It's hard to give you guys heart failure in, like, 15 minutes. It's been 15 years for me, and I think I'm still, you know, we still learn, we're learning every day. So, just a couple of key things, and I think some of those slides hopefully have some information for you guys that's there just to help. Okay, this is another one that definitely we can fit into 15 minutes. Cardiovascular surgery complications and mechanical devices. Go. Here we go. All right. I have no disclosures. All right, so, case one. Sixty-five-year-old male undergoes CABG, an aortic valve replacement, and is extubated. This is a, these are actual cases. Extubated on post-op day one. PA catheter is removed on post-op day two. On post-op day three, he develops hypotension, increasing doses of epi, so he was on one of epi, and then it became five of epi. Bedside ultrasound is performed based on the available imaging. What is the next best step? So are we going to put in a chest tube? Are we going to do a pericardiosynthesis? Are we going to advocate to the surgeons that the patient go back to the OR? Or are we going to talk to our vascular surgery colleagues? All right, here's the imaging. This is a point-of-care ultrasound. So we have a parasternal lung, a subcostal, an apical four, and an IVC. Okay, based on that imaging, what are we going to do? All right, why, so who says we're putting in a chest tube? No one. Okay, good. Who's doing a pericardiosynthesis? Anyone want to do one? No. Okay, so we took this patient back to the OR. Why? Yeah, yeah, great. We took this patient back to the OR. So it's a mediastinal, a big hematoma, right? We can see it up there. Let's see if this works. There's a pointer. Oh, yeah, there. So we have a collection up here. It's heterogeneous, right? So you can see that there's some anechoic area, anechoic meaning there's no echoes in that area, right? So it's fluid. So it's coagulum, right? So this person has bled, right? And the right ventricle is the most anterior, and the right atrium is anterior, right? So bled all here, and then this is coagulum and a hematoma that's compressing the right atrium, right? And then the IVC is big. So if you have right atrial compression and a big IVC, you have focal tamponade, right? So that's what we're seeing here is a tamponade process. And tamponade, right, can happen. You don't need to have fluid all the way around the heart. It can be focal. And what we have here is focal. And this is color flow. And we see that there's essentially there's a gradient that's developed across the tricuspid valve. So the right, if you look here, oh, go back one, the right ventricle is actually small. It's underfilled, right? So the right ventricle is underfilled even though the IVC is big. So it's a compression issue on the right atrium. The reason to bring this up with respect to post-cardiotomy or post-cardiac surgical care is that tamponade is really something to think about. And it can happen late, right? It can happen seven days out from surgery. But really what you need to do in that setting is take the person back and wash them out and get rid of that. We have all the things here for diagnosis. You can use invasive hemodynamics. You can use pulsus paradoxus if it's there. You can use echo. The huge thing is if you're concerned and you don't see something with transthoracic echo or your point of care, do a TE. And someone asked about a TE before. This is absolutely the case where you get a test question and they would say that the bedside ultrasound didn't show much, but the CVP is high and the cardiac output's low. You need to do a TE in this patient. And that is, this is a patient actually that we took back to the OR. This is the transthoracic here. This was the only image we had. This person had two valves put in, two mechanical valves, and had had a commando. And what we see when we do the TE is that this is a different case of right atrial and right ventricular compression with the TE. Again, this is a TE image. So the probe is sitting here. That's the left atrium. This is the right atrium here, and that's compression here of the hematoma that had to be washed out. So these are the classic sort of things to think about when a patient comes back from the OR, from cardiac surgery. What are the issues that we have to deal with? And there's a lot of them. And we'll go through just a couple of important points. So vasoplegia, I think this is what we deal with the most. And it's hypotension with a low SVR, and we need vasopressors. Just a couple of things that sort of to touch point on, to talk about. One is the risk factors. So this is why we stop ACEs or ARBs before people go to cardiac surgery. It is definitely a risk factor for it. Primary therapy, well, we always fluid resuscitate. We like to follow invasive hemodynamics in these patients and fluid resuscitate them until we think that they have adequate volume. But vasopressin is probably the better medication with respect to norepinephrine, and that's based on the VENX trial. Vasopressin, there is less atrial fibrillation, right? So norepinephrine can lead to a little bit more. It's more beta, so you get possibly more arrhythmia with it. So we like to use vasopressin in those patients. And definitely vasopressin if you have RV dysfunction post-op is a helpful medication because it can help you with SVR, but it doesn't impact the PVR quite as much. And then in those patients that are doing really poorly, we need to scavenge for nitric oxide and either inhibit the synthesis of it with methylene blue, or we need to