Valvulopathy Part I: Regurgitation

Hey, everybody. This is Sarah Craigher. I am an emergency physician and intensivist at UCLA, and this is the ICU-EDU podcast. Today we're talking about acute medical management of valve neuropathy. This first episode is going to focus on regurgitation. In a couple weeks, the second episode focusing on stenosis is going to come out. So why are we even talking about this in the first place? This is something that, at least hypothetically, we don't see all that often. But these patients fall into that category, which I think we should really be owning as resuscitationists. They're complex, and if you get it wrong, they can rapidly deteriorate. But if you get it right, then you can really turn them around acutely, and you often have an end game to actually solve the underlying problem if you can optimize them for surgical or percutaneous valve replacement. And valve neuropathies are really easy to miss. I mean, this is something that we all say we don't see that often, but I suspect we actually probably see it much more often than we think we do, and we just don't recognize it. Because valve neuropathies are something that we often just don't think about when we have a shocky patient in front of us. And this is problematic because they usually require some very disease-specific treatments, and many of the things that we tend to do otherwise in a shocky patient will not make these patients better, and actually have potential to make them a lot worse. Medical management of severe valve neuropathies is one of those situations when you just have to really trust the physiology, because appropriate management of these patients often requires you to do some seemingly counter-intuitive things that you might be hesitant to do unless you've really wrapped your head around why you're doing them. The good news here is that understanding the physiology pretty directly translates into your management strategy. Now, what we're not going to talk about, we're not going to get into the details of chronic management of these patients, and we're not getting into surgical decision-making around valve replacements. Instead, we are just going to focus on what to do with valve neuropathies when they come in acutely sick and how you're medically going to manage them. So, in valve neuropathies Part 1, we're here going to focus about regurgent head valves, then in Part 2, we'll talk about stenotic valves. In both episodes, we're going to first talk about the key pathophysiology, and then we'll talk about how that pathophysiology translates into management. So let's start with regurgitant valves. So it turns out that your circulatory system has one-way valves for a reason, and when that one valve becomes a two-way valve, you end up with all kinds of major problems. We're going to focus on aortic insufficiency, mitral regurgitation, and tricuspid regurgitation here. We're not going to talk about pulmonic regurgitation, because this is mainly an issue in congenital cardiac patients, which is a whole different topic, and not one which I am anyway qualified to talk about. So regurgitation, AIMR-TR. You can get regurgitation in two different ways. Primary regurgitation, which is a problem with the valve itself, and secondary regurgitation when you are severely volume overloaded and you may have some underlying valvular problems – but your main issue is severe volume overload. Primary regurgitation when there's a problem with the valve itself. This is the kind that's most problematic and also dramatic, or at least much more dramatic when your valve malfunctions acutely. Now, despite how dramatic of a presentation these patients can have, acute regurgitation is something that's actually very easy to miss, because we just aren't thinking about it. One of the things that can make both diagnosis and management of acute valvular regurgitation particularly challenging is that it's relatively rare, although definitely possible for it to happen spontaneously, and it's usually precipitated by something. And that something can often be a fairly dramatic thing in and of itself. So for example, acute MR may be precipitated by a large MI, acute AI may be precipitated by a dissection, and acute AI, MR, or TR can all be precipitated by endocarditis. Now, why is this problematic? Because it makes it really easy to become distracted by the precipitant cause. The patient with an MI will have some impressive EKG findings. The patient with a type A dissection causing acute AI is going to have a very impressive CT scan. The endocarditis patient may come in febrile and bacteremic, like legit septic shock. And so it becomes really easy to pat yourself on the back because you have correctly identified a major thing wrong with your patient, and then not look any further. Because from a management standpoint, the key question in these patients often becomes what is the primary driver of their shock physiology? Is it the acute valvular regurgitation itself? Or is it whatever precipitated the acute valvular regurgitation? And both need to be addressed to be clear. Like you need to address that MI, you need to address that type A dissection, but it can often be the case that it is in fact the acute valvular regurgitation that is actually the primary driver of the patient's shock. And in order to be able to get that patient to a place, both physiologically and logistically, where you can start addressing the underlying