Valvular Heart Disease with Tim Madeira, DNP

In this episode Tim Madeira, cardiothoracic DNP,  provides an overview of the primary heart valve diseases. He expertly guides us through the complex physiological processes underlying conditions like stenosis and valve regurgitation arising from congenital abnormalities, calcifications, infective endocarditis, and trauma. In addition, Tim outlines the latest evidence-based standards in surgical, percutaneous and medical interventions that nurses find themselves managing in the hospital.

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Valvular Heart Disease

Annie: If you’re anything like me, you found valvular heart disease to be. Overwhelming. As we all know there are four different heart valves. Tricuspid pulmonic, mitral and aortic, and each of these vows can have a myriad of things. Go wrong with them, such as stenosis, regurgitation, prolapse, and congenital defects. 

I used to think that I needed to know these four valves, times three main categories of defects. So 12 distinct conditions. 

But in practice, we really only see a handful of fabulous. Heart diseases. Most of the time. And that is what we are going to be talking about today. So sit tight as my guest, Tim Madeirra, and I dive into the causes of valve disease, it’s medical and surgical treatments. Common presentations and what to be on the lookout for when caring for these patients.

Tim: Hi, everyone. I’m Tim Madera. I am a dual nurse practitioner and clinical nurse specialist specializing in acute and critical care. I currently work as a nurse practitioner in the CV SICU at the Johns Hopkins Hospital in Baltimore, Maryland, and previously was a clinical nurse specialist for cardiac surgery in both the CV SICU and the step down unit. 

Annie: I met Tim when I attended the progressive care boot camp session at NTI last year. Tim has really climbed his way up. Starting as a patient transporter. Then to becoming a nursing assistant emergency tech, OR secretary, and eventual nurse in the ICU, ED and all the way now to having a doctorate and a nurse practitioner. 

So I asked him to come on the podcast today to talk about valvular heart disease. It’s something that I personally have learned and unlearned and relearned again about 10 times.

And I kind of want to start with a kind of a weird question it seems like heart valves are problematic, right?

Like, we get rheumatic, valve disease, we get endocarditis, we get stenosis, regurgitation. Is there something anatomically, different or unique about heart valves that make them prone to valvular heart disease?

Tim: That’s a great question. I think it’s a hard one to answer because valvular heart disease honestly can be a consequence of many different types of problems. You know, some patients are born with valvular disease. They have a congenital heart defect or, you know, malformation of some sort, and will struggle with heart valvular disease all their lives, and may need multiple surgeries for correction.

Other people, it can be secondary to another disease, one we, I think of as cancer. We have patients who come in maybe for breast cancer, for example, get radiation and chemotherapy. And that radiation to the chest, will sometimes cause the chordae tendineae, those little ropes that hold some of these leaflets to, you know, to the myocardium. Those may get stretched over time or actually break or sometimes what will happen is the heart may start to kind of grow or overgrow in a, in a abnormal way that they stretch out and those little valve leaflets no longer can communicate and touch each other and they stretch and stretch over time. And in that way, even though the valve is moving the way it should, it’s more that stretch of the valve leaflets away from each other that causes that heart failure type symptomology. 

Annie: If you think about it, a lot is asked our little heart valves. Heart valves are a thin flapping like leaflet that has to be flexible enough to open fully with each heartbeat during sisterly, yet strong enough to close tightly in prevent leaks during diastole. The uni directional flow of blood is crucial in is really the basis of our cardiovascular system and our heart bowels play a crucial role in this function. When you were saying some people are born with heart conditions what are some common examples of this?

Tim: So one favorite of mine, if I should even say favorite, is of congenital heart diseases. Like, this is the nerd in me coming out, is tetralogy of Fallot. I think it’s really interesting, these people all have four problems that are They’re universal. They have an overriding aortic valve that kind of goes in that septum. They have a ventricular septal defect. They have pulmonic stenosis, or stenosis of that valve, that pulmonic valve in the pulmonary artery that goes to the lungs. And we also have hypertrophy of that right ventricle. These four things we call Tetralogy. And I’ve always been fascinated. I was like, how can these four problems all affect the heart. 

