Good morning, everybody. This is day two of our marathon, and so glad everybody's here. So we're going to, one quick reminder for everybody is that if you want access to all the lectures and things, you have to complete a pre-evaluation. So make sure that you do that. It's on the SCCF website. All right, should we go into the questions, do a question and answer session? Also want to introduce Dr. Brandon Wiley. All right, so hi, everyone. I'm Brandon Wiley. I'm a cardiologist and a critical care physician from Los Angeles. And it's a pleasure to be involved today. You're going to hear me speak for the first bit of this course, so I hope you've had enough coffee. So we'll start here. 75-year-old man presents to the emergency department with acute chest pain that radiates to the back. Initial blood pressure 160 over 90. Heart rate is 100. ECG and troponin are negative. Chest CT is negative for PE, but there is evidence of an intimal flap in the descending aorta. Which of the following is the most appropriate initial management? Open surgical repair, endovascular repair, medical management to get a heart rate of around 60 and a systolic blood pressure of 100 to 120, or medical management to achieve heart rate less than 100 beats a minute and a systolic blood pressure of 120 to 140. All right, so there's the QR code. I think I started it. Whatever your mouse highlights over here will highlight that on the pie chart. Oh, OK. And then if you hit that show, that says show correct answer. So once everyone has clicked that, it will highlight whatever answer is correct. OK. All right. You ready, Brendan? Yeah. OK. All right. Good. So it looks like we sort of have a race between. So no one is electing for repair. And then we have a race between medical management, either for a heart rate of 60 and a blood pressure of 120, or a heart rate of 100 and a systolic blood pressure of 120 to 140. So can I go ahead with the answer? Yeah. So the answer for us was keeping that heart rate down to around 60. And that's the systolic blood pressure of 100 to 120. Now, what we want to do is reduce the stress, right, that is causing that tear. And if you look at the most recent guidelines, this says 2010, but there's 2018 guidelines from the STS. And they recommend a heart rate of around 60 to 70 in that range with the systolic blood pressure of 100 to 120. Now, medical management is the standard. Endovascular repair or surgical repair, you think about when you have a complicated dissection. And there's a whole host of criteria for that. But the big thing to think about is malperfusion. So if you have malperfusion with a type B, then you're going to think about actual repair in the patient. Where the dissection starts, and if they have persistent pain, these are all things that may push for a repair as well. OK, so next one. 75-year-old man is admitted to the ICU with shortness of breath, lightheadedness, and bradycardia. His ECG is shown. It'll be our next slide. Which of the following is the most appropriate next step? So based on the ECG, which we're about to see, is the next step going to be, hey, this is benign. We don't need to treat, which then we would wonder why they're in the ICU. Administer atropine, administer IV amiodarone, or apply transcutaneous pacing pads. There's our ECG. That's pretty good. We'll have some discussion. Yeah. All right. Okay. Great, so it looks like the winner was apply transcutaneous pacing pads. That is the correct answer. And we'll go over why that is if we go back to the ECG. So what we have here is heart block, right? This is Mobitz 2. And the reason that atropine is not considered the right answer here is because it's kinda hard to see here, but there is a bit of a conduction delay, right, so that's saying that the heart block, the block is likely to be infrahissian. And atropine in that setting typically does not improve the rate. And in some cases can actually worsen the block. So the correct answer is usually to pace the person. Now, transcutaneous pacing, I don't know if any of us here have done it, not the most comfortable thing for the patient. So, you know, I tend to put a TVP in, but that is the idea. A lot of times these patients, by the way, do get atropine, usually it's in the ED, right? And they say, well, atropine didn't help. And that's probably because it is an infrahissian block. And again, infrahissian usually, when you see a wider complex, that there's conduction disease of the bundle itself. Okay, I think this is my turn. A 61-year-old man hospitalized for COPD comes in with acute severe chest pain and dyspnea. He has ST elevation and lead AVR. He's pain-free after treatment with aspirin, clopidogrel, IV heparin, IV nitroglycerin. Which of the following diagnosis is most likely? Core pulmonality with acute decompensation, acute PE, acute pericarditis, acute coronary syndrome due to severe stenosis of the right coronary artery, acute coronary syndrome due to severe stenosis of the left main coronary