cause to cat lab, to the OR, you know, treating them with long-term antibiotics, you're going to need to stabilize the hemodynamics by managing their acute valvular regurgitation. Now, aside from this kind of hyperacute presentation of valvular regurgitation, you can also see significant valvular regurgitation in a patient who has been developing regurgitation chronically. So they've been developing a primary problem with the valve chronically, and it's now gotten to a point of valvular apathy severe enough where they just can't compensate anymore, and they transition from compensated regurgitation to decompensated regurgitation. And a frequent precipitate of that presentation is in a patient with gradually worsening chronic valvular regurgitation who then comes in due to massive volume overload. And this is where these primary causes, where there's a primary problem with the valve itself, starts overlapping with secondary valvular regurgitation. And this is where the major problem causing your regurgitation is less due to a problem with the valve itself and more due to severe volume overload. And these patients often come in where this severe volume overload is seen in combination with acute decompensated heart failure. And in fact, you can often have very impressive looking MR or TR on an echo in these patients who are severely volume overloaded. And unless you have a recent prior echo, there really just isn't a great way to distinguish whether that's because the valve itself is a problem or because the patient is just massively overloaded. Now the good news about this situation is that management is essentially the same either way, or at least the medical management is. The surgical management or cat lab management becomes different whether it's just a volume overload problem or a problem with the valve itself, but again, it's hard to tell that if you don't have a previous echo. And so the key thing if you think the regurgitation is mainly secondary to acute decompensated heart failure and volume overload is to get a repeat echo once you've optimized their heart failure and volume status, because that's the only way to figure out to what degree the valve itself is a problem versus just the volume overload. And it's important to do this because that has significant implications for decisions about valve replacement and subsequent management. In terms of diagnosis, regurgitation is just really easy to miss. And I think a decent amount of the reason that it's so easy to miss is we just don't think about it. It's not top of our brain as a cause of shock, it just doesn't occur to us. So to me, just having it in the back of your mind as a possibility in the acutely-sockey patient is a really good place to start and makes you less likely to miss it. Now in terms of diagnosis, I'm not going to get into the art of listening to murmurs. Even aside from good luck listening to the subtleties of a murmur when your patient's in the ED hallway or in the recess bay with you and 15 other very loud people, it's something that there's a large selection of book chapters and articles that you can look up and read on this topic, which it would be long and boring for me to recapitulate now. I think it's also important to note that the absence of a murmur does not rule out acute valvular regurgitation. And I hear this a lot where somebody's like, "No, no, no, it can't be a regurgitant valve or I'm, you know, going to vaguely consider that," but taking it off the differential because I didn't hear a murmur. And that assumes you're pretty good at hearing murmurs. Too it assumes that you'll necessarily see that specific physical exam finding and the absence of it has a good negative predictive value and it turns out it doesn't so much. Also at the end of the day, I personally at least am much better at echo than I am at auscultating murmurs and I kind of suspect that I'm not the only one. The main thing that hearing a clear murmur on a physical exam will do for me is less about identifying the specific meaning of that particular murmur and more about sending me down the path chasing a valvular catastrophe as a diagnosis, when I otherwise might not have thought about it. So if I hear a murmur on my initial assessment of the patient, it'll definitely spur me to take the time and energy to think about it and more time and energy on my bedside echo to put color Doppler over the valves and start assessing them. Now, while I may be better at echo than I am at auscultating murmurs, I 100% do not have a level of skill or I'm doing much of a quantitative valvular assessment. And often, for regurgent envelopes, color Doppler is about as far as I am realistically going to get at the bedside. But direct evaluation of the valve itself is only one piece of what you're looking for on a bedside ultrasound because you're also looking for a pattern of echo findings that you would expect based on the physiology of a given valvular resuscitation. So is the atria big? Is the ventricle hyperdynamic looking? Is the ifc plump? So again, put color Doppler on it, look for that, but also recognize that that's one finding amongst a pattern of echo findings that should be in context with your clinical hypothesis. If you want to get a really good primer on pocus assessment of valvulopathy, there's a great segment on this on core ultrasound that you can take a look at and I'll link to it in the show notes. So aside from various clinical