Annie: Yeah. Something I I see in those who are born with some sort of congenital condition for example, Marfan syndrome is one I’ve seen, and Tetralogy of Fallot is that there are surgeries throughout life, like maybe, you know, as a child, they had a some sort of repair, but then there’s ongoing management . It’s something that has been an ongoing thing throughout their whole life.

Tim: Yes, definitely, definitely. We as a medical society are trying to think of more innovative ways to help these people long term, especially those who have to have multiple surgeries or multiple interventions throughout their life, as some of these heart valves may stop working or maybe you’re working efficiently. Or maybe you get infected, like we see with endocarditis you know, there’s a litany of things that happen long term to these people with prosthetic valves and, different, gadgets and gizmos that, that we put into them. 

Annie: Yeah, and I’m, I’m excited to, to talk to you about those when we get into the the treatment part of this discussion.

So just off the bat, like what are some common, valvular heart diseases that, that you see? What are some of the big ones that we should know about?

Tim: Sure. So, you know, you have to think of the heart as a two sided type of pump. There’s the one side that takes the arterial blood, which is the higher pressure type parts of the heart. And then we have the venous side of the heart, which is the lower pressure type valves.

And, first of all, is important because the types of pressures that these valves have to deal with every day, with every single pump of blood. blood , that can sometimes,tell you about what types of diseases you might see of the valves. 

I think the ones that we typically think of more so are diseases of the left side of the heart.

So our mitral valve and our aortic valves, those patients tend to be very symptomatic because those are the valves that when they’re not working, impact the quality of life. These are people, who have shortness of breath, who may be passing out. 

In aortic stenosis, for example, when that valve is, you know, stenotic and really, like, really rigid to get anything through over time, you know, They become what we call preload dependent.

We have to, they have to have enough blood and volume in their system in order for that blood to get squeezed through that little tiny valve. And these are folks who commonly will come into a clinic or an emergency room saying, I just passed out. It’s so hot today and I wasn’t drinking water. Oh, I must be dehydrated. And sure enough, a good nurse in the ED or, you know, in that clinic listens to the heart sounds and says, Hmm, do you know you have a murmur? Has anyone ever told you that? And those are commonly, those are the people who are like, Wow, no, I didn’t realize I’ve had a murmur. 

Annie: That’s such a great pearl. about, you know, a patient who’s presenting with, loss of consciousness, syncope, you know, whatever you want to call it, that you can easily explain it away with, you know, simple dehydration or you take an EKG and correct me if I’m wrong, but I don’t think , valve disease is going to be easily pointed out in an EKG. But listening to heart sounds is really going to be your clue for a patient who passes out, likely from dehydration, but… with the root cause being, aortic stenosis.

Tim: Definitely. Definitely. So, I know for some nurses out there who took pathophysiology, and thought, I’m never going to need any of those heart. sound, you know, borders and knowing where my aortic and my Erb’s point is. But I, as a cardiac nurse practitioner, and even as a nurse, I would listen to all four of my heart sound locations with every assessment just because, you know, there’s always that one off that you find a murmur or you find something that is significant to the patient. Needs to be explored further. 

Annie: Exactly. So, it sounds like aortic stenosis is a big one. What are some other, big valvular heart diseases that we should be aware of?

Tim: I would say is really important is mitral valve. prolapse or insufficiency sometimes. It depends where you work, but mitral valve regurgitation is when that mitral valve really fails to effectively close upon systole of that left ventricle. So when that left ventricle is trying to push blood forward through the aortic valve, oftentimes blood will also back up through that incompetent mitral valve, and more fluid than should be , ends up in that left atrium. And over time, when that blood keeps squirting into the left atrium the pressures in that left atrium increase. And over time, that causes atrial stretch. And then we start to then, with atrial stretch, notice that all of the normal electrical pathways of our heart. start to get distorted because we have such a big atrium to kind of get the electricity through, and that’s when we start to get atrial fibrillation. All of these stretched cells can’t communicate well, and then other ectopic little spots perk up. So people with mitral valve disease specifically, even mitral valve stenosis, it’s the same type of physiology when you think of it.

A stenotic valve, it’s hard to get that blood from your left atrium down into the ventricle, so it just builds up in that atrium and stretches it out. Those are the folks that have the rhythm issues, in my experience, and heart failure symptoms. , they tend to go in and out of a fib, sometimes they don’t know it, they might feel palpitations at home, but because their ejection fraction and the quality of their heart is generally strong in the beginning, they may, you know, Be like, Oh, I felt funny, but it moved on. And I moved on with my day, but it’s generally when people let it go to too long that then the left ventricle starts to suffer because of this inequality of pressures and then we start to get more and more heart failure type symptoms. 

