptively kind of covering here that this will help to treat.
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Because we just don't want to have these high angiotensin II levels, the high sympathetic nervous system activity and just to complete this concept aldosterone
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and adh will be higher
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and you know what this does this increases your reabsorption now the patient's reabsorbing lots of sodium
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and water and if you reabsorb sodium and water what is
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that going to do it's going to cause the patient to retain a lot of this fluid
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and they're going to start developing edema they'll have more preload
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so the ventricles will have to dilate more but one of the problems
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that you'll see here is they'll start developing a lot of edema because of this.
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So this is the concept that I really, really want you guys to be able to understand here with this nasty disease process.
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There's one more thing, which is actually super cool though.
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So this system here is called the ranin -angiotensin -aldosterone system, right?
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You know, whenever your heart, your cardiac output's really, really low, another really interesting thing that happens is,
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is that your heart, whenever it's like really low cardiac output, the hearts actually kind of get filled with blood.
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And so they can release this molecule in response to a lot of stretch.
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So let's say that the heart is really, really, really being stretched.
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It's being stretched a lot.
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When the heart is being stretched a lot, it makes a molecule called atrial natriuretic peptide.
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And it makes a lot of it.
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And the whole point of increasing this atrial nectarine peptide is it wants to go and inhibit.
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The hope is that it inhibits angiotensin 2.
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And if I inhibit angiotensin 2, I prevent this whole disastrous process from occurring.
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Well, that's cool.
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I would really like drugs that increase AMP then.
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I would really like drugs that decrease angiotensin 2, block aldosterone, and block the sympathetic nervous system.
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And that's what we'll talk about in the treatment section.
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But this is what I want you guys to understand about left heart failure.
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Now let's quickly go through right heart failure and high output failure.
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Bye my friends, so now we got to talk about right heart failure.
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So we talked about the left heart failure.
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The right heart failure is actually a lot easier.
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When we talk about right heart failure, it's the same kind of concept.
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We take this normal heart and we jack it up to cause systolic heart failure.
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Now when we talk about this, it's again, you're dropping what?
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The contractility.
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So what generally drops contractility on that right heart?
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Well, in the left heart, the most common cause was an mi guess what it would be here an mi okay
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so generally a right ventricular mi is going to be the
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most common cause generally of this systolic right heart failure
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so you're dropping the contractility here
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and that's leading to the formation of this systolic heart failure now again what you're going to notice is is
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that this puppy's going to start beginning super dilated all right
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so what you're going to notice is this dilated type of right ventricle.
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Now, another concept here with this dilated right ventricle here is that your right ventricle,
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the contractility is reduced, right?
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So this whole right ventricle, let's say, is really, really messed up.
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Because it's messed up, it's going to have a hard time being able to pump blood out into the pulmonary artery, right?
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So it's going to have a hard time with forward flow.
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so what you'll notice out of these patients is
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that they are going to have a low right ventricular cardiac output right because of the contractility and
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so because of
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that they're going to have this low contractility
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this is going to lead to a decrease in their right ventricular ejection fraction
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now we don't generally give these you know as we compare prior
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The heart failure with a reduced ejection fraction, that's primarily only consistent with left heart failure.
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But again, you can think about it in this particular way.
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But again, a reduction in contractility will lead to a reduction in the right ventricular ejection fraction.
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And the problem is
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that these patients are going to have a hard time generating a good cardiac output out of the right ventricle.
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And so that's the concept here.
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It's pretty straightforward.
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Something is decreasing contractility because you infarct at the right ventricle.
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In the other aspect over here, you have something increasing the afterload, right?
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So if I have something increasing the afterload, in the example for left ventricle, it was hypertension, it was aortic stenosis.
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For this one, it's anything that increases, I'm going to put a little parenthesis here, anything that increases the pulmonary vascular resistance.
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So for the systemic circulation, it was called systemic vascular resistance that was hypertension or aortic stenosis and this thing it's anything that causes
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pulmonary hypertension so we say this is pulmonary hypertension
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and there is different types we'll talk about this in palm
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when we go over pulmonary hypertension but there's type one
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which is idiopathic type two
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which is due to left heart failure type three due to some type of like lung disease like copd
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or interstitial lung disease type four due to some type of chronic pulmonary emboli
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and then type 5 is there's usually something like sarcoidosis like something compressing the pulmonary vasculature
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but this is the concept i want
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you to understand pulmonary hypertension for right heart failure systemic hypertension for left heart failure for
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that diastolic type now what do you notice here about this right ventricle it's thick right
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so they have some hypertrophy generally of that right ventricle so we could say right ventricular
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hypertrophy and this is usually because
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that ventricle is going to have to thicken to be able to accommodate the high pressure of the pulmonary vasculature.
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That's the only way it can do it and so
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because of that it's going to have a hard time being able to fill with blood.
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So the problem with this situation here is the same concept.
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They have a reduction in right ventricular filling which causes them to have a again a normal ejection fracture.
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They don't have a problem with their ejection fraction
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so they have a normal right ventricular ejection fraction
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so again decreased filling process
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but normal right ventricular ejection fraction that's the big kind of thing
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that i want you guys to understand here
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now again remember both of these are going to have a reduction in right ventricular cardiac output
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it's just again the mechanism behind them developing this all right
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that covers this one for right heart failure the pathophysiology and the causes.
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What about this weird one?
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There's this weird entity called high output heart failure and generally high output heart failure is particularly only consistent with generally left, so the left heart.
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And what I want to do quickly is talk about this one.