scenarios and examine echo findings that will set me on the path of chasing an acute valvular catastrophe, the other thing that does it, or at least gets me really thinking about it, is when I have a patient in shock and they are just not responding to treatment and getting progressively worse. I've assessed them multiple times, I've tried multiple strategies to use for shock and I'm racking my brain to try and figure out what I've missing because I have done all the things and they're still getting worse and worse. When I find myself in this situation, I have learned that I should start wondering if I'm missing a valvular catastrophe. Because as I said earlier, the thing about valvular catastrophes is that they require very specific management strategies that don't necessarily overlap with most of the other things that you might have been doing to treat shock and they will not get better until and unless you initiate specific management that addresses that underlying pathophysiology. So now let's talk about that management. So management of regurgitant valves really, really requires you to have a solid understanding of the pathophysiology and trust your understanding of said pathophysiology. The pathophysiology of regurgitant valves, I feel like can really be distilled into two core principles. One, pressure gradients and two, high output heart failure. So let's start with pressure gradients. By far the most important thing to understand about the physiology of regurgitation is that really it is all about pressure gradients. If you remember back to physics 101, you will recall that valves roll down hills rather than up hills or in the case of fluid dynamics, a fluid will flow forward along a pressure gradient from areas of high to low pressure. Now your heart tries to kind of stack the deck here by way of these handy dandy one-way valves that don't allow fluid to flow the wrong direction, even in a situation when your pressure gradients may not be optimal to make it flow the right direction. Unfortunately, when you have a regurgitant valve, our nice one-way valve has now become a two-way valve. And what this means is that you have become entirely dependent on pressure gradients to maintain forward flow. And so what you need to do from a management standpoint is figure out how to optimize your pressure gradient in order to encourage the blood to move forward instead of backwards. Functionally, what this translates into is decreasing the resistance to forward flow and increasing the resistance to back flow. So that's thing one, to understand about pathophysiology of regurgitant valves, the critical role of pressure gradients. But there's a second component that we really need to recognize here, which is acute decompensated heart failure. In acute valvular regurgitation, you are functionally in high output heart failure. This physiology is not really different fundamentally from any time you have high output heart failure, where basically it's not a problem so much of the intrinsic systolic function of the ventricle, it's that the ventricle needs to work really, really hard to get enough forward flow. And in the specific situation of acute decompensated heart failure due to valvular regurgitation, the issue here is that your heart's not pushing against so much resistance because you have this pop-off valve, you have all this back flow. But because, since now quite a bit, if your cardiac output is going backwards instead of forwards, your ventricle is being forced to work really, really hard to get a sufficient amount of forward flow to perfuse your body. Basically, your ventricle is experiencing a pretty poor effort to results ratio. Now, it's really important that you understand this when you're looking at the heart on echo, because if you just quickly throw a probe on there, your contractility is going to look awesome, but don't trust it, because this is a case of "I do not think it means what you think it means." Your contractility only looks awesome, because your ventricle is not pushing against much resistance, it has a pop-off valve. So, this is a situation that is pretty similar to vasoclegia. The idea being, if I'm pushing a box, and you watch me and it looks like I'm pushing it really easily, it might be because I'm really strong, or it might be because the box is really light and I only look strong because I'm not pushing against much. So, now, if we translate that pathophysiology of pressure gradients and acute decompensated heart failure into management, we end up, then, with two key components of management strategy for valvular regurgitation, and those are vasoactives and volume status. Now, what we're going to do is talk about how the general principles of core pathophysiology and management strategies of valvular regurgitation play out in the specific scenarios of A to A-I, MR, and TR. And let's start with aortic regurgitation. So, these patients can be particularly deceptive. They really like to trick you into thinking they often have septic or hypovolemic shock, because what you're going to see is a blood pressure with a very wide pulse pressure, a very low diastolic pressure, and then you echo them, and their left ventricle looks hyper-dynamic. Voila! They can be especially sneaky if they have acute A-I due to endocarditis and show up with a fever. And you think to yourself, "Aha! I see a really low diastolic, I see a hyper-dynamic LV, and a patient with a fever, clearly