Annie: To summarize: aortic stenosis, mitral prolapse, and mitral regurgitation are the three most common types of vascular heart disease that you will see in the hospital. And this makes sense, right? Because these conditions are located in the arterial, the high pressure side of the heart. And because of that, they wreak the most havoc on our patients. 

Now what exactly causes valve disease. Now I have to admit, I was hoping that there would be one kind of overarching theme that somehow explained how bows start to malfunction. But there’s really not one thing. To start with people are born with heart defects. Their hearts are simply built with some sort of structural abnormality. This would be as mentioned at the top of the episode, our tetrology of phyllo and Marfan syndrome patients. Now Marfan syndrome leads to an abnormality in both the structure and composition of connective tissue, especially in the mitral valve leaflets. These changes may include increased laxity or floppiness of the leaflets, making them more prone to mitral prolapse the bolding backward into the left atrium during systally. 

In addition to tetrology of below and Marvin Centrum. Bicuspid aortic valve is another congenital heart abnormality. 

Tim: So, for example, for the aortic valve, some people are born with a by leaflet valve, meaning they have two leaflets instead of three leaflets. Many people don’t know they have this, , and they may present with chest pain or pain in the back of their shoulder. Come get seen in an emergency department, get a CAT scan, and find out that they may have an aortic aneurysm now of their aorta. And they didn’t know that they had an aneurysm, and they didn’t know that it was because they were missing a leaflet to their aortic valve.

And for all this time, they had a lot of pressure building up in that ascending aorta because the aortic valve wasn’t able to fully close or open properly, because of that missing leaflet. So sometimes it’s a surprise to people. 

Another problem I’ve seen with aortic valves, people with bicuspid aortic valves specifically tend to have higher chances of having endocarditis or infection of that heart muscle. And there is a strange and not fully explained connection between dental hygiene and, aortic valve infections. , we have seen that, with especially aortic valve, people with poor , dental hygiene tend to get infections of the aortic valve. They come in with fevers and they can’t explain. They might have, markings in their hands called Osler’s nodes. They may have, They might have chest pain. They may not have chest pain. Wemight decide to do blood cultures and find that there’s an infection.

And we do an echo and find that there’s what we call a vegetation growing on their heart valve, which is really kind of like a ball of infection on the valve. 

On the other side of the heart, on the right side of the heart. Tricuspid valves on the right side, which take the blood from your superior and your inferior vena cavae that those can get infected by people who may. you know, be using, illicit drugs such as intravenous drugs and may not be using an aseptic technique when administering these drugs and those, because that tricuspid valve is the first venous valve, or the valve that the venous blood first contacts, that one sometimes can get infections more readily than heart. valves on the left side of the heart. So that right there is a difference between the right side and the left side. It’s just kind of what comes in contact with which valve first tends to win the race, I guess.

Annie: That’s so interesting that poor dentation affects the aortic valve. However, aseptic IV drug use affects the tricuspid valve. 

Let me just see if I, you know, understand this correctly. Endocarditis would cause, would it cause, regurgitation or stenosis?

Tim: It could be either. 

So we tend to see the infection sometimes eating away with those chordae tendineae that hold the leaflets together So then you would get a regurgitation of that tricuspid valve, for example, You know, we could also sometimes see the infection being on the leaflets so severely that it almost makes the leaflets stick together, and that could cause like a stenosis. So you could get either or. 

Tricuspid stenosis is not really something that we see often. We tend to see more of the regurgitation more so from the infection eating at the leaflets and eating at those chordae tendineae. 

You tend to see stenosis more in patients with radiation or maybe congenital heart disease where they were born with that tricuspid problem, rather than acquiring it late later than in life. 

Annie: Congenital defects endocarditis. And as it turns out, trauma. Can cause valve problems, too. 

Tim: I recently had a patient come to me recently in the intensive care unit after having a car accident, and they didn’t have an airbag deploy in time, and they were not wearing a seatbelt, their chest hit the, the steering wheel, and that caused a cardiac contusion which is pretty much a bruise of the heart.