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So for the most part what you've noticed that
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when we talked about left heart failure before is
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that there was a low cardiac output and then when you talk about right heart failure there's a low cardiac output.
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There's this weird entity in the world where this is called a high cardiac output heart failure.
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You're like, what?
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That seems odd.
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It is weird.
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But here's, let me, let me kind of explain why this happens.
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And this patient here, we see that their vessels are super dilated.
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So they have extremely super vasodilated blood vessels.
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So what you'll notice here out of these patients is they have a massive vasodilation.
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All right.
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And when you vasodilate vessels that's a big thing we'll talk about what causes
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but this is massive vasodilation all right
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so there is massive vasodilation here the question
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that you have to ask yourself is what's causing these vessels to become super super dilated
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and there's a bunch of different things one reason
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is very common is sepsis sepsis will cause massive vasodilation another one
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which is an odd one is when you have thymine deficiency such as beriberi.
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This will for some reason cause massive vasodilation.
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Thyrotoxicosis, so when a patient has thyroid storm, this can also cause massive vasodilation.
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Other kind of interesting things could be things like AV fistulas as well as severe, and I mean really, really severe, anemia.
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These are particular things that in these diseases
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but i would say sepsis being kind of one of the most common ones these will cause massive vasodilation
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when you massively vasodilate these vessels
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What happens to the systemic vascular resistance now?
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Soccer's huge.
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resistance has got to be low.
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So now their systemic vascular resistance is crazy, crazy low.
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Now, go back to that formula.
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What was the formula called?
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For everything with low output heart failure, we said that we have blood pressure is equal to cardiac output times systemic vascular resistance.
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And all the ones that we talked about, cardiac output was low,
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which dropped the blood pressure now in this disease process the systemic vascular resistance is low
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which will cause the blood pressure to be low what has to compensate the cardiac output
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and that's why we call this high output heart failure
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so then what happens is
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when your systemic vascular resistance drops what it does is it creates a reflex kind of situation
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so what it does it'll drop the blood pressure
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so the patient's blood pressure may drop when you drop the patient's blood pressure
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What that's going to do is it's going to activate the sympathetic nervous system and the renin,
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angiotensin, and aldosterone system, and that is going to increase the sympathetic nervous system.
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Now, look at this.
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If I increase the sympathetic nervous system, that's then going to go and work on the heart.
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And when it goes and works on the heart, it's going to work on a bunch of different components here.
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One is you have your SA node, your AV node, your bundles of Hiss and bundle branches.
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That's all going to be activated.
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And your heart rate is going to try to go up because it's going to hopefully try to increase your cardiac output.
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And you're going to contract your heart like a son of a gun.
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So then on top of that, you're going to try to cause the heart to really, really contract.
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And the stroke volume will go up.
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and both of these are going to be an attempt to
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try to push as much blood possible out of the heart
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so what you'll notice here is
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that these patients will have a massive increase in their heart rate
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and a massive increase in their stroke volume but here's what's really odd
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you would think okay these guys are pumping
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and i mean pumping blood out of their heart into the corner i mean into the systemic circulation
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so the cardiac output has to be high enough right
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it's got to be good enough to be able to meet the actual tissue demands it's not
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and that's where the problem here in the cycle occurs
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this disease causes vasodilation leads to this whole process tries to increase the cardiac output
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but no matter what it's not enough to meet the body's demands
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and so what happens here is it's not enough and that's the issue so you see how we talk about heart failure,
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it's the inability to perfuse the tissues and meet their demands.
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That would be a definition then.
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So high output heart failure is the cardiac output's high,
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but it's not high enough to overcome this massive vasodilatory effect to meet the tissue's oxygen demands, and that is heart failure.
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So, so far we've gone over left heart failure, low output, right heart failure, low output, and the rarity of high output heart failure.
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Now let's go over what are the complications of a patient developing heart failure.
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Alright my friends, so now if a patient has left heart failure, whether that's diastolic or systolic heart failure,
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or right heart failure, whether it's systolic or diastolic heart failure, we have to understand the particular complications that can arise.
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When a patient has left heart failure, one of the big things that you'll see with these patients is features of pulmonary congestion.
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So either way, the patient's cardiac output stinks.
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They're not able to get enough blood out of their left ventricle.
419
So what happens is because they have a cardiac output that is being reduced, if you will, in other words,
420
in these patients, it's hard to get the blood out of the heart.
421
Because of why?
422
Because they have a reduced cardiac output.
423
Now, because of that, if the blood can't get out of the heart, where's it going to go?
424
It's going to start backing up into the left atrium
425
when it backs up into the left atrium
426
it goes into all of these like cute little pulmonary veins here see it starts moving into the pulmonary veins
427
and then what happens is it starts kind of like congesting these pulmonary veins intensely now
428
when the pulmonary veins start coming very very filled with all of this blood the pressure in those go up
429
and we specifically use a terminology here called pulmonary capillary wedge pressure so we use that on both of these here.
430
And this will go up.
431
And the pulmonary capillary wedge pressure is a measure of left heart pressures.
432
So if the left heart pressure is high, the pulmonary capillary wedge pressures will also be high.
433
When that happens, the pressure in the pulmonary capillaries rise enough that guess what starts leaking out of this actual vasculature?
434
Fluid.
435
So you're going to have fluid leaking out of this vasculature and into the interstitial spaces. and into the alveoli.
436
So now this alveoli is gonna become filled with fluid, you're gonna develop some edema here in the interstitial spaces,
437
and now these patients have pulmonary edema.