this is septic shock and a patient who needs fluids and vasopressors," except that when you give them fluids and vasopressors, they completely fall apart. So, how do our two core pathophysiologies of valvular regurgitation, pressure gradients, and acute decompensated heart failure, apply in the context of aortic regurgitation? Let's start with pressure gradients. Remember, we are now completely dependent on pressure gradients for forward flow. So, how are we going to optimize our pressure gradient in the context of A-I? In general, we want to decrease the resistance to forward flow and increase the resistance to back flow. In the case of A-I, increasing the resistance to back flow is not as relevant when we're talking about A-I, provided that the mitral valve is doing its job. Because the whole purpose of being of the mitral valve is to prevent back flow from the LV to the LA during systole. And since the mitral valve is used to doing that with, you know, usual high systolic back pressures generated by an LV that has to overcome the resistance of a normal aortic valve in a normal situation, your mitral valve is usually pretty solid. It doesn't usually have a lot of difficulty doing this in the patient with a recurgent and aortic valve, or at least it doesn't at first. Now, eventually, once your LV starts to blow up and get hypervolemic, two things happen. One, you're stretching the mitral valve annulus, which doesn't help it close completely. And when your LV gets sufficiently overloaded with regurgitant volume, then you absolutely can't start developing some mitral valve regurgitation. But that is a secondary problem that you can't fix directly, and the way you fix it is by fixing your primary problem of aortic insufficiency. Now, really, where the money is in terms of optimizing pressure gradients in your patient with AI, it's really all about decreasing the downstream pressure. And the most important thing you need to do here is decrease your left ventricular afterload by dropping your SVR. Now, this can feel like a really counterintuitive thing to do, because you're looking at this patient and they have a blood pressure of 105 over 30 with a map of 55, and you look at the LV on Echo and it looks like it has awesome contractility, and so people often do what seems like a very reasonable thing in this situation and start Norepi. Which increases rather than decreases the SVR. And if you start Norepi in your patient with AI, you pretty quickly end up in this vicious cycle, where you increase the SVR, which worsens the pressure gradient, which then worsens the AI, decreases your forward flow, causing the patient to become more hypotensive, at which point you go up on your Norepi, further increasing your SVR, worsening the pressure gradient, and off you go. What you actually need to do here is start your patient on something that will decrease the SVR. And in order to get comfortable doing that with our patient with a BP of 1 over 5 over 30 and a map of 55, you really need to accept the idea that the wide pulse pressure in this situation is not a result of vasodilation. The SPP is relatively high because the aortic valve is not providing any resistance to LV contraction, and the diastolic blood pressure is low because your aortic valve is allowing blood to backflow into the LV during diastole, not because your SVR is low. So what you really need to do here is give something that systemically vasodilates and decreases that SVR, because that's the only way you're going to be able to optimize that pressure gradient. My drug of choice here is dobutamine. Dobutamine is an inodilator, meaning it will give you both vasodilation and inotropy. And you definitely want that vasodilation to improve that pressure gradient, but you also want the inotropy. Why? Why would you need to do something that supports contractility here when the LV looks so hyper-contractile on bedside echo? Because of the second core pathophysiologic principle of regurgitated valves, which is acute decompensated heart failure. In a patient with aortic regurgitation, the LV systolic function will look great when you eyeball it on echo, but again, do not be fooled, right? It just looks that way. And you've got to remember that, in fact, this patient is functionally in high output heart failure. The left ventricle is having to work really, really hard to try to get even a vaguely acceptable amount of forward flow to the body, and so you really want to help it out with some inotropy here. Now, similar to most patients with acute decompensated heart failure, the other thing that these patients need is diuresis. In order to feel confident doing this in these patients who have a low map at a low diastolic and you're like, "Oh, are they septic?" It's important to understand that intravascular volume is not, it is not, your rate-limiting step to forward flow here. You have plenty of volume that's being handed to the LV. The problem is that when the LV then tries to move the volume forward, most of just comes right back and moves backwards. And as the LV starts ballooning out with volume, you now can start getting some mitral regurgitation and backing up fluid to the lungs and blowing out that LV. And so even though their map is low, you've got to diaries them. You've got to help that LV regurgitant volume, especially because often if they come into the ED and we initially don't recognize what's happening, these patients often get a decent