All right. How are you everyone? Sorry, my voice today, it's like I think I had something or a virus or I don't know what happened. Last night I came in here and then today morning I woke up with this voice. So maybe this is the Aloha voice. So I'm happy and honored to be a part of this expert group, and I'm the least expert in this group, and I'm honored to be one of them, and I'm honored to be with Chess and presenting this. But I will give the time to each presenter to introduce themselves and we'll have time at the end of the session for questions, and please feel free to stop us or ask us if you have any question. If you would like to wait at the end, we'll wait to the end to ask any questions. Thank you. Thank you very much. I'm David Boaten. I'm from Wake Forest in Winston-Salem, North Carolina, and happy to be here. I have no disclosures relevant to this presentation, and hopefully we can understand the utility of treating options for AFib and differentiating supraventricular from ventricular arrhythmias. So this is a regular wide complex tachycardia, something we're faced with fairly frequently in the ICU, and I think when we see this, what's the first question we should ask? Probably isn't, can I have calipers? Or gee, can I get a rhythm strip? It's, is the patient hemodynamically stable? If the patient is not hemodynamically stable, electricity. Whoever your current power supplier is, is who needs to be involved to synchronize cardioversion immediately. If the patient is hemodynamically stable, then you have time to look at criteria. And these are the Bregada criteria. They're now 30 years old. But realistically, they have been the backbone for most people's efforts to distinguish supraventricular from ventricular tachycardia. But I find the algorithm daunting. And so, you know, if I am faced with this, I'll ask you to answer, is this VTAC or is it supraventricular hemorrhagic tachycardia? And we don't have a person to do this. So I think this is VTAC. And the reason I think so are these criteria that are really variations of Bregada. I think for me, they're a little easier to keep track of. SVT with aberrancy would typically be a classic right bundle branch block or left bundle branch block pattern. And for most of the time, this is going to be a FIB, sometimes just a regular supraventricular tachycardia. But classic bundle branch block patterns favor an SVT. Non-classic bundle branch block patterns, especially QS and V6, little r greater than r prime in V1, and an RS less than 1 in V6 all favor VTAC. And this person has all of those. So this is VTAC. Extreme left axis deviation, very wide QRS, and even a single lead, very wide being greater than 160 milliseconds. Fusion or capture beats are classic for VTAC, but only seen perhaps in 15% to 20% of VTAC. And RS greater than 100 milliseconds in a single precordial lead is a pretty good indicator that it is VTAC. And so, gee, this is VTAC. How do I treat? And these are the European Society of Cardiology guidelines. And I picked them because I like them better. And so, you know, this is strictly... It is guideline-based. There are differences between the US and the European guidelines. I think I'll point those out. But I think that, clearly, if you think it might be SVT, non-atrial fib, adenosine is reasonable, or carotid sinus massage. Most of the time, though, that's not the usual case, and we'll talk about that in a bit. And known or suspected heart disease. Gee, that includes about 95% of our ICU population, perhaps. And so, you're going to go down the pathway to your right, which is, is anesthesia for cardioversion going to be tolerated? And if it is, go to cardioversion. I think that makes the most sense to me. If you're worried about anesthesia for cardioversion, or you don't want to do it, or don't have an anesthesiologist available, and you don't want to do it yourself, procaine or amiodarone. And I think it's interesting that the European guidelines are really heavy on procaine. It turns out that if you look at most of the data, procaine is a very effective drug. Probably our most effective drug for ventricular arrhythmias. Got a bad rap because chronic use, 50% of people will develop antinuclear antibodies. About half of those are going to develop an SLE-like syndrome. So it's not a drug you would use chronically. But acutely, procaine works pretty darn well. It is a significant myocardial depressant. About 5% to 10% of patients who get procaine will have a drop in blood pressure. And you just got to be aware of that. But I think it is a reasonable alternative. In the US, amiodarone is going to be the first choice. And in the peri-CPR state, lidocaine is not a bad choice. And so if you look at recommendations for pharmacologic treatment of VTAC, there is no consistently best single drug. Every one of the drugs has adverse effects. Every one of them has advantages and disadvantages. Amio has the least impact on cardiac function, but not a zero impact. But it's significantly slower in onset than the other drugs. 150 milligrams over 10 minutes, then a milligram per minute infusion for six hours. And you can repeat the bolus if you need to during that six hour interval. Procaine, probably the most effective. 20 to 50 milligrams per minute until the VT is resolved. And reconsider though if long QT or severe heart failure because heart failure, it can depress myocardial contractility if it's severe. And if you've got a Brugada syndrome, it can unmask the sodium channelopathy and make things worse. Uncommon, but possible. Sotolol, again, reconsider if QT is prolonged. Potentially fairly effective. And then lidocaine. In this setting, it's probably the least effective of these drugs, but it is pretty good in terms of not depressing myocardial infunction. And it is the pharmacologic treatment of choice for polymorphic VT. But if you've got a long QT in polymorphic VT, remember magnesium, two grams IV, and you can sometimes give beta blockers. And I'm going to switch then to atrial fibrillation. Not one that most people have trouble recognizing, but one that we get confused sometimes about who to treat and how to treat. This is a gentleman who was in sinus rhythm, developed