And that contusion was so severe that it ripped some of the chordae tendineae and they ended up having a valve prolapse from that. And I was like, really? I’ve not heard of this, but it can happen. Just basic trauma. 

Annie: I guess it makes sense, like the chordae tendineae are, they’re small, delicate structures, but yeah, that’s not what, your go to diagnosis for for chest trauma.

Tim: In trauma, we always say they’re bleeding before they’re found innocent, right? So we’re thinking that they’re always bleeding, bleeding, bleeding. And we, in trauma, I used to do trauma as a fun gig on the side once upon a time. And, you know, you kind of look in every, every nose hole orifice looking for blood because you’re, you’re just going to assume that they’re bleeding until you prove that they’re not.

And I would never have thought that. You can get a valve contusion or injury to your valve, you know, just from hitting yourself in a really weird spot at a really weird time. 

Annie: So, we talked about, congenital reasons for valve disease, infection, endocarditis, radiation. What about downstream effects of, an MI, for example? Would, would that cause, stenosis or regurgitation? 

Tim: So, let’s just say, 50 year old person smoking, has a history of smoking, high blood pressure, maybe poor diet, maybe diabetes. That seems to be the perfect cocktail for heart disease, right? They have an MI. They have damage to their heart muscle. In the inside of that heart muscle, in what we call the endocardium, there might be, chordae tendineae, that snap, and that might cause the heart problem, or what happens is over time you know, the heart valves were fine, the person , recovers from their heart attack, and they go on about their lives, but over time they might start to remodel the heart, and the heart, as it remodels and grows in a very peculiar way, in an abnormal way, that muscle now, that overgrowth of muscle, makes that heart contract in an abnormal way. And over time, the heart doesn’t like to contract in an abnormal way, and it starts to, reduce its efficiency. And with that reduction of efficiency means building up of pressure in the heart because of all that backing up of blood. And then we start to get weakening of that muscle and we call that a cardiomyopathy. That’s the weakening of that muscle. And sometimes we get a dilated cardiomyopathy. That’s one form of it. And I think we see that a lot in the, in the inpatient setting, these dilated hearts where they’re big. boggy basketballs in the chest on the chest x ray and they aren’t ejecting very well. They have an ejection fraction of 20 to 30 percent. Those are the folks that with that big dilated heart, all of those heart valves eventually get split and and brought kind of further and further away. So functionally those valves are flapping up and down. Normally, but it’s that muscle damage that is causing the stretching of the muscle to cause those leaflets to no longer touch each other. And we start to get a functional problem, such as regurgitation,for example. 

Annie: That is the kind of explanation I needed to understand kind of the etiology here of regurgitation. So if you’re talking about a dilated cardiomyopathy, I can easily see how, you know, that would, that would stretch the muscles, that would pull the valves apart. So in that setting, would it be. An aortic regurgitation, would it be mitral or would it be both for a dilated cardiomyopathy. 

Tim: So, it could be either or. So, for example, aortic stenosis, my valve is really rough and tight. It gets harder and harder to push blood through that valve. And over time, the heart’s going to try to compensate by increasing the muscle mass of that left ventricle. And then it’ll get bigger in that, for that reason alone to try to overcome the pressure of getting through a little tiny valve or a really stenotic valve. Over time that heart will probably not be able to keep up with it. And sadly, as that heart muscle thickens, the volume of blood that the actual left ventricle can receive from the atrium, starts to decrease because it’s now being filled in. with muscle. So that’s what we call a dilated heart failure or a diastolic heart failure, I should say because it’s not necessarily a problem with the squeeze.

We actually have a problem with the filling. And those are we’ll hear these terms now, which have been coined over the last few years called HFrEF and HFpEF Heart failure with reduced ejection fraction, such as our folks with the dilated cardiomyopathy. And then we have the HFpEF. They have a preserved, ejection fraction, but they suffer from heart failure because they’re not really filling well. And so it’s, it’s fascinating. So it’s a hard question to answer at the end of the day, but you have to kind of individualize it to the person and see what is the cause of their heart failure. Is it a filling? Is it a squeeze problem? Is it a valve problem? Is, it both?

Annie: How is that determined? Is ECHO the test ?