amount of volume. And so I start diariesing them right away. Then the LV progressively balloons out with regurgitant volume. This is actually one of the reasons that bradycardia is really bad for these patients. So patients with acute AI who get bradycardic can often decompensate quite rapidly, why? Because by spending more time in diastole, what you are doing is increasing the amount of time you have to regurgitate volume back into that left ventricle, which then causes progressively worsening LVEDP and LV dilation. The other reason why bradycardia is bad and in fact higher heart rates, tachycardia tends to benefit these patients is because remember back to basic, basic physiology where your cardiac output equals your heart rate times your stroke volume. And you're in a situation here when the heart can't do a whole lot to increase the amount of stroke volume that's actually moving forward. Your LV is already doing as much as it can. So the heart needs that higher heart rate in order to maintain their cardiac output. So this is the other reason why you want something like dobutamine here. You want the chronotropic effects of dobutamine, as well as the inotropic effects and the vasodilation. To summarize, aortic regurgitation management along our two key management strategies, vasoactives and volume status first, vasoactives. These patients need vasodilation, inotropy, and chronotropy. They need vasodilation because since you're formerly one way aortic valve has now become a two-way valve, you become entirely dependent on that pressure gradient to move things forwards so you've got to decrease your downstream pressure. Two, they need inotropy because they're functionally in high output heart failure and the LV needs support to push all that regurgitant volume forward. Three, they need chronotropy both to maintain their cardiac output in a situation when they can't functionally increase the stroke volume that much and because spending less time in diastole helps minimize your regurgitant volume. As such, your vasoactive of choice in a patient with AI is probably dobutamine because it'll give you your vasodilation, inotropy, and chronotropy, and it's fast on/off, which can make it less scary for you to start if you're like, "Oh, I don't know, this seems like a bad idea," because you can just turn it off. I usually prefer it to melanone in this situation, both because it's fast on/off and because it gives you more chronotropy than melanone does. Now, our second major principle of vasoactives and volume status, your regurgitation management, is volume status. These patients need diuresis almost always because you've got to offload the left ventricle or else it'll blow up like a balloon and explode your mitral valve. In order to feel confident diuresing these patients, you really have to internalize the fact that the rate limiting step to forward flow is not the amount of volume in the system. It's how much of that volume is moving forward into the aorta rather than regurgitating into the left ventricle. And all feeding that left ventricle more volume will accomplish is increasing the recurgent in volume, blowing up the LV, which is in fact going to make it harder for the LV to move volume forward. Now, let's talk about mitral regurgitation. We're again going to start by talking about how our two core pathophysiologies, pressure gradients and acute decompensated heart failure, now apply in the context of mitral regurgitation. Pressure gradients. We are again here going to go through the exercise of trying to optimize our pressure gradient in order to encourage the blood to move forward and not backwards. How are we going to do this? By decreasing our downstream pressure and increasing our upstream pressure. Now, our downstream pressure here is also our systemic vascular resistance just like with AI. And so when your left ventricle is contracting, you want to make it easy to push the blood forward against the SVR instead of having it go backwards, and decreasing your SVR will help you do that. So in the case of MR, it actually also really, really helps for you to increase your upstream pressure because by increasing your upstream pressure, that discourages things from going backwards rather than forwards, and overall gives you a pressure gradient from upstream to downstream, favoring forward flow. Then what's the pressure upstream to the mitral valve? That's your pulmonary pressures. As such, this is one of the not very many times in circulatory physiology where actually having high pulmonary pressures is really, really helping you because it's improving your pressure gradient. So you want to increase your pulmonary pressures and decrease your systemic vascular resistance. Now what about our second core pathophysiology as it applies to MR? Our acute decompensated heart failure. So with acute MR, just like with AI, your left ventricle is having to work really, really hard here to try and keep up any kind of forward flow, any kind of solid cardiac output. And this is another case where your LVEF is going to look artificially awesome on Echo because it has a pop-off valve. It's not really being forced to push against the full afterload of the SVR since it can just offload volume right back into the left atrium, which improves your cardiac output not at all, but makes your LVEF's systolic function look artificially good on Echo, which is again why you always need to be suspicious if you see