atrial fibrillation. His blood pressure is pretty good now, but he has significant heart failure with risk of ejection fraction. EF is less than 40%. Says he feels the palpitations, but denies chest pain. And his shortness of breath is better than it was on admission, but he's still not back to baseline. His SpO2 ain't bad. And it is, though, on significant oxygen with a high-flow cannula. So how would you treat him? And the choices are going to be cardioversion, amiodarone, beta blocker, or nothing. And I'd argue amio here, though I recognize I put a question mark behind it. I think a lot depends on my conversation with this gentleman. If he truly says, I'm really doing pretty well, doc, I feel it, but it's not bugging me. And that blood pressure is not a significant change, if it's not a significant change from his baseline. And everything else appears to be trending. I may leave him alone. Because AFib in the ICU in new onset, and we'll talk about this, especially in someone who has sepsis, usually resolves spontaneously. And so why add another drug to the regimen that might have adverse consequences? And I would consider not doing anything and just waiting. And I think it's worth talking about AFib because it is the most common new onset dysrhythmia in the ICU. It's really common in post-op hearts, the population that I usually dealt with. A quarter of our patients would develop post-op AFib in many cases. Sepsis, a fifth of them are going to develop AFib typically at some point in their ICU stay. And burns also have a high incidence. AFib is associated with a higher mortality in virtually every single study that's looked at. If you have AFib, your chances of dying are higher. But it is almost never the cause of that increase in mortality. When people try to look at cause-specific causes of death, it's not the AFib. So I think it's a great marker that you're sick, but in and of itself, I'm not sure how often it requires treatment. The difficulty is in folks who have stiff myocardium or just very poor contractility, gotta be very careful about rate control in AFib. Remember that your cardiac output in reduced stroke volume states is pretty rate dependent between 90 and 140. You get over 140, your stroke volume starts to fall. You get much less than 90 and your cardiac output begins to fall because the stroke volume is good, but your rate isn't high enough. And so when you say, well, gee, if his rate's a little fast, I'll just give him a beta blocker. If you looked back at this fellow, his heart rate overall on that bottom rhythm shows probably about 100. I would worry about a beta blocker in him, even though I like Esmolol without Ebola. But I think that his rate is getting in that low range where I worry in a fellow with 40% AF that if I lower his heart rate too much, his cardiac output's gonna fall. And so again, beta blockers are generally faster rate control. Metoprolol, five milligrams IV, repeated again, or Esmolol. Amio, generally better rhythm control when given at 150 milligrams IV and then repeating it as needed. Calcium channel blockers use something else. They're less effective. They have a higher risk of hypotension. They just probably aren't terribly useful for atrial fibrillation. Our hospitalists like it and we tell them try not to do it. Digoxin is the least effective primarily because it's not very good drug for rate control. It will eventually, but typically in almost toxic dosing ranges and it takes a lot longer to get control. The choice between beta blocker, amnioron is patient and practice dependent. Markedly impaired myocardial function favors amnio. Rate dependent favors beta blocker. I like Esmolol again, but I generally avoid Ebola's. And anticoagulation is not necessary if you are reasonably rapidly converting them to sinus rhythm. What is reasonably rapidly? It's probably, again, practice dependent somewhere between two and five days. I would argue you don't need anticoagulation for atrial fibrillation. And there's a fair body of evidence that, and this is from post-CABG patients and I'm eagerly awaiting the CABG PACES trial which is scheduled to end recruitment next year. But in patients with new onset AFib with a risk of stroke and death during hospitalization. And at 90 days, the risk of stroke is higher in patients with AFib. But it doesn't change even if you convert them to sinus rhythm. That they still have the same risk of stroke. So I don't know that we need to be overly concerned with either anticoagulation or with conversion to sinus rhythm as long as we think it's a temporary thing, it's a new onset AFib. And so we'll have more data probably in a couple of years, but I think this reflects a lot of current thinking. Thank you. All right, now you have to deal with my voice. My advice to you, don't party a lot the day before your presentation. So, today, what I'm trying to do, I will talk about how you use the arterial line waveform in the ICU to represent the function of the heart, represent like the diseases could happen in the heart. So, we have this screen every day in front of us in the ICU. And every day, we can see the heart line and the waves of the heart line. And usually, as a resident, I use it just for mean arterial pressure. What's the MAP? The MAP is more than 65 or less than 65, and that's it, be done. So, what we're trying to do today to try to use it more than this, try to see if it can represent the heart function and how can we use it to help you to represent the heart function. So, when we divide the arterial line, we divide it into two parts, the anaerobic part and the diacritic part. And the way how I look at it, I look at every part of it to see if that can represent, like it can help me to know what's going on with the heart in that sick patient in the ICU who has multiple other comorbidities. So, the beginning of the heart line, as we know, it's opening of the aortic valve. And after the aortic valve is open, that's when we have the upstroke of the blood flow to the aorta. And from the beginning, we can know if this, not we can know, but can help us to determine if this patient has severe aortic stenosis or has severe aortic regurgitation by looking at