Tim: Yes, ECHO. There’s two types of ECHOs that we can do. We can do a transthoracic ECHO, or called TTE, which is the most common. It’s when we do the, put an ultrasound onto your chest wall, and we look at it through that way. Or we can do something called TEE, or transesophageal ECHO, and that you have to be, you know, under sedation, and they put a pretty large echo probe down your throat, and look at your heart from behind the heart through the esophagus.

Annie: What’s the benefit of a TEE versus, you know, kind of your traditional transthoracic ECHO?

Tim: Great question. So the benefit of a TEE is that there’s not a whole lot of tissue and muscle and fat between the esophagus and the back side or the, that posterior part of your heart. So we get, as clinicians, great pictures of all of your heart valves. and all the function of the heart compared to that trans thoracic echo. 

So that, that’s the benefit mainly. It’s, we just get much better images, and can tell that person more definitively what the problem is.

Annie: So that, that’s the diagnostic part of it. Now, what about treatment? Maybe you could help me, break down, the different categories and, and how they’re treated. 

Tim: So we can start with the aortic valve, aortic valve stenosis, in the, earlier days, we used to do what we call balloon angioplasty. And we, we did this with a coronary arteries also for people who are having heart attacks. We would put a catheter through that valve and we would blow up a balloon and it would, , you know, pop open the valve and for stenosis, you know, that would sometimes buy that person a few extra years of, you know, improving the function of that heart. A problem with that though is these people tend to have calcifications of their aortic valve as well that cause the stenosis and we can sometimes flick off a piece of calcium off into the, arterial blood flow and we worry about things like stroke. , cause the first three vessels that come off the aortic arch tend to go up to our arms and to our head. So we worry about stroke or acutely throwing off a clot of some sort. 

So the other options then that developed were surgical valves. And with surgical valves, people tinkered with mechanical valves and we also looked at. The valves of different animals that were similar in size and composition to humans. So, now, really, patients are usually offered a mechanical valve or a tissue valve most commonly, especially for the aortic valve and the mitral valve. 

Now, people might ask, what’s the difference? So, for tissue valves, tissue valves, these tend to come from either pig or, or cow, and we call them porcine or bovine valves, and these are tissue valves, , and they tend to do well, do, function just like the human valve, but tend not to need any blood thinners, which is great. It’s a win win. So for some patients and their lifestyle, , a young woman who may want to become pregnant, For example, with I recently had a patient with Marfan syndrome, and she had an aortic aneurysm, and one of my surgeons is a, was a leading expert in fixing aortic aneurysms with sparing their native valve. And by sparing and keeping a tissue valve, you don’t need lifelong Coumadin. Which, Coumadin in itself is not a great drug if you’re trying to get pregnant and want to be childbearing. So we get a lot of young women with Marfan syndrome that come to my facility looking for a valve sparing aortic root replacement as one example because they don’t want that toxic side effect of Coumadin for the rest of their lives.

But the problem is, is that these tissuevalves don’t last as long as our mechanical valves. The mechanical valves last longer, so for someone young, they have to also think about, you know, do I really want to have this surgery maybe 20 years again down the road? You know, if they’re already maybe say 35, 40 years old and they need to have a tissue valve or a mechanical valve placed, do they really want to get another surgery at age 70? So that’s something to think about.

Inversely, with some of our older folks, we might offer them more the tissue option than the mechanical option because older folks tend to be higher fall risks as they age. And being on Coumadin and a fall risk is not a good cocktail. So sometimes we’ll offer more so where we tend to see our older patients pick a tissue valve so that they have a better quality of life. don’t need to take Coumadin, don’t have to go for frequent blood draws for their INR, and they get the one time shot. They are just, they’ve got that valve and their longevity is not more than 20 years or so, so it kind of works Out for them. 

Annie: Why Coumadin? Out of all the anticoagulants, the wonderful ones we have now where you don’t have to test your INR, why Coumadin?

Tim: That’s a great question. So, Coumadin sort of was the first cool blood thinner that we, you know, sort of got a handle on as a medical society. And, the FDA has seen the majority of studies with Coumadin. Now we have these really cool new drugs called our NOACs or novel oral. Anticoagulants. And they’re not as well studied long term as warfarin because warfarin was first. 

