This is great. Hi, everyone. I'm Brandon again. I'm going to be here for the next hour and a half. To 945. To 945. OK, till 945. OK. Again, yeah, so we're going to go over a lot for about an hour. And I'll do my best to kind of take us through some of this stuff. And so we're going to start with heart failure. And I have nothing to disclose. So we'll go through a cased approach here. We'll talk about some key points. So our first case, 67-year-old male, no past medical history, presents with acute dyspnea and edema. He goes to the ICU on CPAP, gets some diuretics. Exam, he's warm. He has jugular venous distension. He has edema, but no murmur. Heart rate is in the 90s. Blood pressure is 130 over 90. He's sat in 92% on a PEEP of 8, FiO2 40%. Chest X-ray, there's vascular congestion and pleural effusions. ECG is sinus with LVH and left atrial enlargement. There are the labs, right? BNP is elevated. High sensitivity to troponin is elevated but flat. Lactate is 1.1, creatinine's up a little bit. What's the next best diagnostic step? Right heart catheterization, so put in a PA catheter. They're in the ICU. Why not, right? Endomyocardial biopsy, left heart catheterization, or echocardiogram. Oh, OK, echocardiogram, there we go. All right. Should I ask you guys each one of these things? Everyone can raise their hands. So why an echo? Well, so this is from the guidelines, the heart failure guidelines. And essentially, the diagnostic algorithm for patients with suspected heart failure, and these are the sort of things you could be tested on. Very classic stuff, right? So your exam, class one, chest X-ray, ECG, all class one. Echo is a class one. So we echo ECG, ECG, ECG, ECG, ECG, ECG, ECG. This guy has new heart failure, right? Has no past medical diagnosis. We want an echocardiogram to understand something about the biventricular function, as well as whether or not there's any pathology, such as valve abnormalities. We can get something about diastology and our filling pressure, as well. A cardiac MR, right? So MRI, that's a class 2A. We do do that in patients that have non-ischemic cardiomyopathies. Think about, is there an infiltrative process that we're missing that could be leading to the heart failure that we're seeing? The point I want to make here is that a right heart catheterization is not indicated as a routine thing for patients that present in heart failure. It is not routine. And a biopsy is also not routine, right? So those are just wrong. Now, an important point to make here is that routine right heart catheterization is not indicated because of a lot of trials that showed, and the most important one being the ESCAPE trial, that routine catheterization in heart failure patients did not lead to benefit. However, it's important to note, as we are all intensivists here, that this trial, which is cited all the time, excluded the most critically ill patients, right? So if you were on dobutamine, dopamine, or milrinone, you are not enrolled in this trial. And if you were felt to be too sick, you're not enrolled in this trial, right? So although routine right heart catheterization is not indicated in sick patients, in patients that are in cardiogenic shock, there may be a benefit. And definitely in my practice, and I deal with a lot of cardiogenic shock, I'm pretty aggressive about putting a PA catheter in in those patients that are demonstrating shock or malperfusion. And this is just something for you guys to look at. This is a retrospective thing, but it looked at 1,400 patients in a registry for mechanical circulatory support. And essentially what they found here was patients that had a full set of hemodynamics done, meaning they had a PA catheter in, did better than those patients that did not. And these are, again, shock patients. These are not your bread and butter coming in with some wet heart failure patients. Other things to think about, possible test questions. We do do an ischemic evaluation for patients with new heart failure. That's a class IIa indication, and that's because the top three causes of heart failure in the United States are ischemia. Ischemia and ischemia, you know? So it's all coronary artery disease. But then there is a list of other things that we can see, and these are the things that we want to think about and rule out because a lot of them, or some of them at least, are reversible and can be treated. Okay. So move to the next question. 62-year-old male, history of non-ischemic cardiomyopathy, was admitted to the ICU for acute heart failure, secondary to AFib with RVR, and medication non-adherence. He converted to sinus with metoprol. Diuresis was started with furosemide. Creatinine's 1.2, potassium 3.9. He's warm. He has elevated JVP. Blood pressure is elevated at 150 over 80. Heart rate is now 80. He's sat in 92% on four liters. ECG, LVH without acute ischemic changes. The echo shows a dilated LV. EF of 35%. Global hypokinesis of the left ventricle. Mildly reduced RV systolic function, no valve disease. In addition to a loop diuretic, metoprol, and enoxaparin, what is the next best step? Start hydralazine. Anyone? Start amlodipine. Start saccubitrile valsartan, low-dose spironolactone, and plagliflozin. So three meds. See some people raise their hands. And start digoxin. Okay. So a couple of people raised their hands for starting three meds at once. It seems like a lot, but I think that's where we're going now. I'm not sure that you would be tested on this per se, but important points here are that amlodipine, you're not gonna start. This person has an EF of 35%, so you wanna get them on GDMT, what's considered GDMT for heart failure with reduced ejection fraction. Amlodipine is not a part of that in the