the steep part of the valve and of the heart line tracing. If it's very steep, that goes with more like normal to aortic regurgitation. If it's like less steep and goes slowly up, and that goes with aortic stenosis because the heart is facing a lot of resistance to push the fluid, the blood out. And that's the first part of the heart line tracing give us like the systolic upstroke that how is the contractility of the heart doing if I have like a very good cardiac function with a good EF and contractility, I will have like a very good steep upstroke heart tracing. And if it's not, it will be like very slow being down. And then at the peak of it, we have the systolic peak pressure. And we'll talk more about the systolic peak pressure. Because me, personally, I thought this is just the systolic pressure and it's a result from just the flow of the blood through the aortic valve and the aorta and that's it. But this part of the tracing, it's actually affected by the reflected pressure. What exactly happened is when I have the heart is pushing the blood in the aorta, and I have like if I have a normal compliance fizzle, and the blood flow will go into the smaller and smaller fizzles, it reached a point that we have the stiff fizzles. And that's the reflected backflow and like the blood comes back to that resistance that will increase your peak systolic pressure. So if you have an elderly or like someone who's a smoker with the stiffness in his blood fizzles, you will have a higher systolic peak pressure. And actually that was studied and they tried to give some resistance at the femoral artery while looking at the heart line. And they found that there's around 10 to 20 millimeter mercury changes just by increasing the resistance. And that will increase the peak systolic pressure. And then we have the systolic decline, which is we are still in systole. And then we have the aortic valve closure. And our machine, our smart machines in the ICU, it will use that to look at the area under the curve. And that goes with the stroke volume. What's the stroke volume from that heart? And we can use this when we talk about fluid responsiveness, and we talk about the flow track, and we use it to see the stroke volume variation. So that's the way the algorithm that looks at the area under the curve to look at how is the stroke volume of this patient and how does it variate with the maneuver that you're going to do. And then after the closure of the aortic valve, we have the diastolic runoff. And that depends a lot on the systemic vascular resistance. So the higher the resistance, as we know, usually when we look at septic shock patients, I teach my resident and the fellow, I say, like, if the patient has very wide pulse pressure and the diastole is very low and the systole, like, there's a wide pulse between the systole and diastole, that goes with vasodilatation because the diastolic runoff will be low because of the vasodilatation decrease in vascular resistance. And it's the opposite in someone with obstructive shock or cardiogenic shock. So when we talk about the heart line, we said, like, we have systole and diastole and pulse pressure. How can we use the pulse pressure? Nowadays, we can use the pulse pressure in volume resuscitation as well. Like, if you have a patient who has septic shock or he's hypotensive and you're thinking of giving more fluid and your patient has all the qualification for doing this test, what does that mean? Not every patient that you can just do the pulse pressure variation on. There's a lot of significant criteria that you will make your patient can have accurate pulse pressure variation. And most of the machines in the ICU, they will give you the pulse pressure variation according to the changes in the maneuver that you're going to do, like with leg raising or with changes between the heart and the lung interaction. So pulse pressure variation can help you in diastolic, like if there is a big pulse pressure variation can give you a clue this is most probably distributive shock more than cardiogenic or obstructive shock, and the opposite is right. All right. So that's the part that I talked about, which is the top part in here. That's the augmentation of the waveform. So that's usually the more stiff vessels that we have. That's the more reflection of the flow, and that will give us a higher peak flow. And the machine will not just take the, like it will take our machine, and I will talk to the next slide. I don't want to talk about it right now. But our machine does not just take this systolic pressure and diastolic pressure and calculate the map, and I will talk more about this. But the changes, you can see it if you have your line in the femoral artery or your line in the radial artery, your line in the dorsalis pedis artery. So the smaller the blood vessel, you go down, you will see that that reflection higher and higher, and like in this picture in here. So you see that the difference between where the lines ended up, like in comparing the aortic root to the dorsalis pedis artery. So you see like the peak, because that's just for the reflection of the blood flow from the resistant small vessels. All right. So if you look at this two lines in here, or this two tracing, you can say, oh, the systole and diastole, it's the same. And if I just do the map according to the two-third diastolic pressure plus the one-third systolic pressure or any other equation, it will give you the same mean arterial pressure. But the machines, it doesn't work in this way. The machine, it works by just measuring the area under the curve. And by measuring the area under the curve, it's obvious that it's not equal in here. And that's how it gives the map, and accordingly, it will give us the systole and the diastole. All right. So that's why it's very important to look at each part of this tracing and try to use it toward your benefit in treating this patient. The first part, which is mainly for the contractility, and then the stroke volume. And you can see the aortic compliance. And the last part of it can give you the vascular tone and the afterload. So by knowing this, by looking at the heartline many times and trying to put the