scavenge it with hydroxycobalamin. There's no R there, but that's cyanakate. We use a lot of cyanakate. We tend to run it long, right? Instead of like a bolus, we run it over time. And there is a small study out of Mayo Clinic that shows that maybe that is a better way to keep the SVR up and to keep a blood pressure. Postoperative bleeding, just maybe the test question that you would get here is like, what do we transfuse to? And it's a restrictive transfusion, right? That's our criteria. That's based on a lot of studies. Is that just for non-hemorrhaging anemia or hemorrhaging anemia? Yeah, that's a good question. So if the person is bleeding, we give blood and we tank them up. This is, if you're going to get, the typical sort of thing is a person has a CABG, they come back with a hemoglobin of 7.8, and the nurse is like ready to give blood. In that setting, we don't give blood, right? We're okay with 7.5 to 8. This is the 2021 guidelines, which I've included down there for you guys. And then we like to think about how we transfuse and why we transfuse. And so the other thing that's recommended in the guidelines is to use your Rotem or your TAG to really like think about your blood products that you're transfusing and to transfuse in a targeted way. Another key thing is post-cardiotomy cardiac arrest. This is a big one because people aren't used to the idea of not starting CPR immediately. And we actually, we do this always for the new nurses in our cardiac surgical ICU. And we recently did this and a couple of nurses just started doing CPR initially, immediately in the mock code. And in a cardiac arrest, in a post-cardiac surgical patient, it differs from your typical ACS because you can wait up to a minute to either shock the patient if they're in VT up to three times, or if they're pulseless or in asystole to try and pace them, right? To try and get the pacemaker to capture and pace. Because CPR, external cardiac compression, can damage what the surgeon's done. And so typically what we're trying to do, and this is why we do our mock codes, is try and shock the patient, shock the patient, and then we have open chest protocols to open the chest quickly. So these are the things maybe to think about for a test question. And again, we typically don't give epi in this setting before we're opening the chest, unless we're, you know, we do use a little bit of push dose sometimes. We had a patient with tamponade recently that we used a little bit of push dose to keep the map up while the surgeon was getting ready to open the chest. So I think this could be a good test question for you guys. So case two, the telemetry strip demonstrates which of the following? Normal ventricular pacer function, output failure, capture failure, or pacemaker-mediated tachycardia. Who's going with normal ventricular pacer function? Good. Yeah, because we're not going to show it if it's normal, I don't think. Output failure? Capture failure? Yeah, okay. All right, we got capture failure. And pacemaker-mediated tachycardia, we don't have the tachycardia there. So that's good. It is capture failure. Why is it capture failure? Because we see pacing spikes and we're not capturing. We're not capturing the myocardium, right? So this is capture failure. Capture failure is when there's pacing spikes present, but we're not capturing. The most common cause in non-cardiac surgical patients, so these are patients that you have in your ICU that, like that case that we did, came in with MoBITS 2, you float a TVP, and then all of a sudden it's not capturing. Usually it happens like 3 o'clock in the morning when no one's around, and they're calling and they're like, it's not capturing. And it's usually because the patient is moved in bed, right? Because we use balloon-tipped catheters, balloon-tipped catheters, a lot of times they move. So if the lead is not well-positioned, you're not going to capture, right? The big thing that will lead to failure of capture that I see often is with the balloon tips, you float it like a swan and you float it into the RVOT and you don't get great capture in that setting. You actually want it to float kind of directly down towards the apex of the right ventricle. And so I actually tend to remove, I tend to, you don't want the curvature that you have with a typical PA catheter. For a PA catheter, when the fellows are doing it, I try to give them a nice curve and make sure that they're putting it in if they're from the right IJ so the curve will follow and you'll go up like that through the RVOT to the PA. You don't want that with a TVP. So not well-positioned, that's the first thing. In cardiac surgical patients, kind of a big thing is fibrosis that happens or inflammation that happens when the patient is being persistently paced. And a lot of times what people do is they turn the output up super high because they get worried, well, we got to capture. The higher your output is though, the more likely you're going to have lead failure over time, especially if that person just had an AVR and they have some heart block and you want to see if it resolves over the course of the next week or so before you have to put in a pacemaker and then someone turns up the output a lot and it fails, right? So you don't want to do that. That's why you don't want to increase the output a ton. You want to find where you're capturing and then go up a little bit above that. And then other things that will lead to failure to capture, myocardial ischemia, electrolyte or pH derangement. This is a classic sort of thing where the person