438
And so this is one of the potential complications is they get a little bit of pulmonary edema.
439
Now why is that bad?
440
When you have pulmonary edema, some patients can present a couple different ways.
441
One is they particularly present with what's called dyspnea.
442
Now dyspnea, it may just be a generalized dyspnea.
443
This may be with exertion.
444
This may be at rest.
445
That depends upon the severity of their CHF.
446
But another very interesting presentation is that whenever these patients lie flat,
447
the fluid tends to kind of separate out into multiple parts of the lungs.
448
Normally, they'll be in the dependent inferior portions.
449
But as you lay flat, this edema can become worse and spread throughout multiple alveoli
450
and this can worsen their actual shortness of breath when they're laying flat
451
and so there's two terminologies one is called paroxysmal nocturnal dyspnea this is whenever they're at their sleep
452
and they're laying flat they're super short of breath
453
or just in general maybe they're not sleeping they're laying down flat
454
or laying on a recliner
455
and they have some shortness of breath there it's the same concept
456
it's called orthopnea these are big big common features that we see with pulmonary edema.
457
One is just dyspnea, whether it be exertion or rest, or the other one is when they're laying flat, proxysmal nocturnal dyspnea or orthopnea.
458
Another potential problem here is that whenever these patients, let's say they really, really have a massive reduction.
459
So let's say that their cardiac output massively reduces, maybe for whatever reason.
460
Common triggers for patients to develop what's called acute decompensated heart failure is they have an MI
461
or they have a massive tachyarrhythmia or they stop taking their medications they're supposed to be taking.
462
And what this does is this massively drops the cardiac output, massively increases the pulmonary capillary wedge pressure, and worsens their pulmonary edema like terribly.
463
And sometimes this pulmonary edema can be severe.
464
I'm talking severe pulmonary edema and this is something
465
that we would generally see when a patient has what's called acute decompensated heart failure
466
and what happens is is this fluid will really start kind of leak like all over multiple different alveoli
467
and interstitial spaces will become filled with fluid
468
and this can cause a massive vq mismatch
469
when you fill up multiple alveoli with fluid
470
that causes a vq mismatch decrease in ventilation normal perfusion there's a mismatch and that leads to hypoxemia.
471
So watch out for a VQ mismatch here, and what will happen is the patient's SpO2 will be very low,
472
and they can exhibit features of what's called hypoxia.
473
The other thing is that this fluid that leaks into the interstitial spaces, when it actually does leak there,
474
sometimes it may just cause the patient to have generalized dyspnea or increased work of breathing.
475
So they may be working hard to breathe, or they may have a higher respiratory rate.
476
So that's another kind of thing
477
that you want to watch out for is watch out for an increased work of breathing or an increased respiratory rate.
478
So these are some of the big findings that you want to watch out for.
479
So again, watch out for a stimulation of VQ mismatch
480
because of all of these alveoli being filled with fluid and then hypoxia.
481
So watch their O2 sat to see if they have desaturations.
482
This is super, super common in left heart failure.
483
So big things to look out for is go to the patient, see if they have any respiratory distress or hypoxia on their O2 saturation,
484
ask them if you have any shortness of breath at rest, exertion, or when they're laying down flatter when they're sleeping.
485
The other thing, get your stethoscope that you paid
486
so much money for and go and listen and see if you hear any rails or crackles.
487
All of these are potential signs of pulmonary edema.
488
This is very common in left heart failure.
489
The scariest complication that I say that you would potentially see in a patient who has left heart failure is cardiogenic shock,
490
and this is definitely the scariest one.
491
Generally, again, a very common trigger here that can happen is an MI, a massive tachyarrhythmia, or you stop taking your medications.
492
These are very, very common triggers.
493
Now, again, same concept.
494
The patient has a massive drop in their cardiac output.
495
If you drop their cardiac output, you're not going to be getting enough blood flow out of their heart.
496
When you don't get enough blood flow out of the heart, particularly enough volume, you drop that cardiac output, what happens to their perfusion?
497
Oh, that's stinky.
498
That systemic perfusion goes down. So not only whenever
499
you have a low cardiac output do you have a hard time getting blood out of the heart
500
and it backs up into the lungs, but you have a a hard time getting it out of the heart and delivering it to multiple tissues.
501
When you have a decrease in systemic perfusion, The problem with this is that your body kind of says, okay, perfusion's kind of stinky right now.
502
That's because the cardiac output's really low.
503
You know what the body tries to do is it says, okay, what I'm going to do is if the cardiac output's low, what's that formula?
504
BP is equal to cardiac output times the systemic vascular resistance.
505
Let's write that out.
506
So BP is equal to cardiac output times the systemic vascular resistance.
507
And these patients who are in cardiogenic shock, this is low, causing this to be low.
508
What has to compensate my friends?
509
SVR.
510
And this will shoot through the roof.
511
And when SVR goes up, it clamps down on your vessels, squeezes them.
512
And now you have very little blood flow going to your extremities.
513
You know what this is going to do?
514
This is going to cause these patients to have very cold or pale extremities.
515
Another really, really terrifying sign here is they have like modeling, and this is really, really kind of scary.
516
It's where they have this weird kind of discoloration, usually at the knees, and that's a very sign of, that's a very poor sign of perfusion,
517
and this is usually because you're clamping down on those vessels to compensate.
518
Another thing is that when you have decreased systemic perfusion, not only do you create this reflexive vasoconstriction, but you also get organ malperfusion, right?