whole, like, I cannot lie and say, yes, just the heartline will give you the full answer. But it gives you a clue to direct you toward, oh, I need to do an echocardiogram. This looks like this. It will give you a clue, like, this patient most probably needs more fluid, or this patient has very low contractility. So it will give you a clue to do your next step. All right. The other thing, just like in the heartline, when you look at the tracing for the EKG and the heartline, usually there is a delay, as we know, between the electrical and the dynamic movement of the heart, like around 180 millisecond delay in that. So by doing this, so in my first or second year fellowship, I was like, yeah, now I can look at the heartline. I can help myself a little bit. But it's very important to know what you're looking at. And can I use this heartline tracing or not? Or does heartline tracing need adjustment before I use it? Because sometimes you will just go and use the heartline that is, like, giving you wrong answers because there is something wrong with the system of the heartline itself. So when you look at the heartline, we do what we call the flush test or the square test. And that's to help you to look at the accuracy of your heartline, if the heartline has a good waveform, and you can use it for interpretation, and you can use it for your map and everything else. So when we look at the difference between this heartline and this one, it's obvious that the systolic pressures, it's not the same. And diastolic pressure is not the same. So the systolic here will be lower, and the diastolic will be higher. And I cannot see the dichotic notch. And in here, if I do the flush test in here, I will see less oscillation at the end of the flush test. Why is that? Because in here, like, I know this is what we called the overdamped tracing. So that's what will happen when you have overdamped tracing due to bubble in the tubing system, or you have long tubing, or you have any problem in the system itself that will give you, like, it will understimate the systole and overestimate the diastole, but the map will be the same. And the other problem is the underdamped, which it looks very good. And that's the question that I have always from the nurses, hey, Dr. Migri, can't just we go with the systole in this patient? The systole looks fantastic. His map is low, but systolic blood pressure looks good. Can we just, like, forget about the map and go with systole? And I come and look at the tracing, and I see, like, this tracing. And that gives you overexaggeration to the systole. And how can I know? I do, again, the flush test. And I see how many oscillations do I have. And that will give me if this patient have, like, underdamped or not. And the map, gladly, the map will be the same. It will not change in overdamped or underdamped. But the systole and diastole, that will change. All right. And this is the system of the, and my advice to all the residents and fellow, like, be familiar how to put the system of the ART line and how to level it. And yes, maybe you feel like this is the nurse do all of this for us. But try to be familiar with doing it and looking at the tubing system. Look at how to troubleshoot it. Look at the transducer. Where is the level of transducer? Is it, like, at the midclavicular line or not, mid-anxiety line, I mean, or not? Or the tubing itself, did they put any extension or that's the tubing? Because it's specific tubing that it comes with the ART line set, it has, like, specific resistance and everything. You don't want to do any extension or anything because, like, you are trying to help with your lines and everything. So that's ART that causes of the overdamped and underdamped. As we said, like, we have loose connections, air bubbles, and kinks. That's most of the, or blood clots. And that blood clot could be in the system, the tubing system itself, or it could be in the catheter itself of the ART line itself. So this waveform in here, this tracing of the ART line, I had in one of my patients in the ICU. And I didn't know about it at the beginning, to be honest. And I was looking, like, oh, why this patient has, like, three, like, has two aortic notches. That's the first one, if you see in here, it has the aortic valve, oh, you don't see the mouse. Oh. Sorry, I thought you are seeing what I'm. So if you look at the beginning aortic valve opening, like, and the stroke of the cardiac output, it give you the first peak, and then it goes down and give you another peak again. And then it goes down and give you, like, diacritic notch of the closure of the aortic valve. And this is usually happening in patient with hypertrophic cardiomyopathy, or patient has a closure, like, we see it a lot in the ICU. This patient will be dry with hypertrophy of the heart and will give us these two peaks that you have. The first peak, because of the push of the blood, and then because of the obstruction that it goes down, and then the reflection of the blood again will go up again, and then slowly the systolic decline and then the closure. And that gives you a clue, like, that's what made me, like, my attending told me that that's what's going on. So we did an echocardiogram at bedside, and that was the answer, this patient has LVOT flow obstruction. And thank you so much. Thank you. All right, so we're going to be talking about pulmonary artery catheter tracings. I'll say a few things that Mohamed already talked about, which are very important. I think the first thing is, I'm not going to discuss the setup of a PAC catheter, but if you guys are going to be using a pulmonary artery catheter, you guys need to know the right way to set it up, because it becomes a very problematic thing, especially in today's day and age, where we don't have a lot of experienced ICU nurses around, that you might be able to put the catheter in and not get readable tracings after that. So my name is Abhi Jogle, I'm from Cleveland Clinic, and these are my disclosures, but nothing is directly related to this talk. So in today's talk, what we're going to do is, we'll identify the different parts of the pulmonary artery waveforms, and discuss key values of note that you guys