artery. OK, great. So this is, um, uh, oh, let me see more answers. All right, I'm going to show the correct one. Oh, more answers. All right, so good. We have some discussion on this. All right, so I'm just going to skip over core pulmonality because no one answered it, or acute PE. And so really, the three answers are acute pericarditis, ACS, either from the right coronary artery or from the left main artery. And you know the answer is either the last two because they're longer than the first three, but the answer is right. But acute pericarditis, generally, you have as diffuse SD segment elevation, not depression or anywhere else. And you have PR segment depression. And there's no evidence that that was described in the question stem. In this case, there was SD elevation in lead AVR. And whenever you see abnormalities in AVR, it's generally a diffused process. It's either proximal LAD or a left main lesion. So this is a big deal. And so the correct answer is actually the last one. And those patients usually need surgical treatment. All right, this is mine as well. 65-year-old woman admitted for aneurysmal subarachnoid hemorrhage presents with dyspnea and substernal chest pain two days after admission. She had anterior lead SD elevations, and her troponin level was mildly elevated. However, when she went to the cath lab, there's no geographic evidence of coronary artery disease. She then develops hypertension to a blood pressure of 80 over 60, and is found to have moderate left ventricular outflow tract obstruction, which of the following is contraindicated in the treatment of this patient? Alpha agonists, beta blockers, inotropic agents, and a balloon pump. So we've got the next one. Curious to see what the answers are here. I think we have a quorum in terms of answers. So this is kind of asking a negative question. What is contraindicated for this patient? First thing is to realize what is the disease process. You have ST-segment elevations, right? And so you worry most often about acute coronary syndrome and a plaque rupture. But you've ruled that out with a cardiac catheterization. So generally speaking, when you see that, it's generally due to stress cardiomyopathy. It's about 20% of patients who come in with ST elevations have this. And when that happens, the neck of the left ventricle basically contracts. But the apex and the mid portions of the left ventricle do not. And what worsens is if you give something to aggressively cause more contraction of the heart, because that'll worsen the obstruction. So the things that's contraindicated is inotropic agents. I don't know. For patients with stress cardiomyopathy, I never really give inotropic agents, because it just worsens the situation. So what they wanted you to think about is, can you use an alpha agonist for these patients? You can, because if you're increasing afterload, it kind of forces the neck of the left ventricle to open up a little bit. And so it would help. It also helps with hypertrophic cardiomyopathy patients as well. Beta blockers, I haven't generally used for patients who are hypertensive, although in this question, it says that. And balloon pump, you can use, although it's less often used. I don't know if you want to add anything. Yeah. I mean, these are challenging patients to take care of. If it's a stress cardiomyopathy, then more catecholamines is a bad idea, right? So hitting them with a lot of inotropy is not great. If they're hypotensive, you can be kind of stuck. And so alpha agonists, fine. A balloon pump, you can use in that setting as well. We've done that. In your hypertrophic cardiomyopathy patients that come in, for example, with sepsis and have outflow tract obstruction, in that setting of a low SVR state, then it's like alpha. That's one of the few times I use phenylephrine, phenylephrine in those patients, and actually sometimes a beta blocker. You're not going to get tested on that. That's more of like how to sort of manage what can be very challenging physiology. Okay. I think this is mine. So intra-aortic balloon pump pressure tracing that's going to be shown is most likely associated with correct timing, early inflation, late inflation of the balloon, early deflation of the balloon, or late deflation of the balloon. That's our tracing. OK, I think we have quorum. Yeah. Let me, I'm going to just go back to that. Yeah, go back to this. Yeah, that'd be nice. Thank you. Yeah, I don't even, I don't remember what everyone answered. So what we're seeing here is early inflation. We've lost the, you know, we're not, we're inflating before the necrotic notch. The reason it shows you the unaugmented beat there, or the non-augmented beat, is you can see where the necrotic notch is. So the balloon is actually inflating early here. And this is kind of a tracing. Yeah, yeah, so this is a nice tracing. You know, we use a lot of balloon pumps in our practice. And the trainees are, it's usually a confusion on what, how things are working. But what you have to