519
If I have organ malperfusion, oh man, that ain't good because now I'm not perfusing various tissues.
520
What are some of these tissues that actually become affected because of an increase in more organ malperfusion?
521
One is the brain.
522
The brain is super sensitive to blood pressure.
523
The coronary circulation, which supplies the myocardium of the heart, well, it's going to make things a lot worse.
524
It becomes very susceptible.
525
The kidneys become susceptible and the GIT would probably be the last one of the line, but it's also super susceptible.
526
If I don't perfuse the actual brain, then I can develop encephalopathy, and this is probably going to be one of the most common causes.
527
Sometimes, if the actual mouth perfusion is severe enough, it's possible it could cause a TIA slash CVA, all right?
528
So that's another thing you want to watch out for.
529
The other thing is that if you don't perfuse the actual myocardium well enough, it may cause a myocardial infarction.
530
So you may see things like an N -STEMI or a STEMI potentially.
531
So these are things that I think are really, really important to remember.
532
The other thing is it may stimulate, son of a gun, it may stimulate injury to the kidneys.
533
This is called an AKI.
534
There is a very common terminology that you may hear here.
535
When patients have very severe left heart failure and they don't perfuse their kidneys very well because of decreased systemic perfusion,
536
but also their CVPs are really high, so it's hard to get blood out of the kidney.
537
They can develop something called cardiorenal syndrome.
538
Very common trigger of AKI, so don't forget that one.
539
And the last one is they may cause acute mesenteric ischemia.
540
This is another really, really big one, or ischemic colitis.
541
And this is another big trigger, so you're going to want to watch out for any kind of like bowel ischemia and abdominal pain.
542
The last thing that's always a feature of systemic perfusion
543
that's being very very poor is your tissues whenever there's very little oxygen that's being delivered to the tissues
544
so here this tissue is supposed to be getting oxygen
545
if it's getting very very little oxygen they do not like that
546
and what they do is they trigger the production of a molecule
547
that's usually a sign of poor perfusion you guys know what that's called lactic acid
548
but lactic acid gets broken down into lactate and
549
so you want to watch out for this because one of the things
550
that this will do is this will really cause the pH to drop and it'll trigger an acidosis.
551
So watch out for acidosis that can occur in the setting of cardiogenic shock.
552
So again, when a patient has heart failure, it can kind of look a little bit different.
553
The patient may have chronic CHF or their primary symptom may just be dyspnea, paroxysmal nocturnal dyspnea, or orthopnea.
554
But if they develop an acute decompensated heart failure from those triggers, MI, tachyarrhythmias, medication, non -compliance,
555
they can develop severe pulmonary edema, hypoxia, respiratory distress.
556
And most patients who have chronic CHF, they may just have minimal decreased systemic perfusion.
557
And the way that they compensate is an increase in systemic vascular resistance.
558
So they may have cold, kind of pale mottled extremities.
559
But whenever it's really bad, to where there is an acute decompensated heart failure due to an MI,
560
tachyarrhythmias, medication non -compliance, now they don't perfuse multiple organs.
561
And they can develop things like encephalopathy, MI, AKI, and acute mesenteric ischemia, and lactic acidosis.
562
These are big things to think about, my friends.
563
All right, we come to the last one here.
564
Patient has right heart failure, all right?
565
So if the patient has a right heart failure, it's because they had something wrong with the contractility or the high afterlope, pulmonary hypertension.
566
This one's super easy, thank goodness this.
567
Whenever the right heart is damaged, what happens is again the whole concept here is
568
that it's either you can't fill it
569
or you can't get blood out of it right
570
so that's either one of those concepts you can't get blood in
571
or you can't get blood out of it when
572
that happens what happens is the pressure in the right heart increases
573
and we use a terminology to really describe that
574
and that's called your central venous pressure so your central venous pressure becomes very high when your central venous pressure is high,
575
what happens is the blood is kind of a measure of the blood backing up into your superior vena cava
576
and blood backing up into your inferior vena cava.
577
And what this will do is this will kind of present in two different ways
578
that you want to try to look for.
579
One is it'll present with a patient having a lot of jugular venous distension.
580
So they'll have a plump jugular vein.
581
And the other one is they'll have some edema of their lower extremities, usually what's called pitting edema.
582
So when you press on it, it kind of really dips in and gives this kind of deformity there.
583
This is super common in right heart failure.
584
Another common presentation, again, regardless of the type, whether it's problem filling or problem getting out,
585
the concept is the same is that you have a very high central venous pressure
586
when your central venous pressure is high the blood is going to back up into the inferior vena cava
587
and what it does is it causes one particular problem
588
which leads to hepatic congestion
589
so you know the liver
590
I'm kind of zooming in on a basic model of the liver let's say
591
this is a liver cell this is an artery this is the hepatic veins
592
which empty into the IVC and this is a biliary duct.
593
Whenever this hepatic vein is congested and it can't get blood to go up,
594
it congests in the liver and causes the liver to become injured and damaged.
595
And you know what this could potentially present as?
596
This could cause a patient to develop liver failure.
597
More specifically, I would say you see this more commonly as a cirrhotic kind of presentation
598
but you can see this as a potential trigger of liver failure
599
because of the increased hepatic congestion all right the other thing
600
that it can do is it can increase your portal pressure
601
so what happens is your hepatic veins what happens is it can actually cause
602
this to really cause the portal pressure within the venous circulation the hepatic portal circulation to become very very high
603
so if you increase your portal pressure
604
what this does is this causes the hydrostatic pressure in the portal veins
605
and the peritoneal capillaries to be super high and leak fluid into the abdomen.