should be aware of, and then we'll go into some common abnormalities that you should be aware of as you take care of these patients. So I find this useful, the insertion guide distance, this really kind of tells us where exactly I expect my PA catheter to be, based on the numbers. In a contemporary ICU, 95% of your patients, you'll be putting it in the right IJ, so the numbers that you should be aware of is that at about 20 centimeters you'll be in the RA, at about 30 centimeters, you'll be in the RV. And around 35 to 45 in most cases would be where you'd start seeing your PA catheter tracings. So when we think about the different parts, as I move forward with my PA catheter, you need to understand what you're looking at. Because if you don't know what you're looking at, it becomes extremely difficult for you, especially in cases where people have underlying disease processes. If someone is coming in with, let's say, pulmonary hypertension, has really a dilated RVRA, those numbers might not be the right numbers for them because you are now seeing a much dilated chamber. So the pressure tracings and identifying exactly where you are becomes one of the most important factors to think about. So the first thing that you're gonna look at is the right atrial waveforms. Now, remember, there's five phasic events that happen whenever we are looking at an atrial waveforms. Three positive waves, the A, the C, and V, and two negative deflections, the X and Y descent. All right, now this is important. Like physiologically, we've all looked at this. This really goes over the different aspects of systole-diastole and how our valves are opening or not. The A wave represents the atrial contraction, which occurs at the end of the diastole, and it's an important thing for you guys to remember. And if you kind of trace it with your echocardiographic assessments, you will see that it kind of is a little bit delayed. And Mohammed already talked about the fact that you're going to have a time delay associated with pressure waveforms when you look at electrical activity. The C wave is another important thing for you guys to remember, is the result of the tricuspid bulge in the atrium. And it happens during the isovolumetric contraction of the ventricle. And this coincides with the QRS complex. Now remember, it's important because if there's anything happening with your tricuspid valve, you're going to see very different pressure tracings for the C wave, and then that becomes important for you guys to be mindful of. Now, whenever we're looking at the right atrial waveforms, always locate the A wave and then measure the top and bottom of the A wave to average these values out. If you're seeing a dichroic notch, that usually means that there's some changes that are happening with the tricuspid valve closure. And it is important for you guys to be very mindful that these numbers, or these waveforms, are always matched with your EKG to know exactly which phase off of the cardiac cycle you're in, all right? The normal pressure that you guys should see in most patients with the RA waveform is going to be between one and six. And obviously, if you're seeing signs of volume or pressure overload, these will be much higher. As you move forward, what's going to happen is you're going to be moving on and into the right ventricle. The right ventricle basically is, it's a nice pulsatile waveform, and you should be looking at pressures of between 15 to 30 for your systolics, and about, I would say about between one to six, eight for your diastolic pressures, okay? Again, these numbers become important because you're going to be visually looking at it. You need to understand the waveform itself and understand what the normal numbers should look like. As you go into the RV, always be mindful that you might cause some irritation to the heart and develop some degree of arrhythmia. So be always mindful and looking at your EKG as you move forward through your RA. Now, remember this, the RV pressures are always measured at the peak, all right? And again, this is right after the QRS waveform. And an important factor for you guys to remember is that the RV waveform does not have a diproduct notch. Again, this is important because it distinguishes the RV from your pulmonary artery waveform. And it's important for you guys to be aware of that. As we move into the pulmonary artery, the things to remember for you guys are that as soon as you pass through the pulmonic valve, you will see a slight change in the waveform. What usually will happen is that you'll see the diacrotic notch appear, but also your diastolic pressure will go up. So remember your RV, a normal RV diastolic pressure is going to be about six to eight or so. And as soon as you go into the PA, what you'll see is a jump in your diastolic to about anywhere between 10 to 12, 14 or so. So that's important because as soon as you see that, visualize and make sure that you're seeing a diacrotic notch. Now, when you're doing these things in real time, like this is as you get more comfortable, these are really fast things that you can do within seconds, right? Like experienced providers will do it very quickly. But remember that if you've not really thought about these, it can become problematic. Why? Because if you have an abnormal heart and you're not looking for these specific things, you might see erroneous pressure tracings, you might see erroneous pressures, and you might not be able to understand exactly where you're at. So the core concepts of understanding the shape of these waveforms becomes extremely important. Now, as soon as we are into the pulmonary artery, like you're gonna get your pressure tracings from there and you're gonna think about going ahead and wedging this PA catheter. So what are the things that you should be thinking about as you are going to be performing a wedge for a pulmonary artery occlusion pressure? So slowly advance the catheter. And once you're around, I would say not even 50 to 60 centimeter, like once you're around 40 to 45, be mindful of exactly how your pressure tracings are changing and go slowly. And you're gonna wait till you start seeing this pulmonary artery waveform change into