beginning. You don't need digoxin. The person's in sinus rhythm now, right? And then hydralazine, we can use. It is in the algorithm, and we'll go over that for heart failure with reduced ejection fraction, but it is not an ideal first medication in a setting with someone that has reasonable kidney function. But what we are doing now and thinking about is how to treat patients with heart failure and how to treat them aggressively. In the ICU, we're dealing with stage C heart failure, right? Those are patients with current symptoms or previous symptoms or signs of heart failure. And then we stratify them based on their functional status. Most of the patients that you guys are gonna see are gonna be class three to class four. This is the guideline for what we're talking about now with heart failure with reduced ejection fraction and what's sort of thought of as the four pillars of therapy. So we have ARNIs or ACEs or ARBs. Those are RAS inhibitors. We have our beta blockers. We have our MRAs, our mineralocorticoid receptor antagonists, and then we have our SGLT2 inhibitors. These are all class one indication for heart failure with reduced ejection fraction. That's considered to be an EF of 40% or less. Heart failure with mildly reduced EF, 41 to 49%. We can see that most of these have 2B indications, except for our SGLT2 inhibitors. And then HEF-PEF, there's not a lot of great therapy, but what we tend to use now is our SGLT2Is, and then we start MRAs in those people. What we want to do and try to do in practice now is get them on these therapies quickly, right? So this is, again, from the most recent guidelines, update to the guidelines for the treatment of HEF-REF stage C. And what we see are, again, our four pillars, our RAS inhibitors, mineralocorticoid receptor antagonists, our SGLT2Is, and our beta blockers. We add diuretics, right, because we want to relieve congestion. Those work synergistically with the SGLT2Is and the MRAs. And then if patients are still symptomatic despite optimal GDMT, then we start hydralazine and isosorbide dinitrate. Or if we can't get them on RAS inhibition or an ARNI due to a renal dysfunction, then we can insert hydralazine and isosorbide dinitrate. Why do we start patients quickly on these medications? Because the most recent study was the STRONG-HF trial. Long and short of it is, this was an international trial, multi-centers, 1,000 patients. Patients that were started on GDMT quickly and then ramped up quickly over time did better than those that didn't, and there was a mortality benefit. So although this may not, probably won't be in the test that you guys are taking right away, this is something to think about in your practice. It's definitely in the ICU, the way I practice now is when I stabilize the patients and they're perfusing, I try to get them on therapies and try and get them on therapies quickly. Because if we don't, they tend to be discharged from the hospital and they don't get put on these medications right away. And so we have an opportunity, a true opportunity to get them started on these meds in the hospital. I'm happy to talk to your pharmacist about it. But no, I think it's a great point. People get concerned about, for example, renal dysfunction and if the GFR is a little on the low side. I'm aggressive. You should see a bump in creatinine when you start these medications and that's tolerable. And even a 20% bump is tolerable if the person is perfusing and doing reasonably well. I try to start them all at once. I'm at a public hospital and we've been able to, it took some time to get us to a point where we're able to do that. The things to think about, and you and I can talk about this afterwards, is what some of these medications can do when they're started together. So empagliflozin or Jardians, when you have a loop diuretic going and you start spironolactone, the person's gonna make a lot of urine. So you may have to back off a little bit on your loop diuretic, for example. That's one of the things you can see in some electrolyte disarray because they're just gonna be peeing a lot. I like that in a lot of patients that are grossly volume overloaded because I'm able to decongest them faster. And there are some studies that have shown that when we do get these medications started quickly, people decongest faster and their length of stay shortens. And that's what the hospitals want, right? So I think we do have to be aggressive. And when the pharmacy calls, push back a little bit and say, no, this is important, we need to do this. Does that help a little bit? Yes. Okay. Yeah, yeah, absolutely. Yeah, no, it's a really good question. So again, you have to individualize the care. I try to be aggressive in most patients, but in some patients you can't be. Older patients, sometimes you have to be a little bit more judicious in how you start and then sort of look at what's going on with the patient at the time. I, a GFR, most of these medications, for example, Jardians or Impagliflozin or SGLT2 inhibitor, you can start, you can use in a patient with a GFR of 20. DAPA, which is the other SGLT2 that's used a lot, it's 25 or 30. So you can use these medications in people with low GFRs. The Secubitriol Valsartan or Entresto, it's not as much an issue with your GFR, but it causes hypotension. It's more prone to hypotension than, for example, Losartan. So if you have a patient, a trauma patient, for example, and you're dealing with blood pressure issues and they're an older person, you may not use that medication, right? You may back away from that and use something different. Yeah, so you can start with, for example, Captopril, which is a short-acting ACE inhibitor, and you can start a very low dose and see