do to understand whether or not your balloon is augmenting appropriately is you have to change yourself from 1 to 1, to 1 to 2, or 1 to 3. You need to see what non-augmented beats look like. And so that's a non-augmented beat. That's a non-augmented beat. And so you can see here that the balloon is inflating right at the diacrotic notch, diacrotic notch closure of the aortic valve. You don't want the balloon to inflate when the aortic valve is open. And so what's happening in that prior one is the balloon is inflating when the aortic valve is open. And I think the next slide will go over what happens with that. So if the balloon inflates when the valve is open, you get premature closure of the valve. You get decreased stroke volume. And actually, you're increasing the work that the ventricle is doing. You can increase the LV end-diastolic pressure. You get aortic regurgitation. And with that increased work, you get increased myocardial oxygen consumption. So these are the things that we don't want to do with the balloon pump. So we want to make sure that we're timed appropriately. Oh, yeah, this is me. All right, so I like looking them up here. I swear I looked at all these beforehand. 56-year-old man admitted to the ICU with hypoxemic respiratory failure, oxygen saturation of 76% requiring intubation. Wife says that he had heartburn-type symptoms for three days and became increasingly breathless for an hour before admission. So became breathless, had heartburn, and then respiratory failure. On exam, he has diffuse RALs and elevated JVP. He has a short early systolic murmur heard at the apex. Extremities are cool. ECG demonstrates sinus tachycardia with Q waves in the inferior lateral leads and nonspecific ST changes. Chest radiograph demonstrates diffuse bilateral infiltrates. High sensitivity troponin is 4,000. LV function is hyperdynamic with an ejection fraction of around 70%. And there's some focal akinesis of the mid to distal inferior lateral and inferior segments. Valvular structures are not well seen with the POCUS imaging. Which of the following is the next appropriate diagnostic test? Do you get a CT of the chest? Do you get a transthoracic or transesophageal echocardiogram? Do you do a bronc? Do you check a procalcitonin? Or do you send the patient for a nuclear perfusion scan with a Lexa scan? OK. Oh, there we go. Nice. So the answer is a transthoracic or transesophageal echocardiogram. Now, if we go forward, I think we can talk through the other answers really quickly. I'm trying. Oh, yeah, no problem. Here we go. All right. So a person's presenting with respiratory failure, a high sensitivity troponin that's 4,000. So that's a pretty reasonable, that's telling you that there's been significant myocardial injury. And they have a hyperdynamic ventricle in the setting of shock, hypoperfusion. They're cold. When you have a patient that's presenting with a lot of myocardial injury, and you're worried about an MI, and they have a hyperdynamic ventricle, and they are in shock or they are malperfusing, you need to think about mechanical complication. And one of the classic ones is a papillary muscle rupture that leads to severe MI. In that setting, the murmur of mitral regurgitation can be very short and can be hard to hear because there is such rapid equilibration of pressure between the left ventricle and the left atrium. So the murmur occurs from blood flow. The blood flow is only going to flow when there's a pressure gradient between the two chambers. And if you have a ruptured papillary with torrential MR, there's a rapid equilibration in the pressure of the two chambers, and this murmur is short. Classically, you miss it. And so if you are concerned and your bedside imaging doesn't show you something, then a transthoracic, or honestly a TEE, a transesophageal, is the way to go to make that diagnosis. Can I ask a question of that? If they give the choice of only transthoracic or esophageal, which one would be the next? One or the other? I don't think they would give you that question, quite honestly. I think that the right thing to do, if you can't see something with a surface study, so point of care ultrasound is a surface study, then the next thing you do is a TEE. And in our practice, that's what we do. If we don't see it by transthoracic and we're concerned, we do a transesophageal echocardiogram. Yeah, it's easy enough to do in that setting. All right, 20-year-old gentleman has a diagnosis of dilated cardiomyopathy, he's admitted to ICU. He has heart failure, refractory medical management, and necessitate placement on a bifentricular assist device. The intensivist is called to the bedside because he's developed an abnormal cardiac rhythm, as shown. He's awake and follows commands, which defines the most appropriate immediate course of action for managing the abnormal rhythm. We talked about this yesterday, right? Immediate defibrillation, starchesque compressions, amiodarone, magnesium, or no immediate interventions. And