a venous looking waveform. So we talked about the RA waveform in terms of the arterial changes that you're seeing. So what you're looking for is a venous form, a like change that's happening very similar to what you had been seeing in your right atrium, because as soon as you go into a wedge position, what's really happening is that you're looking at your pressures in the left atrium, okay? So your left atrial pressures would be the surrogate marker that you'll be looking at when you look at the PA catheter in the wedge position. Key things to remember, the pressure usually in a normal person is going to be six to 12. Your pulmonary artery diastolic pressure will give you a rough estimate of what your PA occlusion pressure should be. And remember that your PA occlusion pressure should not be higher than a PA diastolic pressure. And we'll talk about that in a second. The main thing is if that's happening, most likely what's happening is that you have over-wedged your catheter. All right? Now, a key thing for you guys to remember is that when we do this, this is an important factor for you to be looking at your left atrial pressures that really tells you if there is anything changing in the left atrium that is causing subsequent changes in your RA and RV, all right? So, remember a wedged PA catheter is basically facing a column of fluid. And that's basically going to give you the pressures that you are interested in. Now, once you have developed your, like you know, you've wedged your patient, the other thing to remember always is that you want this PA catheter referentially be in the west zone three. If you're not in the west zone three, most of the times it's because you've over-wedged the catheter. You might get erroneous readings because your pressure waveform, especially your A and V waves, are not very effectively seen in an over-wedged catheter. The other thing to always remember is that when you do wedge, right, you don't want to leave it wedged for too long, okay? You will cause harm if you forget. So, always, always, always make sure that you have deflated your catheter after you have wedged and gotten your initial readings for these patients. So, what are the things that you need to be mindful of when we do look at the pulmonary artery occlusion pressures? So, remember this, that unlike the RA waveform, the A wave occurs near the end of the QRS or the QT segment here, just because what you're seeing is pressure transmission delayed over time because of a longer column of blood that you have seen. And that's important for you guys to be mindful of. And like I said before, right, whenever you look at these pressures, get in the habit of looking at them in the context of the EKG associated with that because that gives you an idea exactly where you are in your cardiac cycle. The other important factor that I see a lot of people kind of mess up is exactly where am I going to look at my pulmonary occlusion pressures? Like, you know, when I have a venous waveform, I'm going to see a lot of variation of pressures. I'm going to see a lot of upticks with my different waves, but also you're gonna see variations associated with respirations. These might be very pronounced specifically in patients who are volume down or in patients who are in mechanical ventilation. So, you need to be very mindful of where exactly you're looking at your pulmonary occlusion pressures. So, the common thing for you guys to remember is always try to locate your A wave before the pressure decline is happening. Measure the top and bottom of this A wave and average these values out at the end of expiration. And that's an important factor for you guys to remember. So, pulmonary occlusion pressures are always looked at the end of expiration. And it's always prudent to get the average off your A wave because it gives you a whole important number for you guys to look at. So, I'm gonna go over a few key exercises. Like, you know, we'll just look at a few waveforms and try to work out what exactly is going on. So, this is a patient where we have wedged the pulmonary artery catheter. And what we're seeing is as soon as the patient was wedged, we see a slow uptick off the pressures as we kind of leave it at wedged. This is a classic example of over-wedging, all right? So, what we're really seeing is that the balloon's basically trapped against the vessel wall. And as time's going on, basically, you're seeing the pressure slowly rise because it's just really deep in. The key thing here is always back off on your PA catheter, get a repeat x-ray, and make sure you're in your vest zone three if you see a waveform such as this. Another thing that you have to be mindful of is what's called an incomplete wedge. This is something that we see a lot in our patients in the ICU, patients who have some degree of pulmonary artery disease already. What happens is that you go in and you will get a venous waveform, but that venous waveform will slowly devolve into something that does not look exactly like a PA waveform, but a mixture of the two. And this is a common problem because I've seen a lot of people basically take this and then take the A-wave and start looking at getting their pressures. The problem is if it's an incomplete wedge, there's a pretty high likelihood that you're gonna overestimate your pressures because you've not wedged completely. So, this is in the same case. So, the incomplete wedge, you can see, like we're seeing very high pulmonary artery occlusion pressures. As soon as we got it to a complete wedge, we saw that the pressures were pretty low and almost normal. The other factor to always be mindful of is that when you do see waveforms that are very much different than what we have talked about, this is again a pulmonary artery occlusion pressure tracing where you're seeing a very high uptick of your pressures. Now, sometimes it's very easy for people to look at this and say, oh, you know, are we still in a PA waveform? But it's not, right? So, that's where I will say you have to go back to your basics and look at exactly which wave am I looking at, right? So, remember, like we always try to find the A and the V-wave. So, we have a pretty nice A-wave