And, there is a little bit of ethical dilemmas with these studies because it’s hard to sell a patient saying, Hey, I’m going to give you a mechanical valve. , how do you feel about signing up for a study where you’re going to try an experimental blood thinner that might clot off your valve and Cause a stroke or death, how do you feel you wanna sign? So that has sign of sort of delayed and you know, it’s definitely a barrier to some of these research studies, but they are doing them. So as we have developed these newer, newer anticoagulants we’re starting to see different mixtures of drugs. We’re starting to see studies now with Doac, which is dual anti-platelets.

That’s aspirin plavix together, versus just aspirin, we’re seeing studies with aspirin and coumadin versus just aspirin. We’re having comparisons of all three. , so right now I think we’re in the midst of it and the next 10 to 15 years I think we might start to see more heart valves being allowed to switch over from coumadin to something different like Eliquis for example.

Annie: For sure. 

So, personally, I have seen a lot of TAVR patients in my career as a nurse, and I was wondering if we could kind of walk through what happens in a TAVR and what nurses need to know when caring for these patients post operatively?

Tim: Sure. So, TAVR is one of the really cool innovations that we’re seeing now with heart disease management. So TAVR stands for transcatheter aortic valve replacement. And, 10, 20 years ago, when patients needed to have an aortic valve replaced, you know, we used to look at the person’s age, you know, what comorbidities do they have?

Diabetes? Are they mobile? Do they have assistance at home? Are they more disabled people, you know, Like wheelchair bound and some of these factors used to make it kind of prohibitive to do a surgical aortic valve replacement and now We can offer a different choice for some patients, especially our older patients So back, you know 20 years ago If you were 80 years old and you were told that you needed a new Aortic valve, a lot of cardiologists and cardiac surgeons would probably turn you away saying that you’re too high risk, you know, your diabetes and your kidney disease and all your other things, confound your age as well. And we would recommend you just go home on medical management. But now our older patients anywhere from 65 plus, but more so 80 years or greater. Or patients who may have a longevity of 10 years or less. What we can do is offer them this TAVR, transcatheter aortic valve, and put this valve, through your femoral artery in your groin, and kind of just push it up, all the way up to your aortic valve, and deploy this valve.

In through the native valve, and it just pops right in, and now we can give our older, patients more choice longevity, adding a few years to their life, and even more so improving their quality of life now that they have a new valve, and not having to undergo a huge operation that’s very risky at an older age. 

Annie: Why would you not do this on a younger patient? You seem to be emphasizing like the older populations.

Tim: Yeah, and that, that’s a great point. So because TAVR and these other transcatheter valves are newer, we don’t have as great long term data as we do with the surgical ones. So that’s one thing, you know, if a 20 something person came into clinic TAVR, we can’t really, tell people how long that valve would work for them. So for right now, we can’t really say with great confidence. Oh, well, this valve is going to last for the rest of your life because we really don’t know. We don’t have great long term data. We have some data that shows five year outcomes are about comparable to surgical valves, but . We’re still kind of learning, learning the 10 year plus data because it’s a newer technology. 

The other thing to it is, no procedure comes without risk, , even with transcatheter, you know, of occlusion of coronary arteries by, by, by chance or tearing something even though the likelihood of that is low, sometimes you know, based on the person’s anatomy, we just might say, you know, you should really think about a surgical option. You know, because it’ll last longer, you’re in a controlled space, we can expect you to bleed and we’re right there ready to go in an operating room versus in an interventional lab such as a cath lab.

Annie: What does surgical intervention look like? 

Tim: So surgical intervention is an open heart surgery. It’s a four to six hour case, sometimes longer, just depends on how you know, robust the patient is and how many valves are being fixed. , we would have to do what we call a median sternotomy. We would cut through that sternal bone and open up the chest. And then when we go in, we could either do a repair of your valve. or a replacement of your valve. 

If you don’t have a lot of stretch of your left ventricle, we can sometimes just place a ring and tighten up that that valve and keep those native leaflets. So that might be an example where 20% something you rolled, really should consider a mitral valve ring, for example, to just kind of tighten up the mitral valve itself and let those natural leaflets work together naturally versus offering them a more invasive procedure which might cause bleeding and stroke and other things.

Do that might be one consideration as an example, to go for an open procedure versus a percutaneous-like procedure.