how the patient tolerates it. If they don't tolerate it well, it will be gone pretty quickly. The only issue with an ACE inhibitor is that you need to wash out the ACE inhibitor before you start the Arni or the Entresto. So it really depends on kind of the patient that you're dealing with. In some of these older patients where I think that, for example, they may not be able to tolerate, they have a lowish blood pressure and they may not be able to tolerate Entresto, I may use Losartan, like a low dose of Losartan, or I may use Captopril to kind of see how they do. This is just, again, a slide for you guys. This is from the guidelines, just a summary of the therapies and how we do it. Again, step one, kind of getting all those medications on board, and then as we move forward, utilizing things like CRT, or even now we're using MitraClip in patients with significant mitral regurgitation to optimize them. And then heart failure with preserved ejection fraction, again, that's an EF of 50% or greater. We don't have, we really don't have the studies that have shown tremendous benefit. I'm happy to talk to people about using a Secubitril, Valsartan, or Entresto in these patients. The studies can be a little equivocal, but definitely diuretics, you need to decongest the patient, and SGLT2 is beneficial in that setting, and there is definitely reduced hospitalization in patients using that, and then MRAs, and then the ARNIs and the ARBs for high blood pressure. All right, so case three. 62-year-old male with ischemic cardiomyopathy. So this is ischemic cardiomyopathy, HEF-REF. So heart failure with reduced ejection fraction. Presents with dyspnea and orthopnea, chest X-ray and the ED demonstrated pulmonary vascular congestion. So the lungs are wet. IVC is dilated on POCUS. He is given furosemide IV and admitted to the ICU. The JVP is difficult to see. There are rows, no murmurs, but he's cool, distally, right, his extremities, and mild lower extremity edema. Blood pressure's 100, I'm sorry, heart rate's 100, blood pressure is 120 over 90, and he's satting 93% on six liters. What's the next best step? Dopamine infusion, dobutamine infusion, nitroprusside infusion, or metoprol, and there are the labs. We see he has an AKI. High sensitivity troponin is elevated but flat. Lactate's 1.7. There's liver injury, and the bilirubin is up. So who would do a dopamine infusion? Okay, who would do a dobutamine infusion? Okay, we got some hands. Who would do nitroprusside? No hands, and who would do metoprol? Okay, so nitroprusside is what I would use in this setting, reasons being, one, you have a map of 100, okay, and this person has evidence of hypoperfusion, right, so they're cool, they have liver injury, keratinin is up, right, so they have an AKI, they have liver injury, and they're cool peripherally. Dobutamine is a reasonable thing here, but not ideal. You wanna start the nitroprusside first, bring that map down to probably around 65 to 75, and improve for flow in that setting. Dobutamine is an inodilator, so it gives you inotropy and vasodilates, but again, it can drive the heart rate. It's associated with arrhythmias, and then dopamine we tend not to use in patients with cardiogenic shock, or because of bad outcomes in prior trials and increased arrhythmia, so nitroprusside's probably the best answer here. A couple of slides just to point out some things. Hypoperfusion is important, it's really important. This is a slide that shows a study that was done by one of my colleagues who looked at heart failure admissions and looked at mortality, and mortality was higher in patients that had hypoperfusion but had normal blood pressure, right, so not classic shock, than those patients that were hypotensive. So when you see these patients, you need to think about hypoperfusion. Hyperperfusion, what we use to classify hyperperfusion is a lactate that's elevated, urine output that's low, creatinine that demonstrates an AKI, and then this is the SKY criteria for cardiogenic shock. Again, this is something to review. Classic shock is stage C, which is hypoperfusion without deterioration, and then when you get to sort of stage D and E, those are patients that a lot of times we see in the ICU, right, that we're thinking about putting on mechanical circulatory support. The assessment of perfusion, again, super important to think about whether or not the patient is warm or not. Pulse pressure is very important. So that patient in that prior case had a very narrow pulse pressure. It was 120 over 90, right? The pulse pressure would be 30 divided by 120, which is about 25%, so that's low. That tells you something about cardiac output. If there's low pulse pressure, then the cardiac output's gonna be low, the stroke volume's gonna be low. For those of us who use echocardiography, we can just look at the LVO-TVTI, and that can tell us something. But the exam is really important here. And then this slide illustrates the Diamond-Forrester classification, which is the idea of whether or not someone is warm and dry or cold and wet based on what their filling pressures are and what their cardiac output is. The point of this slide was that we used echo to do it, and we were able to get the same classification. And those patients that had evidence of high filling pressure, so an E over E prime of greater than 14, and had low cardiac output by echo, those patients had the worst mortality. So again, thinking about using noninvasive stuff such as echocardiography to help you re-stratify patients. But this is the way to sort of think about how to care for these patients in the ICU. And this is a very classic slide. I made this based on what's in the guidelines. But again, it's that