has a K of 7 and they call and they say, well, we need a TVP because they're bradycardic, they're in heart block. And you can put a TVP in those people and it's not going to capture, right? You have to fix the potassium. Failure to pace, that's absence of a pacing spike, all right? The thing to do there, if you don't see a pacing spike, is switch the device to an asynchronous mode, for example, VOO. It should pace. If it doesn't pace, if you don't see anything, then there's a problem with the actual device itself, maybe the battery. And then you can have over-sensing, which we'll talk about in crosstalk inhibition. That's where, for example, if you're in DD mode, so you have your atrial sensing and pacing and ventricular sensing and pacing. For example, the atrial lead could sense the V-spike, the V-pacing spike, and think of that that it's an intrinsic atrial contraction and then not pace, right? So that's crosstalk. Daily assessment, and my talk has a lot on this, so if you guys want to learn a little bit more about that, I go into depth on pacing. But the daily assessment of epicardial wires, to assess the rhythm, don't unplug the leads. I've seen that happen, and there's nothing underneath. And then my heart stops beating for a second. But just reduce the rate down and see if the idea is to sneak up on the intrinsic rate. So go down slowly and sort of let the intrinsic rate sort of peek through. We assess capture. That's important, because I can tell you something about if there's going to be impending lead failure, if you're needing more and more and more milliamps to capture. It can also tell you if you did a TVP, if it's now in a different place, right? If you were capturing at, like, one, and all of a sudden you're capturing at, like, seven, then maybe the lead has moved. And then sensitivity is really important. So sensitivity is what the pacemaker is able to see, how sensitive it is for an intrinsic conduction. So to increase sensitivity, you actually turn down the threshold, right? So it's sort of this paradoxical thing, but you turn down the threshold to increase the sensitivity. The higher your sensitivity, you can have over-sensing, so you can, and we'll show what that is, where you actually, the device is picking up stuff that's not really there. And if you under-sense, right, you have the threshold a little too high, then you can have intrinsic contraction that the device doesn't see, and then you can have an R-on-T phenomenon. So this is under-sensing, and this is that R-on-T, right? So the sensitivity is too high, it's not seeing, the device is not actually seeing the ventricular contraction. You have R-on-T, and then you have torsades. And this is over-sensing, again, failure to pace, and here, the sensitivity is probably too high, and so this noise that's here, the device is seeing that as intrinsic conduction, and it's not pacing. Okay. Case three. Patient is admitted to the CT ICU after uneventful CABG and AVR. Pre-op, the patient had biventricular dysfunction, EF of 40%, and mild to moderate RV systolic dysfunction. So the EF was down prior to surgery, and the RV was down. Underlying rhythm is sinus bradycardia, a heart rate of 35, with intact AV node conduction. So post-operative, they're bradycardic, and there is intact AV node conduction. Which of the following pacer modes would be most likely to improve cardiac output? AAI, VVI, VOO, or AOO? You want to improve cardiac output by optimizing your pacer. Is it going to be AAI? Couple of hands. VII? VVI? VOO? Couple of hands. AOO? Okay. So this is your pace, sense, and then what you're going to do, right? So you're going to pace in the atria, you're going to sense in the atria, and then you're going to inhibit if there's atrial conduction. So the answer is A. And why is it A? Because you want AV synchrony, right? So the best way to improve cardiac output, one of the best ways to improve cardiac output with a pacemaker is to ensure AV synchrony. I didn't give you guys the option of DD, right? And a lot of times, you know, putting the epicardial lead on the atria is more challenging than on the ventricle. The atria, they're thinner. When you pull the lead after surgery, there's more risk of tear. So not every patient gets an atrial lead, depends on the surgery. But typically, we pace people in DD if they get both leads. I didn't give you that option, but I gave you atrial pacing and atrial sensing, and you would do that to improve AV synchrony. VV, right? This is your safety mode, right? So your VVI, that's your safety mode. That's going to be if they come out with just a ventricular lead, and you want to make sure that the person does not go asystole on you, but you're not going to necessarily, you won't get synchrony with that because you're not sensing in the atria. And then your VOO, any of these OO modes, right, where it's not sensing, right, that's just asynchronous pacing. It's just going to pace. And in that setting, you're definitely not going to get synchrony. And again, this is sort of what I went over. So AAI, atrial demand pacing. So again, you pace, then you sense, and then what do you do? VVI is ventricular demand, so pace, sense, and then inhibit. Indicated for bradycardia with AV block, I said in the question in the stem that the patient did not have AV block, or if they're atrial fibrillation or atrial flutter, because you can't capture, right, with the atrial lead. If they're in AFib, you're not going to get capture, so you want to be in VVI. But again, it can reduce cardiac output due to impaired AV