So we're going to continue the interactive session with additional cases. I have no disclosures relevant to this session. So I'm going to use a case to base all of my comments today. So we're going to talk about a 56-year-old woman presenting to the hospital with new onset heart failure. She has a strong family history and there are multiple apparently affected family members, including her mother, her maternal grandmother, maternal aunt who has a defibrillator and two siblings with heart disease. She's currently on no medications. And she presents to you quite decompensated, tachycardic, elevated JVP and S3 gallop, and an apparent mitral regurgitation murmur. She's cool, but her labs look okay. Her sodium is normal. Her creatinine is relatively normal. She has an echocardiogram, which shows a dilated left ventricle with an ejection fraction of 20% severely hypokinetic. And then, so our first question regards hemodynamics, and I need you to all get your calculators out because you have a right heart catheterization here with arterial pressure, mean of 78 and an RA of 22, elevated left-sided pressures and a low cardiac output and index. And the question is what is the SVR in this patient? So for those of you who don't have this equation at the top of mind, to calculate a systemic vascular resistance or any vascular resistance, you need the pressure on either side of the bed. So in the case of SVR, you take mean arterial pressure here, 78, subtract from it right atrial pressure, which is 22, divide that by cardiac output of 2.2, and then you need to multiply by 80 to get it into the units, dynes, seconds, to centimeters, to the fifth. So most people are answering C, and that is in fact the correct answer. I find the most common problem here is that you don't complete the subtraction before you multiply. You have to remember where the parentheses are in this equation, but the answer, correct answer, is in fact C, 2,036 dynes, seconds, centimeters, to minus fifth. So this patient is quite vasoconstricted. An optimal SVR is around 1,000 to 1,200, 800 to 1,200 probably. So this is a very vasoconstricted patient. And remember from Dr. Fang's talk that the heart is very afterload sensitive. Here I want you to focus on the graph, not in the sub box here, but as afterload increases, as a ventricle is very sick, stroke volume falls very quickly with high afterload. And so in a patient who will tolerate it, vasodilation can lead to profound increases in stroke volume in these patients, and you'll see cardiac output and index go up, often with very little change in blood pressure. And we show this, oops sorry, first question, first A question, which is, which of the following neurohormones is not elevated in this patient? So remember this is a new presentation patient. She's on no therapy, and we want to know which of the listed neurohormones is not elevated. Probably won't occur on the boards this way, as Maria Rosa has pointed out to us, but for purposes of our session. So that's fine. What percentages do we have for the others? Okay. All right. So most people are getting this right. Transcyretin E is the correct answer. The A through D are all vasoconstrictor hormones or indirect vasoconstrictor hormones that are elevated in untreated heart failure. It's an extraordinarily vasoconstricted state when untreated. And as you know, many of our therapies target blocking these hormones and their effects to reduce that vasoconstriction and vasodilate the patient. So this is a screenshot from Harvey. You can see we have a relatively low blood pressure in this patient. And as you vasodilate this patient, because the end systolic pressure volume slope is quite shallow, you do see a drop in blood pressure, but it's relatively minimal. But you do see an increase in stroke volume as you drop the blood pressure. So this is just showing in a pressure volume loop format that you can see an increase in stroke volume with a relatively small decrease in mean arterial pressure with vasodilation in a patient with a quite dysfunctional ventricle. And this is why vasodilation, neurohormonal blockade are so effective in LV dysfunction. And if you have a vasoconstricted patient and can get away with just vasodilation, it's an optimal strategy. It's definitely on the boards because we have oral equivalent medications that will do this. If we contrast that with the normal patient who has a much steeper end systolic pressure volume relationship, when you give those patients vasodilators, you see a fairly profound drop shown on the bottom panel here in blood pressure, much more significant. So the response we see to vasodilation in people with normal hearts is quite substantial drops in blood pressure, less of a drop in pressure in a patient with severe LV dysfunction, and that's important to recognize. Okay, so you've put Mrs. F on guideline-directed therapy because that's what she really needed, and she stabilized for two years, but then she's again admitted to the hospital. Now on Secubitril-Valsartan, although you recently had to reduce