606
And when you leak this fluid into the abdomen, what do we call this type of fluid that leaks into the abdomen?
607
Ascites.
608
And so that's another very, very common presentation here is ascites.
609
So watch out if a patient develops liver failure and they have a history of right heart failure, think about that.
610
If they have ascites and they have a history of right heart failure, think about that.
611
And again, if they have very plump jugular veins and pitting edema, think about a right heart failure.
612
And the last one, it's not commonly thought of, but it can happen.
613
Left heart failure, we talked about cardiogenic shock.
614
Right heart failure can also get cardiogenic shock.
615
So think about this.
616
This concept is super interesting.
617
In this situation here, you're having, let's say, blood difficulty.
618
This is more common in the systolic types,
619
where the vent right ventricle super dilated in this situation you have problem getting blood out of the right heart
620
and because of that now this right ventricle has a hard time
621
if it becomes super dilated maybe it can't fill properly
622
or it just can't get blood out of the heart when
623
that happens because you can't get blood out of the heart the right ventricle dilates even more
624
so if it's dilated before it dilates more all right
625
so now this sucker is huge
626
so whenever this happens you can't get blood out of the heart
627
it's going to stimulate the right ventricle to dilate even more
628
when the right ventricle dilates more the next thing
629
it does is is it causes the septum to bow over into the left ventricle
630
and now look at the space of the left ventricle it's smaller
631
so then it causes it's called a septal shift
632
so a septal shift and we'll say
633
that this septal shift is occurring from right to left from the right side to the left side what
634
that does is is it makes it hard for the left ventricle to fill with blood because now it's much smaller
635
if it can't fill with blood what happens to the left ventricular cardiac output it drops.
636
So now you have a septal shift and that's going to cause a decrease in the left ventricular filling.
637
If you decrease the left ventricular filling, that is going to then do what?
638
That is going to decrease the left ventricular cardiac output.
639
And if you decrease the left ventricular cardiac output, that can potentially lead to systemic malperfusion.
640
And then if we go on further, cardiogenic shock.
641
So this is a pretty scary one.
642
I'm actually usually, we don't see this one too often, right heart failure causing cardiogenic shock.
643
But when you do, it's pretty terrifying because it's a really, really bad one.
644
But this is another potential one that I want you to think about,
645
but you really primarily only see this one with right ventricular MI as the particular etiology here.
646
Not so much the pulmonary hypertension causes.
647
All right, my friends, that covers the issues or complications, if you will, of heart failure.
648
It's a pretty disastrous thing if it gets really, really bad.
649
What I want to do now is I want to take you through how to diagnose heart failure.
650
First thing is get a chest x -ray.
651
This will help you because if they have cardiomegaly, that's somewhat helpful.
652
Do they have pleural effusions, pulmonary edema, and curly B lines?
653
That's all suggestive of left heart failure for the most part.
654
Now, with that being said, if a patient has these findings, that doesn't define or determine that they have heart failure.
655
I want to combine, oh, they have pulmonary edema, pleural effusions.
656
Is their left heart not doing a good job?
657
Well, one way I could say if their heart is not doing a good job is they could check BMP.
658
This is not a good test though.
659
It's usually used in the emergency department to kind of quickly exclude a CHF exacerbation because if BMP levels are really low,
660
then you can say, okay, their dyspnea is probably not from a CHF exacerbation.
661
If it is really high, then you can't rule that out.
662
The better test is an echocardiogram because it's going to look directly at the heart and it's going to look to say,
663
hey, what's their ejection fraction?
664
Is it less than 40 %?
665
Their left ventricle doesn't look like it's moving at all.
666
That's systolic heart failure.
667
Or does it look like the left ventricle is contracting and pumping, but it's not filling properly.
668
Oh, that's diastolic heart failure.
669
In combination with a chest x -ray, that can be very beneficial.
670
Also do your physical exam.
671
If you don't see anything on the chest x -ray, look at the JVD, look at the legs,
672
look at the abdomen to look to see if they have any features of systemic congestion and combine that with their echo.
673
After you've done that, you should be able to determine is it right versus left.
674
That's pretty straightforward.
675
Now, the most definitively diagnostic test to determine
676
if the patient is an acute left heart failure
677
or in left heart failure in general is to do a
678
right heart catheterization also referred to as a swan gons catheter
679
you take a catheter you run it down the ij
680
you run it into the pulmonary into the right atrium into the pulmonary artery
681
and up into these like pulmonary artery capillary areas inflate the balloon
682
and then measure the pressures i told you
683
that the pulmonary capillary wedge pressure if it's really high that's very suggestive of a failure of the left heart
684
And if it's greater than 18 millimeters of mercury, that's a very suggestive number of left heart failure.
685
So if a patient has elevated BMP levels and echo
686
and a pulmonary capillary wedge pressure greater than 18 in combination with a chest x -ray suggestive of pulmonary edema,
687
I can really be confident in them having left heart failure.
688
Now, with that being said, if a patient has acute left heart failure, it's important to go through their medication list
689
and look to see what their heart rate is and look to see if they have any valvular disturbances.
690
But one of the big ones that I have to do is get an EKG
691
and also consider a left heart cath if I think they're having an MI
692
because that's going to find the occlusion and then treat that.
693
And that might be the thing that knocks them out of this acute heart failure potentially.
694
All right.
695
How do we treat heart failure?
696
This is a really, really important topic.