what looks like a hyper-dynamic LVEF but with a huge blown-out looking left atrium. Even though you see that nicely-contractile LVEF on Echo, MR is another situation. When the rate-limiting step is not the amount of volume in the system, it's that the heart can't move that volume forward, and so giving more volume will help you not at all. All it will accomplish is cause things to further back up and blow out the LA, increase your pulmonary edema, which then eventually gets transmitted to the RV. Now, in patients with secondary MR, where a significant proportion of that regurgitation you're seeing is just due to volume overload, often their heart is just straight-up failing. These patients may have a worse-looking LVEF on Echo, so it can be a bit more obvious what's going on, as opposed to the patient who has acute or hyper-acute MR, and part of the reason they're failing is just high-output heart failure, just like you see with AI. So, in patients with acute heart failure due to MR, you find yourself in a similar situation as you did with AI. Bradycardia's not helping you. You need that heart rate to drive your cardiac output since your stroke volume is not that modifiable, and you're again in a situation that spending more time and diastole is just not going to help you, because you're increasing the amount of time that volume has to regurgitate back into the left atrium. How do those two principles translate into management to sum up? Mitral regurgitation management. The two key components are again, vasoactives and volume status. In terms of vasoactives, these patients also need inotropy, vasodilation, and chronotropy. And so my first line in these patients is usually dobutamine, because it'll give you all three. And again, unlike millerinone, it's fast on and fast off. So you want all those three things, and dobutamine is super useful. Now, it's important to note that the patient with MR needs vasodilation specifically of the systemic vasculature, but not of the pulmonary vasculature. And this can be a little tricky, because on echo and on swans often, you know, often these patients, you look at them and they have high pulmonary pressures, and maybe if things have backed up enough, an unhappy right ventricle. But despite that, this is often a time where it is actively unhelpful to dilate the pulmonary circulation. You want to avoid inhaled pulmonary vasodilators here, and millerinone is probably not your best choice. Now, dobutamine will dilate your pulmonary circulation, some, but not to the same extent that millerinone is. And you need to offset that with something. And so in order to increase your pulmonary pressures here, to increase your upstream pressure to have that favorable pressure gradient, one of the things that can really help these patients is the hemodynamic side effects of positive pressure ventilation, because that is going to increase your pulmonary pressures. Often initially when you see these patients, BiPAP, and when you do BiPAP in these patients, you want a high E-PAP. I would start with 10, 12, maybe more than that, maybe just put them on CPAP, because the main effect you're trying to get here is high pulmonary pressures. If I have these patients on a vent, I'll go way up on the PEEP. And you got to be clear with the team that it's not because of the oxygenation, because often what will happen, your RT will see, oh, they're satting 100%, let's come down on the PEEP. You're not doing that high PEEP for oxygenation, I mean, that's great if it helps, but you're really doing it for their hemodynamics. Conversely, I've seen it multiple times, that if you have a patient with bad MR, and they're intubated and they look great, and then you try and extubate them and take away that positive pressure, they often crump rapidly. It also turns out that because all that regurgitin volume is being transmitted to the lungs, these patients may also have bad pulmonary edema and be in hypoxemic respiratory failure, so people really help them as well. So that is the principle of optimizing the pressure gradient. Vasoactives you're going to use dobutamine, you're going to avoid inhaled pulmonary vasodilators, probably avoid milrenone, and start them on some positive pressure ventilation. In terms of your second major category, volume status. These patients need diuresis, again, just like with AR, your rate limiting step to forward flow is not amount of volume in the system. It's how much of that volume is moving forward into the LV rather than regurgitating into the LA. And so you don't feed the system more volume, all you want to do is actually diuresis, that is really going to help your acute decompensated heart failure, and it's going to help your refrigerant volume, and finally it's going to help your pulmonary edema and help your right heart. Okay, so finally, let's talk about tricuspid regurgitation. So far, we've spent all our time talking about the valves on the left side of the heart, the aortic and mitral valves. Now we're going to switch to talking about the right side of the heart. And again, here we're only going to talk about tricuspid regurgitation because pulmonic is a different topic, which mostly incongenitles, and that is not in my wheelhouse. So let's just talk about tr here. Because we are moving now to the right side of the heart, we need to switch gears a little bit and remember that when we are talking about the right side at afterload, the right ventricular