your dose because she was developing progressive hypotension, she's on very low-dose Carvedilol and normal doses of spironolactone. She takes a diuretic. And on examination, her blood pressure is low. She's again tachycardic. She again has evidence on examination of decompensated heart failure. She's cool peripherally. She now has edema, and now we're seeing some evidence of end-organ dysfunction and poor prognostic signs like hyponatremia. She also has elevated LFTs, so her kidneys and liver appear not to be perfused well. Her echo shows severe systolic dysfunction. She still has an EF that's low at 25%. So now our question is, these are her hemodynamics when you put in your right heart catheterization, and now you don't have to calculate the SVR. I've given you the SVR, and you have to decide based on these hemodynamics what you would do for this patient. And our choices here are to re-increase Secubitril-Valsartan. B is start phenylephrine. C is have the torcemide dose. D is to place an intra-aortic balloon pump. And E is to start dobutamine. Hmm. Nobody for E? Okay. I think the answers are in a different order on the poll. Oh, gosh. Could you tell me the answers in the poll, or the order? Okay. Good. I'm like, wow. And can you tell me the wording of the other answers, sorry, um, that people are choosing? Okay. Have the torcemide. Okay. Excellent. Thank you. Okay. So, um, this is, again, a very typical board question in which it's not wrong to do a number of these, but there's one best answer. Um, so, uh, this patient clearly has organ hypoperfusion despite reasonably low afterload. Her SVR is now 1100, and this is very classic for a treated heart failure patient to show up in a shock state with low output and index and hypoperfusion, but already well vasodilated because of their chronic oral guideline-directed therapy. So, I think the best answer here is to put this patient on inotropes primarily because they also have evidence of RV dysfunction, right? An intra-aortic balloon pump wouldn't be wrong. It might help the left side, but it's not going to help the right side. And this patient has biventricular failure by hemodynamics. So, I think inotropic therapy is the best answer. You wouldn't have the diuretics because filling pressures are quite high, and that's not going to help. Remember, a fluid overloaded ventricle has a lower stroke volume than one with lower wall stress. So, this is an Intermax 2-3 patient, and this patient's in trouble. You're going to put them on inotropes to try and temporize, but again, if you have a shock patient, you want to make decisions about whether your therapies are working relatively quickly and move to mechanical circulatory support in appropriate patients quickly if your pharmacological therapy isn't getting you where you need to get. Sorry. So, despite aggressive attempts at medical treatment with inotropic therapy, this patient continues to deteriorate. She's been listed for transplant, but you haven't yet received offers. She's status three in the current system. She's now aneuric. Her creatinine continues to rise. She's definitely Intermax 2 at this point. Diuresis is ineffective, and low blood pressure is limiting fluid removal, and her PA pressures are higher. Surgeons are nervous about transplant because of the RV and the PA pressures. Even though her transpulmonary gradient remains okay, this is still being driven likely by left heart failure. So, you decide to place an Impella device, and she stabilizes with increased urine output, reduction in PA pressures, reduced pressure requirement, which is great. So, we're going to talk about Impella for a minute. The Impella, as you all know, is placed a trans-aortic valve to provide support, continuous flow support, by removing blood from the left ventricle and ejecting it into the aorta. On the right here are shown the different Impella configurations, including the RP here, which is a right-sided device. From left to right, they provide increased flows, as indicated by the numbers, and they also increase in French size. So, the right-sided devices are increasingly used because they provide more support. Right side of the figure, the right-most devices are increasingly used because they provide more support, but often need to be implanted surgically or with a cut down. Now, the way the pressure sensor in the Impella works is very similar to what we've been talking about with the HQ curves of the HVAD, and Dr. Calger referred to this in her presentation too. The pressure sensor on the Impella device is in the aortic portion of the device, and it's a differential pressure sensor. So, it's looking at the ventricular pressure in the lumen and the aortic pressure external, and it's displaying the difference between those two. So, remember, the difference between aortic and ventricular pressure is essentially zero in systole, but much greater in diastole when ventricular pressure is low and aortic pressure remains high. So, what you end up is a displayed pressure curve shown in blue on this slide, where the low part