697
When I treat them, I specifically went into this for a reason.
698
I want to reduce sympathetic nervous system activity, reduce RAS activity and increase AMP activity.
699
And if you remember increasing AMP activity did what decrease RAS.
700
So my goal is to decrease sympathetic, decrease sympathetic, and decrease RAS.
701
How do I do that?
702
Well, if I decrease my sympathetic nervous system, I have to use things like beta blockers and SGLT2 inhibitors.
703
So metoprolol, carvetolol, or impagiflozin.
704
Usually these SGLT2 inhibitors are very, very important in patients with diabetes, but if they have cardiovascular disease, it's also beneficial.
705
And what happens is they reduce the sympathetic nervous system.
706
That reduces the heart rate, and that also reduces the systemic vascular resistance.
707
I don't constrict the veins.
708
I don't constrict the arteries as much.
709
I don't reduce, uh, I don't actually cause changes in preload and afterload, and I don't cause ventricular remodeling that improves ventricular function.
710
That's mortality beneficial right there.
711
The other thing is that SGLT2 inhibitors also cause aqua uresis.
712
They cause you to pee out of tons of water.
713
And so that can help with a lot of the edema of the patient is edematous.
714
The next concept is I want to reduce a RAS activity.
715
So the reason why is whenever low cardiac output.
716
Again, we said increased sympathetic and low cardiac output activate renin.
717
So renin leads to eventually angiotensin 2.
718
But if I give them a drug called an ACE inhibitor that blocks angiotensin 1 from being converted into angiotensin 2.
719
If I also give them a drug like an ARNI that increases AMP, it prevents AMP from being degraded.
720
If AMP builds up, it shuts down angiotensin too.
721
And then if I also give an ARB, ARB blocks angiotensin 2 from binding to receptors.
722
All three of these drugs will help to decrease angiotensin 2.
723
If I decrease angiotensin 2, I reduce the constrictions of the arteries in the veins and I reduce ventricular remodeling and that's a mortality benefit.
724
Another thing is angiotensin 2, if there's less of it, there's less aldosterone and also ADH,
725
but particularly aldosterone because now there's less sodium and water retention.
726
If I don't retain as much sodium and water, I don't have as much edema, but I also don't have as much preload
727
and i don't cause ventricular remodeling
728
that's where aldosterone antagonists would be really really beneficial in shutting down aldosterone production this is the concept
729
and these are the drugs that we have to incorporate in patients who have heart failure
730
because they have mortality reducing benefits okay that's a part of our guideline directed medical therapy other things
731
that we can add on with guideline directed medical therapy is alternatives
732
so if a patient's african -american they can't tolerate an ace inhibitor and arb
733
hydralazine and isosorbidinitrate is a good combo to add because they're good vasodilators.
734
The other one is an alternative to a beta blocker.
735
If they're maxed on a beta blocker and they are in normal sinus rhythm, ivebrating can be considered.
736
If you want to help them to get rid of a lot of the sodium and water retention,
737
you can make them pee it out by giving them diuretics, loop diuretics and thiazide diuretics.
738
And then the next thing is if a patient has the need for device therapy.
739
So what I mean by this is if a patient has heart failure, especially left heart failure.
740
It stretches out the left ventricle and kind of causes left bundle branch blocks.
741
And then that alters the synchrony of the ventricles.
742
If I give them what's called a CRT, cardiac resynchronization therapy, it'll make sure that the ventricles are contracting kind of in tandem
743
and improve potentially the left ventricular ejection fraction.
744
I should definitely be instituting that in patients with an LVEF less than 35 % and an LVB.
745
All right.
746
That's a CRT.
747
If a patient has a left ventricular ejection fraction less than 35 % and they have ventricular arrhythmias, they need to get an AICD.
748
This will shock them if they go into VTAC or into VFib and prevent them from going into cardiac arrest.
749
The next thing is if a patient is on all of these medications, they have device therapy, their left ventricular ejection fraction is less than 25%,
750
they're not looking good and they look like they're going to need a transplant, sometimes we will play something called an LVAD,
751
a left ventricular assist device, which will take blood from their left ventricle
752
and shunted a different direction into the order to give that left ventricle some time to rest
753
now
754
and patients who are in cardiogenic shock all right their systemic perfusion stinks i want to have one primary goal
755
which is to increase systemic perfusion
756
so increasing systemic perfusion is very beneficial in patients who are in cardiogenic shock so what could i do
757
inotropes or mechanical circulatory support.
758
One way I can do that is I can give them things like dobutamine or milrinone.
759
These are commonly used in acute decompensated heart failure or cardiogenic shock.
760
The benefit of these is that they reduce afterload and increase contractility, which combined increased cardiac output.
761
The downside is that evidence has shown no reduction in mortality.
762
The other drug is digoxin.
763
This is an oral and IV drug.
764
So you can take this out outpatient, you can't take these outpatient.
765
This you can give to the patient and it's been shown to increase contractility and decrease AV node conduction.
766
So it's good in atrial fibrillation as well.
767
It is not shown to reduce mortality, but it may reduce the actual hospitalizations.
768
So there's a potential benefit to digoxin and increasing perfusion, especially in patients with cardiogenic shock, and even as an outpatient continuing that drug.
769
If the patient is failing these inotropes and they're continuing to decompensate and showing signs of potential failure, then we go to device therapy.
770
And there's two ways that we could go here.
771
An intraordial balloon pump has been shown to at least preserve coronary perfusion.
772
So this sucker deflates during systole to get blood to go forward.