afterload, now we're talking about the pulmonary pressures, the pulmonary vascular resistance, not the systemic vascular resistance. But we're still going to go through our two components of key pathophysiology, which are the same, pressure gradients and acute decompensated heart failure. Once you make that mental switch to realizing that the downstream pressure in the context of TR is the PVR, the principles of management of TR are very similar to MRN Really AI, optimizing your pressure gradient. And so in the case of tricuspid regurgitation, that means that where the money is here is improving the pressure gradient by decreasing your downstream pressures, which are your pulmonary pressures. Now, conversely, this means that doing things that will increase the pulmonary pressures will be the opposite of help. So in contrast to MR, putting these patients on positive pressure ventilation will be unhelpful, which is fine, because also in contrast to MR, the patients with TR, they're not backing up into their lungs, right? They're backing up into their SVC, their IVC. And because they're not backing up into their lungs, they don't generally present as hypoxemic. Now, sometimes patients with tricuspid valve endocarditis can present with a bad looking chest x-ray. And if they have septic pulmonary emboli, they can also present looking like they have pneumonia. And this is one of the reasons diagnosing acute TR can be really tricky, because one of the main reasons you're going to have it is endocarditis. And so these are the patients who often come in and they truly, truly look septic and they are septic often. They're bacteremic. They have endocarditis. And they also may have another infection that ultimately was the thing that seeded the endocarditis or something that was seeded by the endocarditis. So these patients can be really tricky. You know, the last time I saw one of these patients with acute TR due to endocarditis who had septic pulmonary emboli, he had this awful looking multifolk pneumonia, quote-unquote looking chest x-ray, had great looking biventricular function on echo, which he did until you looked at the tricuspid valve. But you go in and you see him and you're like, wait a minute, your JVP is up to your forehead. Something is not quite right here. So think about this in sometimes a septic patient who maybe has reasons for endocarditis who's really getting worse with your traditional septic management. So now let's talk about the second component of the pathophysiology of tricuspid regurgitation, which is your acute decompensated heart failure. So you're just like in AINMR, in acute decompensated heart failure, except it's this time your right ventricle that's failing. And so your right ventricle, it's trying really hard. But similarly, half of what it's trying to put out is going backwards, not forward. So it's having to work really, really hard to get enough volume to your left ventricle so that your left ventricle has something to push forward to your systemic circulation. And so your right ventricle needs support. It needs inotropy. It needs you to help it out because it's pretty sensitive to this whole situation and it does not deal well with this whole situation. So you've got to help it out with some inotropy. So to summarize how these principles of pathophysiology specifically translate into tricuspid regurgitation management, vasoactives and volume status. The first is vasoactives. In this case, the key downstream pressure to your right ventricle is your pulmonary pressures. Your primary target for vasoactives is actually your pulmonary circulation, not your systemic circulation. And so by far, the most important thing that you're going to do to help this patient is start an inhaled pulmonary vasodilator. If you're in the ICU or have this stuff available in your ED, that can mean inhaled nitric oxide. It can mean flowlan. If you don't, then you can do what I've talked about in another podcast, Inhaled Milrenote. But this is a critical component of the patient's pathophysiology. You've got to do this. And it's also something, if you are worried that this patient is in septic shock, it's something that you can do anyways without worrying that it's going to hurt their underlying physiology if they are in septic shock, right? Because when you do these things inhaled, it's not going systemically. So it's kind of like a low-hanging fruit that may really, really help this patient. And you don't have to worry about committing to something that may hurt if you're worried that maybe this is septic shock. It also can be a really useful diagnostic tool, because if you have just been working with this patient, they're in shock, things you're doing aren't working, then you start an inhaled pulmonary vasodilator, and all of a sudden they totally turn around. That is a really useful piece of information that may be, it is the acute TR that is driving your primary shock pathophysiology. Now, what are we going to do with systemic vasopressors? So IV vasoactives that we're going to give. Remember, these patients may often need support for their SVR. They may be systemically vasodilated, and they need that SVR support. They need a vasoconstrictor, a systemic vasoconstrictor, not a pulmonary vasoconstrictor. Now, Norepi's not an unreasonable place to start in these guys. The problem with Norepi is that if you go up on your doses and you go too high, you can actually start getting some