of the pressure differential curve is in systole, and the high part is in diastole when the LV pressure is low and the aortic pressure is high, particularly if the device succeeds in pressurizing the aorta, in which case aortic pressure may even be a little bit higher than ventricular pressure, and there's a pressure differential all the way through. So, on your screen, it looks like this, but remember, you're not looking at ventricular pressure here or even aortic pressure. You're looking at the pressure differential. It's high in diastole and low in systole, and similarly, power is shown in or motor current in the bottom tracing, and motor current is going to be higher in diastole because you have to overcome this pressure differential in diastole to maintain flow. Now, a normal function screen can be highly variable depending on the device used and the hemodynamics of the patient, but it should be pulsatile in both the placement signal and the motor current screens. Now, the newer Impella devices have smart assist and actually display ventricular waveforms for you so you can see what the ventricular and aortic waveforms look like, and it's really nice when you have these, but you don't always have these. They also can display cardiac power output for you, which we talked about in the shock talk, as well as some other information which can be really useful, but if you don't have one of these devices, you have a screen that might look like this when you walk into a room on a patient. So, you look at this screen and you might say, I don't think that looks completely right, and you also look at the patient and you see this as well. So, the next question is, what is your clinical diagnosis? Do you have entrapment of the Impella and the mitral apparatus? Do you have right ventricular failure? Do you have leak of purge fluid? Do you have cardiac recovery, or do you have an Impella-induced arrhythmia? And this situation is not that different than some of the situations that Dr. Rogers just showed you with the HVAD, which is again displaying a requirement of power for flow and the differential for flow in the circuit, very similar to what the Impella is displaying. So, most of you are getting this right. This is entrapment of the Impella and the mitral apparatus. This is important to recognize because when the device becomes entrapped, it doesn't function normally, and you need to recognize and correct it. It's almost always accompanied by immediate hematuria because hemolysis increases as the device gets caught up in the valve apparatus. And the waveforms on the screen may or may not be distorted, but clearly the waveform I showed you is not a normal pulsatile waveform. Something's wrong. And so, an echocardiogram can help you see that this Impella distal tip is caught up in the cords of the mitral valve, and that's leading to this clinical scenario. Now, purge fluid, they're probably not going to ask you about purge fluid on the boards, but if there's a problem with purge fluid, there are specific alarms. And also, that should affect every waveform the same, not change like the waveform I showed you. Nancy, I think that on the board, the questions would probably show you this echo, but it wouldn't show you the gross hematuria because that a little bit gives away the answer. Right. But I wanted to have people realize. Right. Following device repositioning, hematuria resolves, and the waveforms assume normal configuration. But six hours later, you're called by the patient's nurse for hypotension and escalating vasoconstrictor needs. When you examine the patient, she's cold peripherally. And when you put your stethoscope on the chest, you hear what seems to be a normal pump hum for this patient. And the screen looks like this at this point. So, what's the most likely problem here? A, the Impella has stopped. B, the patient has become septic. C, the Impella is causing hemolysis. D, the Impella has dislodged and is in the aorta. Or E, acute AI has developed. And again, they might give you an echo to accompany this, as Maria Rosa has pointed out. You know, they'll often give you clues to the problem without overtly telling you what the problem is in a board question. So, go ahead. Excellent. So, most people are getting this right. This is Impella dislodgement. And again, you're not seeing a differential between aortic and LV flow, so the lines are very flat, both the motor current and the position screen. So, the device readout, which is a differential, is showing you no differential. And typically, that's because the device is in one chamber or the other completely. No power is required if there's no pressure differential. And in this case, you might get an echo, although these echoes are harder to see, but the Impella tip is right at the level of the aortic valve in this patient and not effective. So, you get an organ offer and the patient is transplanted, and we'll move to the next presenter.

heart failure

family history

decompensated heart failure

systemic vascular resistance

vasodilation

neurohormones