Annie: What does recovery look like? 

Tim: Yeah, so TAVR, you know, generally people are up and moving pretty quickly, because they go through the femoral site, you have to be on bed rest for several hours, and even that has gotten better over the years. Years ago, when I first started out as a nurse, people were on bed rest for eight to 12 hours.

And now with these really cool per closed systems or percutaneous closure devices, they, they have all kinds of different ones from different companies that close that artery and people can now get out of bed in two to four hours, depending on what you use and how, how big was that sheath in that groin so people are up and moving. They don’t have the pain associated of having their sternal bone cut open. Their lungs tend to not have as much atelectasis. The length of stay is much shorter than a surgical, valve surgery and, generally don’t need as much blood thinners as well. 

Annie: The cases I see, it’s, it’s usually just overnight stay. Where, we, for the first and obviously checking the groin site and telemetry would be the other one. Cause I can imagine that there’s a concern if you,I don’t know, nick, nick something or you know, somehow disrupt the electrical system of the heart during the procedure 

Tim: Yes, and that is a risk. That is a risk. So sometimes when we, when we deploy these TAVR valves you know, the way it’s, it’s so close to our electrical system of our heart that we can get atrial fibrillation, we can get heart blocks, we can get bundle branch blocks. It’s right near that AV node area. And that’s the tricky part to this. It does happen that people will go into heart blocks and things post TAVR when it doesn’t go so well. May need a pacemaker later or may need some heart failure management.

But yeah, that is definitely a risk. 

Annie: Yeah, this is performed by an interventional cardiologist.

Tim: Yes, and whenever we do a TAVR, generally you have to be in a center that also has cardiac surgery backup. Because if it goes wrong, even though it’s a low likelihood, If it does go wrong, it really goes wrong. Generally these patients perforate their their ventricle, or they maybe tear their, their aorta or dissect their aorta. , and they need to have an emergent, sternotomy. So the surgeon runs in, they quickly betadine the chest and open up. So it can be a really difficult type procedure when it goes wrong. 

Annie: So, what does, recovery look like for surgical patients? I imagine this is going to be much longer, if we’re talking about, open heart surgery. Is it automaticICU after surgery?

Tim: Yes. You know, these folks come out of the operating room, potentially very unstable. There can be bleeding associated with an open heart procedure. We tend to have them hypothermic so that their body oxygen requirements are lower during this big surgery. They need to be on a heart and lung bypass machine and the heart and lung bypass will do the function of the. heart and the lungs during the case. It’s, it’s a big surgery. So recovery is usually anywhere from three to seven days at its best, sometimes much longer, depending if there’s a complication. , the sternal bone because we can’t put a cast on it like a broken arm or broken leg. We have to have the patient really reduce their mobility with their upper extremities for a while. Historically, we’ve always taught patients to not lift more than 10 pounds with their arms or lift their arms above their head.

And you’ve heard different things like this. But honestly, the research is kind of weak around this area. My facility has now loosened it up to 20 pounds because it’s really hard to live your life only using 10 pounds of force. A gallon of milk is about 10 pounds, so just making yourself a bowl of cereal can be a challenge when you’re a fresh, open heart patient. 

Annie: So we’ve laid out the interventions for aortic valve stenosis. Taver and open heart surgery. We led with aortic stenosis as it’s the most common type of heart disease in the developed world. Often due to calcifications. In general wear and tear related to aging. Now, moving down to the second, most common valve dealer problem: mitral regurgitation. As it turns out, mitral valve repair is quickly evolving. 

Tim: There are many companies now competing to try to find the cool new valve that they can pop in within most minimal of ways. Mitral valve, transcatheter procedures are now the hot new thing that we’re seeing. There’s two types that come to my mind. There’s one called the mitral clip where we can, similar to a taver, go through your artery and your, in your groin and just deploy a clip for these flailing mitral valve leaflets and kind of tie them together so that they don’t flail as much and it. functionally reduces the amount of regurgitation that that person might experience. Those patients so far seem to be doing quite well. We at my facility are part of an international study on what we call TMVR trans catheter mitral valve replacements, where we actually do a little incision via thoracotomy, but really tiny, about an inch or so in that anywhere within fourth to fifth to sixth intercostal kind of area. And we deflate that lung and we kind of percutaneously pop in a mitral valve similar to the taver and we just deploy it in the mitral spot right now we’re going through the chest wall but we envision this will become a catheter deployed valve in the future. It’s really cool. 