pulmonary vascular constriction with that, which is the opposite of health. That's not what you want. The other consideration to keep in mind is that you want the RV to get some contractility support. Your IV needs inotropy. And so to get that RV inotropy. I usually go with Epi, because Epi will give you that RV inotropic support. It'll give you that increased systemic vascular resistance support. And in contrast to Norepi, especially at lower doses, epinephrine will give you less pulmonary vasoconstriction. So, you know, epinephrine is usually my first line in these patients. And then I usually use my second line vasopressin in the same way that you would for any kind of acute decompensated RV failure. Because a QTR management is really actually quite similar to managing any kind of acute decompensated right ventricular failure. Epinephrine is usually my first line. Second principle of management for these patients with TR is volume status. This is yet another situation where giving fluids is not going to help you here at all, and it's just going to make things worse. Because your problem, like MR, like AI, is not that there's not enough volume in the system. It's that the volume's not going the right direction. And your RV is working to have really hard already to get as much of that volume as it can moving forward. And overloading the RV with volume and blowing it out is, again, the opposite of health care. And will only succeed in increasing the reverberant volume into the RA. These patients need diuresis. Whether this is primary or secondary TR, the patients in RV failure and, again, treat them like acute decompensated RV failure and diures them. To sum up for regurgitant valves, we're talking about TR, MR, and AI. The patient with acute valvular regurgitation is a huge resuscitation opportunity for you. Everything about this situation is complex, but there's a ton of potential for you to affect the outcome if you do it right. In order to do that, you need to manage these patients in a very specific way. Often, the key question becomes, what is the primary driver of their shock physiology? Is it the acute valvular problem? Or is it whatever precipitated the acute valvular problem and both need to be addressed? But often it is the case that it's the valvular issue that's precipitating the acute shock physiology and you've got to stabilize the patient by managing their hemodynamics accordingly and able to be able to get to that place, you can address the underlying cause. The key pathophysiology you've got to understand about all regurgitation is that it's all about the pressure gradient. Your one-way valve becoming a two-way valve makes you completely dependent on pressure gradients to maintain forward flow. The second component of the physiology is recognizing that the patient is in acute decompensated heart failure, even though their RV and/or LV systolic function is going to look artificially good on ultrasound at bedside. In terms of specific management strategies to focus on optimizing your heart failure and pressure gradients, for aortic insufficiency, your management bottom line, for vasoactives, you want dobutamine. This is going to help you optimize your pressure gradient, give you inotropic support, and help you avoid bradycardia. For volume status, these patients need diuresis, I started early and often. With regard to mitral regurgitation management bottom line, for vasoactives, what you're going to want is dobutamine. For the exact same reasons as you want it in AI, it's going to help you optimize your pressure gradient, give you inotropic support, and help you avoid bradycardia. The other thing that you want to do in these patients to help optimize your pressure gradient, give them positive pressure. This is one of the few times that you want to increase your pulmonary pressures. So give them positive pressure, give them peep, put them on bipap, give them a ton of e-pap, that'll help you. Second management category volume status. These patients also need diuresis. It's going to help optimize your hemodynamics, help avoid blowing out that LV in the LA, and they also have pulmonary edema, and so that'll help your hemodynamic and respiratory status. Finally, tricuspid regurgitation management bottom line. In terms of vasoactives, the most important thing you can do here is optimize the pressure gradient by decreasing your pulmonary pressures by giving an inhaled pulmonary vasodilator. These patients also need IV inotropic support. You've got to help that poor failing right ventricle. And they often do need systemic vascular resistant support because they may be vasodilated and have systemic vasoplegia, especially if the cause of this is septic endocarditis. So I usually use epinephrine as my first line here with vasopressin as my second line because it'll help you with all of the above. These patients also need diuresis, just like any patient with acute decompensated RV failure. Having that poor RV now become volume overloaded is not helping anything. And the reason that your LV preload is low in these patients is not because you don't have enough volume in the system. It's because your RV not giving you anything for the LV to work with. So that is acute medical management of valve alopathy part one, regurgitant valves. Keep an eye out for part two of the acute medical management of alopathy series or we're going to talk about stenotic valves. Thanks so much for listening.