here, but we have a very, very high-pressured V-wave. What we are seeing here is someone who has a significant mitral regurgitation that's causing us to have very high pressures. One other thing that I really wanna quickly touch upon is, you know, when we do look at pulmonary artery occlusion pressures, they have to be looked at in the context of what your patient is doing. So, this is a patient where we had the patient come in because of elective right heart cath. And basically, we looked at these very high pressures when the patient was supine. The key thing in this patient was that the patient was morbidly obese. As soon as we got these readings, what we did was we made the patient sit up and repeated the reading. So, what you will see here is, if you look onto your pressures, like you're seeing, like, you know, decently high pressures when the patient was supine. But as soon as we kind of brought them up into a sitting position, we really changed. What really happened was that all the pressure that was developing in terms of your intra-abdominal pressure, the chest cavity pressure, was being transmitted to your heart waveforms. And that's something you need to be very mindful of. So, in this patient, what we did was, we put a pulmonary artery esophageal balloon with the PA catheter, and we got corresponding waveforms with the esophageal balloon. And you can see that, as this patient's sitting up, you're seeing massive, massive negative swings of pleural pressure. So, this is not your, like, cardiac waveforms. These are your pleural pressures. You see really, really significant swings. What that really means is that this is a patient that has very high chest wall compliance that's causing you to have issues. And when we kind of changed them to a sitting position, it kind of changed in terms of, like, us having better waveforms. Now, the same concept you have to be mindful of if you have someone who's on very high peaks, right? Because your very high peaks are going to change your interthoracic pressure in a way that will have transmitted changes on your pulmonary artery readings, all right? I'll end here. I know this was a very brief, like, you know, look at PA catheters. It's a much more complex thing. What I will really reiterate for you guys is this, that this is something that you guys need to go and look at again and again and get comfortable with the normal waveforms. Once you are, it becomes easier for you guys to start thinking about, like, when it is an abnormal waveform. The only other thing I will say is this, a PA catheter is a diagnostic tool. A PA catheter is not a therapeutic tool. I hear this all the time. Oh, we put a PA catheter and nothing happened. Nothing happened because you didn't do anything, all right? So if you are going to put a PA catheter, make sure that you have thought about what exactly your next steps are going to be once you do get these readings. Thank you very much. Thank you. All right, good afternoon. Thanks for sticking with us after lunch. I'm here to talk to you today about temporary cardiac waveforms with intra-aortic balloon pumps. and we'll glimpse it, percutaneous ventricular assist devices. My name is Lakshmi Shretheran. I'm an advanced heart failure and transplant cardiologist, and I run the cardiac shock team in the Cardiac Intensive Care Unit at Emory University. Today we'll focus on the following objectives. We'll understand how an intra-aortic balloon pump works and what normal tracings look like. And then we'll look at abnormal tracings so that you know when to troubleshoot or ask for some troubleshooting assistance. And then I'll briefly show you impello waveforms. Let's begin with the intra-aortic balloon pump. So we have the patient on the left-hand side of the screen and the control system that you are all familiar with on the right-hand side of the screen. The control unit has a monitor that displays an EKG, which is used primarily as a trigger source for the balloon pump, as well as the arterial waveform tracing and the pneumatic balloons tracing of inflation and deflation. Importantly, we check balloon pump positioning every single day via chest X-ray. What you see here is a radio-opaque marker. If you look at the radio-opaque marker, it should be about at the level of the carina, about 2 centimeters from the aortic knob. And the reason for this is you do not want the balloon pump to occlude either the brachiocephalic vessels or be too low that it's occluding the renal vessels. In this particular chest X-ray, you see that the balloon pump is actually inflated, which means that this is happening during diastole. There's a gas source, typically helium, but also carbon dioxide, that has a, that's connected to the pneumatic system and with a valve, inflates and deflates the balloon. So on the bottom right-hand side of the screen, you see the, in row A, an EKG. This is the EKG lead and the tracing that you see on the control unit. And during QRS, what you notice in row B is there's deflation of the balloon pump. And when you look further, what you see in rows E versus F is what are the femoral pressures when the balloon pump is working versus when the balloon pump is not working? And I should say aortic pressures. The big thing you notice in row E is that during deflation, right, systolic pressures with the balloon pump are going to be lower than the patient's own intrinsic systolic pressure. And that is key because that means we are reducing afterload for the left ventricle during systole. The next thing you notice as you look further down is that in row E, when the balloon pump inflates, it's diastole, if you correlate it back up to the EKG tracing. And when that tracing occurs, when the balloon pump inflates, that means diastole, diastolic pressure is actually higher than the patient's own systolic pressure. The gray shaded area shows you what the supported mean arterial pressure is in the setting of a balloon pump, which is going to be greater than that of a patient without a balloon pump. We use a balloon pump for this reason, to increase MAP over a greater period of time. We use it in cardiogenic shock, in myocardial ischemia, when a patient might be getting a