Annie: Early in my nursing career, I had a patient who was a young guy who had endocarditis of the mitral valve. And he was so sick that he was transferred from our small community hospital to a large academic center where he got this procedure done because he was, he was not well enough to tolerate surgical intervention and it saved his life.

He was sent back to us the community hospital, to recover, to illustrate your point, This was the only way he was going to survive, was to get, this percutaneous procedure. Yeah. Yeah. Yeah. 

Tim: These percutaneous procedures to people who tend to be really high risk for the surgical procedure. So, in your scenario, it sounds perfect for him. 

Annie: He was a memorable patient to have as a young nurse. He was a young guy, he had been doing intravenous drugs, and it was really neat to hear him explain in his own words what endocarditis was doing. He had such bad ischemia that a lot of his toes were black. , but he was a, he was a changed man. And he was excited to get on with the next chapter of his life. It was really neat to see that kind of transformation. 

Annie: Up to this point, Tim and I discussed procedural and surgical interventions for Belbuca heart disease. When we started discussing medical management. Unfortunately, Tim’s audio stopped recording. Now medical management is a super important piece of the puzzle to understand as a clinical nurse. So I’m going to forge ahead and summarize what Tim said. 

So medical management of vascular heart disease has two main goals. One to improve the pumping ability of the heart. And to, to address potential dysrhythmias that may result from conduction disturbances associated with structural abnormalities.

So starting with the first theme of improving overall cardiac function, let’s consider aortic stenosis. 

The narrowing of the aortic valve impedes the ejection of blood from the left ventricle into the aorta. And the rest of the body. 

As a compensatory mechanism, the left ventricle hypertrophies you’re getting that left . Ventricular. Hypertrophy to generate enough force to overcome that obstruction. 

However. This is short term games for longterm losses because hypertrophied eventually leads to increased myocardial oxygen demand and decreased compliance. And impairing the overall function of that left ventricle. This is starting to sound a lot like heart failure, isn’t it?

Now over time, the hypertrophied left ventricle may struggle to maintain cardiac output leading to symptoms of heart failure that you all know like dyspnea, fatigue, and fluid retention. Now at the top of the episode, Tim brought up the fact that patients with aortic stenosis are preload dependent. Because they rely on an adequate preload, that is an adequate volume of blood to fill the heart during diastole to maintain stroke value in cardiac output. So patients with aortic stenosis are preload dependent yet often exhibit symptoms of heart failure. 

How can medical management navigate these competing problems? 

It may be helpful to think of this strategy, not as preload dependence so much as preload optimization, because typically with the progression of stenosis, there’s a growing requirement for a greater reduction in preload. Often achieved through the use of loop diuretics, such as furosemide. Beano dilators such as nitroglycerine can also be prescribed for preload reduction as they dilate the veins and thus redistribute blood away from the heart. Okay, so that’s preload. What about afterload? 

After love reduction is also a piece of the puzzle because the narrow aortic valve is creating so much resistance that the ventricles have to overcome. So after load producing agents will include basal dilators, such as hydralazine, ACE inhibitors, and ARBs.

Now, how does the medical management of aortic stenosis? And mitral regurgitation compare up to this point. As we’ve been talking about aortic stenosis, afterload reduction is a key consideration to ease the workload of that left ventricle. 

Where as in mitral regurgitation, afterload reduction is it’s still relevant, but the emphasis may be more on addressing preload through diarrhetics as the regurgitation leads to volume overload. 

Okay. Now, moving on to the second overall aim of medical management is addressing potential arrhythmias through antiarrhythmic medications and blood thinning agents.

If you think about it, rhythm disturbances can happen because valve dysfunction can also lead to structural changes to the heart chambers to. So for example, mitral regurgitation causes continuous dredging of that left atrium due to the regurgitant blood flow. So this atrial stretch and remodeling create a perfect environment for a fib to occur. Arrhythmias, especially AFib can further exacerbate heart failure like symptoms. So antiarrhythmics can be ordered for either rate or rhythm control. 

On top of that, because as we all know, APA puts patients at risk for thromboembolic events anticoagulants are often also ordered.