773
And then it actually inflates during diastole.
774
So here during diastole, it inflates and it keeps the pressure all here in the aorta really high.
775
And what that does is guess what comes right off of the aorta here, the coronary arteries.
776
So if the pressure is high in the aorta during diastole, it's going to improve coronary perfusion and improve myocardial contractility.
777
And that's the benefit of this.
778
Most times, patients who'd end up on cardiogenic shock refractory to a lot of medications,
779
such as dobitamine, milrinone, introverted balloon pumps may require something called VA ECMO.
780
This is called venal arterial extracorporeal membrane oxygenation.
781
We take a catheter, we run it into one of their veins, we run it out of the vein and into a pump.
782
From there, we run it through an oxygenator, and then we put it in a catheter that runs right into their artery.
783
These are big stinking catheters, and they are designed to be able to help to maintain a decent amount of flow
784
and augment the cardiac output and also oxygenate the blood.
785
So this is a potential beneficial therapy that could be used as a patient in refractory cardiogenic shock.
786
The other thing I think that's important to remember in a patient who's in cardiogenic shock
787
or having any signs of cardiogenic pulmonary edema.
788
is what's called BiPAP.
789
Using diuretics to help to get rid of some of the sodium and water, which will help to reduce some of that actual pulmonary edema,
790
but BiPAP has been shown to potentially increase the antithoracic pressure, and that will help to reduce right ventricular prelip.
791
So you don't have as much blood going to the right heart, and you don't have as much blood going out of the right heart.
792
So now less blood is going through the pulmonary circulation and going to the left heart.
793
If there's less blood going that way, that's going to have less blood leaking out into the pulmonary interstitium, less pulmonary edema.
794
The other concept is it drops your left ventricular afterload.
795
So the pressure in the aorta drops.
796
So it's easier to get blood out of the left ventricle into the aorta.
797
So you have less blood coming to the left heart and you have more blood going out of the left heart.
798
That's going to improve your cardiac output and reduce pulmonary edema, but more particularly reduce pulmonary edema.
799
And that's one of the benefits of this drug in patients who are in acute heart failure or potentially cardiogenic shock.
800
All right.
801
I know this is a lot.
802
Let's go through this in a systematic approach.
803
A patient comes in, they have heart failure.
804
You've changed their modifiable risk factors.
805
After that, you start them on an ACE inhibitor, an ARB, all right?
806
Plus a beta blocker.
807
They're still symptomatic.
808
Give them diuretics to reduce venous congestion, whether it's systemic or pulmonary.
809
They're still symptomatic.
810
Add on aldosterone antagonists and an SGLT2 inhibitor.
811
They're still symptomatic, and they're potentially unable to tolerate an ACE inhibitor or an ARB.
812
Well, switch them.
813
Switch to an ARNI if possible, so an angiotensin receptor neprolysin inhibitor.
814
So this would be things where you put them on, like, Secubitril, Valzartan.
815
So these are very good drugs that have been shown to be very beneficial.
816
The other thing is if they can't do that one, or if they're African -American, consider Hydralazine and Isosorbidinitrate it actually has a mortality benefit.
817
If the patients are symptomatic on all these therapies and a normal sinus rhythm maxed out on a beta blocker, give them ivabraiding.
818
If the patient has a left ventricular ejection fraction less than 35 %
819
and a left bundle branch block or a QRS greater than 120, give them cardiac resynchronization therapy.
820
If despite all of these measures, they remain symptomatic, try to increase their perfusion.
821
Usually inotropes would be the next step here.
822
So digoxin would probably be the one that you'd want to continue outpatient if they're in overt cardiogenic shock, melrenone or dobutamine.
823
And then from there, if you have to mechanical circulatory support, if they're in overt cardiogenic shock, intriotic balloon pumps, VA ECMO, hopefully they recover.
824
And then the thing that you would need to put them on to bridge them to a transplant is an LVAD.
825
And hopefully they would get a cardiac transplant and improve.
826
all right my friends that covers heart failure i hope it made sense i hope
827
that you guys enjoyed it and as always until next time
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Từ vựng và ghi chú luyện nói cho bài học này
Bài luyện nói này dựa trên video “Congestive Heart Failure”. Những từ được nhắc lại nhiều nhất trong bài: failure, patient, blood, output, cardiac. Video này có 827 câu và 10365 từ để luyện shadowing. Phần lời nói dài 57:53. Người nói nói với tốc độ tự nhiên, khoảng 179 từ mỗi phút, gần với hội thoại hằng ngày. Chỉ 80% số từ nằm trong 3.000 từ tiếng Anh thông dụng nhất, nên từ vựng khá khó.