synchrony. Your DD, that's your universal mode, so A and V sensed, A and V paced, and then you trigger and inhibit. So what does trigger and inhibit mean? Trigger means that, and inhibit means that if you have an atrial lead, it will inhibit itself if there's atrial contraction, and it can trigger ventricular contraction, right? So it can inhibit and trigger, all right? And that is typically what we use. The only issue with that is it can track atrial tachyarrhythmias, and so if that's the case, then you have to switch the mode. And then we only use the asynchronous modes in emergencies or in the, usually in the O.R. Okay, case four. Six-year-old male presents with chest pain, acute decompensated heart failure, and hypoxic respiratory failure. So chest pain, heart failure, and hypoxic respiratory failure due to pulmonary edema. ECG has ST depressions and isolated ST elevation in AVR. Cath demonstrates multivessel disease, including an 80% stenosis of the left main. CPAP is started in the Cath lab. The point-of-care ultrasound in the Cath lab shows mitral regurgitation and possible thrombus at the apex of the left ventricle. The MAP is 65. What is the next best step? So you're standing there. You're helping manage the patient in the Cath lab. You get CPAP put on. The interventionalist is kind of staring at you, and you're like, okay, what do you want to do? Because we're not going to stent stuff. It's multivessel. There's 80% left main. Let's see what we want to do here. Do you, you say, okay, we'll put an impella in. Someone raise their hand. Okay. Put an aortic balloon pump in. A couple of hands. Just put them on ECMO. Less hands. And start an orepi. Okay. All right. Yeah. So I think the next best step is going to be your intra-aortic balloon pump. You don't want to do the impella because there's an LV thrombus. So one of the things you don't want to put an impella in for, don't put an impella in if there's an LV thrombus, because that can be a problem. You also don't want to put an impella in if you have, like, a mechanical aortic valve. One of the contraindications is severe aortic stenosis. And so just answer that in the test question. But in reality, we definitely just shove it across the valve. That's what happens. ECMO, the person is, in my mind, is not unstable at this point and needing ECMO. ECMO is not perfect in these cases either. If you have increased LV afterload, it can lead to, in someone whose EF is quite low, right, distension. And you actually will end up putting in an aortic balloon pump, possibly, to unload the ventricle. And then norepi, I just said the MAP is 65. So I think that the balloon pump is probably the best. And so why? Well, balloon pumps do have indications. We do use a lot of them. I'm going to say that. Just sort of off-the-cuff comment in the sense that, like, a balloon pump is very cheap compared to an Impella. Impella is about $25,000. A balloon pump is, like, hundreds, you know? And it is indicated for cardiogenic shock after MI or a bypass, acute decompensated heart failure. So the key one here is unstable ischemic heart disease with refractory angina or left main stenosis awaiting surgery. That is an indication for it. So we definitely put balloon pumps in in those patients like this patient who has left main stenosis. And we're consulting surgery. And we think that patient's not going to go right away. We want to stabilize them. A balloon pump improves coronary perfusion. So it can be helpful in patients that are having chest pain. And it's protective in that setting. We also use it for complications of MI. We already had a test question about severe mitral regurgitation due to papillary muscle rupture. So a balloon pump is helpful there, dropping afterload, improving cardiac output. Same for a VSD. We use it for unloading with VA ECMO. I'm sure you guys have probably seen that. High-risk PCI, we can use balloon pumps, although a lot of people have moved towards Impellas. And then it's actually, and we recently used a balloon pump in a patient that had refractory, not totally refractory, but it came in with VT storm. And we put a balloon pump in to cool the patient off for a little bit. Significant AI, it will worsen your AI if there's an aortic dissection or aneurysm. A big one is if there's peripheral arterial disease, because you can develop ischemia of the limbs. And then prosthetic aortic grafts. We've gone over a little bit, we just had a test question about this, but what an intra-aortic balloon pump does. So in diastole, it inflates, right, it inflates in diastole, and you get this augmentation of your diastolic pressure, which I'm trying to make this thing work, but that's what this is here. This is our augmentation of our diastolic pressure. That improves coronary perfusion, right, which is what we want. And then when it deflates, it drops your end diastolic pressure. That's less pressure that the LV has to pump against, right? So the aortic valve can pop open, you get improved cardiac output. And then you get this afterload reduction, right? So your augmented systolic peak is lower, that's lower than your non-augmented, sorry, your non-augmented systolic peak is higher than your augmented, right? So your afterload goes down. And that's what you want to see. And it does all those things. So like I talked about, decreases afterload, decreases myocardial oxygen demand, and it can be a helpful device. And I'll end there.

cardiovascular surgery

point-of-care ultrasound

postoperative complications

pacemaker functionality

vasopressors

assist devices