classification. You have patients that are warm and dry. So those are patients with a normal filling pressure, CVP or pulmonary capillary wedge pressure, and normal cardiac output. We say that, or cardiac index, that's 2.2 or above. Those patients are warm and dry. Those are the patients we start on GDMT. We try to get patients who show up and are wet and cold, dry them towards that position of being warm and dry. So those patients that are wet and cold, for example, our gentleman that came in that we were just talking about, whether or not we're gonna use dobutamine or a vasodilator, he had a high MAP in that setting. So a vasodilator, for example, nitroprusside, is a very helpful medication. If you don't have a reasonable MAP, if the person is hypotensive, right, then you wanna go to the dobutamine, for example. You can't start them on a vasodilator to start with. You're gonna need to start them on an inodilator. Or sometimes in that setting, if they're really not doing well, you're gonna start them on norepinephrine, right? That is gonna be the medication you're gonna use to drive that MAP up so they perfuse, right? And this is just a reference for you guys. So why nitroprusside? I think it's kind of, it's old school, but I've definitely seen it on test questions because it is, there's data for it. This is from the Cleveland Clinic Group, and what they found in a retrospective study through, of their patients, patients that were low output with high filling pressures, and using nitroprusside to titrate to a MAP of 65 to 75, there was a mortality benefit, right? So just something to think about there, and I definitely have seen this sort of question because the people that write the questions are some of these people. Okay, case four. Based on the pulmonary artery tracing, what type of cardiogenic shock is present? Biventricular, left ventricular, right ventricular, or there's no shock? So let's take a look at the tracings that we have. I'll give you guys a second to wrap your head around this. So is this right ventricular shock, left ventricular shock, biventricular shock, or no shock based on these tracings? Who goes with RV shock, right ventricular? Who goes with left ventricular shock? Some hands. Biventricular? Okay, a couple. And then no shock. Oh, it's a shock patient. We're gonna say they're shocked. So what do we have? So we have a right atrial pressure tracing. Again, if you get these, look at what the pressures are, and what each box is gonna be. They may or may not tell you what the pressure is, and you kind of have to figure it out on your own. But if that's 25, five, 10, 15, 20, 25, we see that the RA pressure is right down there, right? So not that high. I gave you guys the mean. It's seven up there. I don't know if you can totally see it. But the mean RA pressure is seven, so the right side is probably gonna be okay. But we know this is a pulmonary capillary wedge tracing because the person pulled back into the PA. That's what we like to do to show that we're wedged, right? So it's a wedge. And then we deflated the balloon, and it's in the PA here. So it's a wedge pressure tracing. The pressure is quite high. The mean pressure here, again, this is 50. I think it's 10, 20, 30, 40, 50, right? So the mean pressure here is gonna be up, right? Around 30, 35, something like that. So this is a high wedge pressure in someone that's in shock. So it's gonna be left-sided shock, LV shock. That's the answer. Hemodynamic profiles. This is a slide for you to use as reference. These are the different subtypes of shock. You know whether or not it's LV-dominant, RV-dominant, or biventricular, and that's based on your filling pressures that are there. And then some numbers that we use in the cardiac ICU to think about, like right-sided function, for example, are PAPI, and people that take care of patients that get LVADs, right? We think a lot about whether or not they have reasonable right-sided function, and they're not gonna go into RV failure after getting a univentricular device on the left side. Cardiac power output is something that's been well-publicized with Impella devices, and it's tracked by Impella devices as an outcome metric. And then you have your SVR and PVR. Again, just important numbers here for you guys to think about. If we wanted to look at this case and sort of think through it a little bit and how we would think about all these calculations, the pressure when we did the patient, when we swan them, the pressure was 98 over 75. We ended up with a cardiac index of two, right? So low cardiac, just kind of borderline to low cardiac output. Right atrial pressure was seven, the wedge was 30, and the PA mean pressure was 38. You can use your CVP over wedge, right? So if the CVP is high and the wedge, and you start to move towards a ratio of one, that's telling you that the right side is not working well. It's an RV problem. This patient's PAPI was really good. It was 3.8. We think about a PAPI of less than two as being abnormal and less than one in, less than 1.5 or 1.85 in LVAD patients, we worry about right-sided failure. And then less than one in an RVMI, we worry about RV failure. Again, the SVR is there. The cardiac power output is there. Cardiac power output is greater than 0.6. We wanna keep it greater than 0.6, less than 0.6 is associated with high mortality. And we have our pressure tracings. Again, with the PA pressure tracing, we see the dichrotic notch of the pulmonic valve, right? So you know it's the PA, the wedge here, and then the right atrial pressure. Okay, any questions? That was a lot. It's a lot. Happy to talk about it with people outside of this as well. Thank you.

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