Từ vựng quan trọng trong video
15 từ đáng học trong video, kèm phiên âm và nghĩa:
| Từ | Phiên âm | Nghĩa |
|---|---|---|
| output danh từ | /ˈaʊtpʊt/ | đầu ra |
| fraction danh từ | /ˈfɹæk.ʃən/ | phần, tỷ lệ |
| decrease động từ | /dɪˈkɹiːs/ | hạ |
| shock danh từ | /ʃɔk/ | choáng, ngạc nhiên |
| vein danh từ | /veɪn/ | tĩnh mạch, ven |
| fluid danh từ | /ˈflu.ɪd/ | chất lưu |
| vessel danh từ | /ˈvɛsəl/ | thuyền lớn, tàu thuỷ |
| pump danh từ | /pʌmp/ | bơm |
| trigger danh từ | /ˈtɹɪɡɚ/ | cò |
| artery danh từ | /ˈɑɹ.təɹ.i/ | động mạch |
| tissue danh từ | /ˈtɪʃ.(j)u/ | khăn giấy |
| formula danh từ | /ˈfɔː.mjʊ.lə/ | công thức |
| medication danh từ | /mɛdɪˈkeɪʃən/ | phép trị liệu |
| beta danh từ | /ˈbeɪtə/ | bêta |
| chronic tính từ | /ˈkɹɑ.nɪk/ | mãn tính, mạn tính |
Cụm động từ bạn sẽ nghe
| Từ | Nghĩa |
|---|---|
| go up động từ | lên |
| check out động từ | tính tiền, trả phòng |
| shut down động từ | tắt nguồn |
| go back động từ | trở lại |
Những câu đáng luyện lại
Các câu ngắn, trọn ý trong video mà bạn có thể dùng lại khi giao tiếp hằng ngày:
- Do you lose contractility there?
- Do you guys know why?
- Do you guys remember the formula for blood pressure?
- What happens if you have diastolic heart failure?
- What happens if you do to the preload?
Ngữ pháp trong video
Những cấu trúc người nói dùng nhiều nhất, kèm đúng cụm từ trong video:
| Cấu trúc | Trong video |
|---|---|
| Thì hiện tại hoàn thành have/has + quá khứ phân từ — việc đã xảy ra nhưng còn liên quan đến hiện tại | you've noticed · we've gone · has left |
| Câu bị động be + quá khứ phân từ — nhấn vào việc xảy ra, không phải người làm | is damaged · is knocked · would be called |
| Mệnh đề quan hệ who / which + mệnh đề — thêm thông tin về người hoặc vật | person who has · fraction, which is · HEFREF, which is |
| Khả năng với “might / may” might/may + động từ — điều có thể xảy ra nhưng không chắc | may be · may drop · may just be |
Phát âm cần chú ý
Người nói dùng 159 dạng rút gọn, ví dụ they're, you're, don't. Hãy nói theo dạng ngắn đúng như bạn nghe.
- Âm “th”: sympathetic /ˌsɪm.pəˈθɛt.ɪk/, thick /θɪk/, breathe /bɹiːð/, rhythm /ˈɹɪð.əm/, catheter /ˈkæθɪtɚ/
- Âm “sh” và “zh”: fraction /ˈfɹæk.ʃən/, shock /ʃɔk/, potentially /pəˈtɛnʃ(ə)li/, tissue /ˈtɪʃ.(j)u/, reduction /ɹɪˈdʌk.ʃən/
- Từ dài — đặt trọng âm cho đúng: sympathetic /ˌsɪm.pəˈθɛt.ɪk/, potentially /pəˈtɛnʃ(ə)li/, medication /mɛdɪˈkeɪʃən/, beneficial /ˌbɛn.ɪˈfɪʃ.əl/, circulation /ˌsɝkjʊˈleɪʃən/
Những âm người Việt thường gặp khó:
- Cụm phụ âm cuối — đọc đủ từng âm, đừng nuốt âm cuối: pump /pʌmp/, valve /ˈvælv/, transplant /tɹænzˈplænt/, consistent /kənˈsɪs.tənt/, dependent /dɪˈpɛndənt/
- Âm /tʃ/, /dʒ/ và /ʒ/ — tiếng Việt không có, đừng đọc thành “ch” hay “gi”: wedge /wɛd͡ʒ/, terminology /ˌtɝ.məˈnɑ.lə.d͡ʒi/, congestion /kənˈd͡ʒɛs.t͡ʃən/, oxygen /ˈɑksɪd͡ʒən/, stretch /stɹɛt͡ʃ/
- Âm /æ/ — mở miệng rộng hơn âm “e”: cardiac /ˈkɑɹdiˌæk/, fraction /ˈfɹæk.ʃən/, vascular /ˈvæskjələ/, mortality /mɔɹˈtælɪti/, valve /ˈvælv/
Cách luyện với video này
- Nghe hết video một lần, chưa cần nói, và ghi lại những từ bạn chưa biết.
- Bắt đầu ở tốc độ 0,75×, nói đuổi từng câu, rồi quay lại tốc độ bình thường khi đã quen.
- Ghi âm giọng mình rồi so với bản gốc, chú ý các từ như output, fraction, decrease.
Phương Pháp Shadowing Là Gì?
Shadowing là kỹ thuật học ngôn ngữ có cơ sở khoa học, ban đầu được phát triển cho chương trình đào tạo phiên dịch viên chuyên nghiệp và được phổ biến rộng rãi bởi nhà đa ngôn ngữ học Dr. Alexander Arguelles. Nguyên lý cốt lõi đơn giản nhưng cực kỳ hiệu quả: bạn nghe tiếng Anh của người bản xứ và lặp lại to ngay lập tức — như một "cái bóng" (shadow) đuổi theo người nói với độ trễ chỉ 1–2 giây. Khác với luyện ngữ pháp hay học từ vựng bị động, Shadowing buộc não bộ và cơ miệng phải đồng thời xử lý và tái tạo ngôn ngữ thực tế. Các nghiên cứu khoa học xác nhận phương pháp này cải thiện đáng kể phát âm, ngữ điệu, nhịp điệu, nối âm, kỹ năng nghe và độ lưu loát khi nói — đặc biệt hiệu quả cho người luyện IELTS Speaking và muốn giao tiếp tiếng Anh tự nhiên như người bản ngữ.