this is the tracing here. So the ECG is on top, the oxygen's here, respiratory rate's there, and blood pressure's here. Yeah, so I think the majority of people here have the right answer, even though it's the wrong answer. Because now I'm thinking about it, I'm like, why not give magnesium, right? This is, you know, it looks almost torsades. But I think it's more like a V-fib pattern. I don't think it matters too much. But if you're going to give magnesium, I'm not going to fault you for it, because if you're thinking it's torsades that's causing this, it's OK. This patient basically has a biventricular support. So even if he's in fib, and if he's talking to you, if he looks OK, you have time to think about him. So the answer that they were looking for was no immediate interventions. But I think magnesium 2 grams push is not a bad idea, right? I would be drawing it up, yeah. Yeah. And then I don't think we need to go over chest compressions or amiodarone, because nobody answered that as well. The whole point of this is that whenever you look at a ventricular arrhythmia, whether it's ventricular tachycardia, ventricular fibrillation, if the patient looks fine to you, you have time to think about what to do next. And the only case where a patient would have V-fib or polymorphic VT and be fine is when you have biventricular support. This is a very old reference, but I left it in here because if you look at the first author, it's Dr. Oz. I just thought that was interesting. It's old, isn't it? All right. Now this is my 49-year-old gentleman, uses cocaine, has hypertension, hyperlipidemia. He last used cocaine five days ago. He comes in with chest pain and diaphoresis. His tox screen is negative. He's diagnosed with an NSTEMI. In addition to giving him aspirin, clopidogrel, and heparin, which of the following medications should be administered within the next 24 hours? So let's give that to you. Okay, so this is great, we have a little bit of variety in the answers. So no one's going to give you TPA and we don't do that because it's an NSTEMI. If it was a STEMI, you would, if you have no cath lab around. I think the key point to this question is when did he last use cocaine? If you use cocaine now or like a day or two beforehand, then things like benzodiazepines and calcium channel blockers make more sense. But the fact that he used it five days ago means that it's safe to give non-selective beta blockers. There was actually a few studies, this is a true story, normal volunteers were given cocaine and then they tried giving them beta blockers to see how much spasm they would have in the corneal arteries. Try getting that by the IRB now. But they did this and things like metoprolol, which is a selective beta blocker, is not as ideal. But things like carvetolol seem to be better because it's more of a non-selective blocker and also has alpha blocking effect. So the correct answer here is alpha, is carvetolol. All right, it's your turn. All right, so 55-year-old patient admitted to the ICU with dyspnea on exertion and orthopnea for two weeks. Afebrile, heart rate in the 80s, respiratory rate is 14, oxygen saturation is 93% on room air. The patient is awake and following commands. The physical exam reveals a pan-systolic murmur loudest at the fourth intercostal space in the parasternal region. The lungs are clear. The patient has 2-plus-pedal edema. The serum electrolyte panel reveals a sodium of 142, potassium of 4.1, glucose 111, ionized calcium of 5.2. Triple lumen catheter is put in to get the right atrial pressure. ECG and right atrial tracing are shown below. Which is the most likely diagnosis? Is it tricuspid stenosis, tricusporegurgitation, mitral stenosis, or mitral regurgitation? Okay, I'm going to go to the answers. Yeah. Yeah, the correct answer is tricuspid regurgitation. Mitral stenosis and mitral regurgitation are going to give you something in your lung fields, right? They're going to cause pulmonary edema. So in this setting with a patient having, you know, clear lung fields, adding 93 percent of room air, unlikely to be a left-sided valve problem. So we're dealing more with right-sided valve issues. Both tricuspid stenosis and tricuspid regurgitation can give you edema peripherally, and that's what the patient has. The systolic murmur, though, tells you that it's going to be a regurgitant murmur. And then what we see here, if you look, again, whenever you're given these, look at what the pressure is going to be here, right? So 25, 5, 10, 15, 20, 25. This is the mean pressure. The mean pressure is going to be high, right? So if that's 20, it's around 15. And what we see, if we're looking at the pressure tracing, we're timing it with the ECG, and we see these waves, right, during systole. So those are your V waves. So that patient has tricuspid regurgitation, not tricuspid stenosis. That's all the questions and answers.

cardiology

heart block

cardiogenic shock

echocardiograms

acute coronary events

stress cardiomyopathy