PCI, and in refractory ventricular arrhythmias. We certainly can't put it in when patients have aortic dissection, since the balloon pump sits in the aorta. It is an indirect offloader of the left ventricle. It sits outside of the left ventricle. And therefore, we also can't use it if someone has significant aortic regurgitation, because blood will go in the opposite direction. As described, one of the primary effects of balloon pumps is that it decreases systolic pressure by about 20% since it deflates during systole. But it increases diastolic pressure by 30%. And as a result, it increases mean arterial pressure, and decreases LV afterload, and presumably wall stress. We also think that it increases coronary blood flow, since the coronary arteries for the left ventricle are perfused during diastole. The balloon pump can only increase cardiac output marginally, typically by about 0.5 liters per minute. Normal balloon pump tracings. This was covered very well in an earlier talk, so I will be brief. But you see that central tracings of the arterial line are noted at the top of the screen, and more peripheral tracings at a radial line are noted at the bottom of the screen. The biggest takeaway from this slide is a concept known as distal pulse amplification, which means as you look more peripherally for an arterial pulse, what you notice is that the systolic peak increases, and the diastolic trough decreases, and this is often because of compliance of various vessels. And in addition, the transmission of the pulse is delayed, hence the delay in the systolic peak that you see radially. And this is why it's important for us to know the difference between understanding the blood pressures that are being read on the controller unit of a balloon pump, versus what you're seeing on a bedside monitor. Okay? So if you want a bedside monitor in a noninvasive setting, noninvasive blood pressure setting, it's basically calculating the highest number it reads over a few seconds, over a few cycles, and the lowest number, and it's assuming that systally and diastolically, and then calculating a map. But that's not what's happening in a balloon pump, which is why your bedside blood pressures, if you have noninvasive blood pressure readings, are going to be different than what you're seeing with a balloon pump. So essentially, we need the balloon pump to distinguish for us the patient's intrinsic systole and the balloon pump pressure during diastole, which will be inflated and higher than the patient's own systole. So to review, if you have this type of tracing, a bedside monitor, a noninvasive bedside monitor will read the diastolic blood pressure as the lowest. It will assume that's the diastolic pressure. And it will calculate it by two-thirds, as you all know. It will assume that the augmented pressure is systole. And it will give you a map that is actually lower than what the balloon pump is providing. The balloon pump augmented map is what you should use for your treatment decisions when you're taking care of patients in the ICU. When we think about normal balloon pump tracings, the biggest takeaway is the assisted peak diastolic pressure from a balloon pump should be higher than the patient's own systolic pressure, since you're inflating the balloon during diastole. In addition, you'll notice that the end diastolic pressure from a balloon pump is going to be lower than the patient's own end diastolic pressure, since deflation is occurring at that point. So the goal of optimizing your balloon pump is to make sure that inflation is happening just prior to the dicrotic notch, when that aortic valve is closing. And again, as we said, that peak diastolic augmented pressure is greater than unassisted peak systolic pressure. As a reminder, deflation, again, during systole. So what about abnormal tracings? Couple of things can happen. You can have early inflation and early deflation. But which is worse? So if the balloon pump starts inflating early, that means it's inflating before the dicrotic notch. It's inflating during systole, and that is bad. That is going to increase afterload for the ventricle, and presumably even decrease cardiac output. So this is a scenario you really want to avoid, early inflation. If it deflates early, however, the bottom line is you're probably just not getting the support you're looking for for the patient, right? You may not be adequately supporting their MAP, but you're not worsening their afterload. On the other hand, you could have late inflation or late deflation. And the question again here is, which would be worse for this patient's myocardial status? Now if it was inflating late, that means it's inflating well after the dicrotic notch that you note on the left-hand side of the screen. And all that means is the aortic valve's already closed. You're already well into diastole by the time inflation occurs. And so you may not get as much coronary perfusion. But if you have late deflation, that means you're deflating once systole has begun. And you're going to have the same issues of increasing afterload and causing harm for the myocardium. So here we're looking at a pressure tracing, where in the middle row you see the balloon pump tracing. And what you notice is there's poor diastolic augmentation. You see both of those waves are about the same level. This can happen quite frequently, and you can see it in a lot of balloon pump issues, most commonly because of positioning. So the first thing to do is get a chest x-ray, see where that radio opaque marker is. Sometimes it's the timing, right? It's late inflation, early deflation, the things we talked about. And if it's that, then you see those two buttons on the bottom right of the screen. That's going to be on your controller unit, and you play with that to see if you can improve the timing, you can improve the waveforms, and hopefully improve the patient's cardiac status. Rarely, it can be because there's a leak in the pneumatic system or in the gas. And even more rarely, it can be mal-sizing of a balloon, if a patient is particularly small or particularly large and outside of sort of the median range of body size. Heart rate becomes a really important reason as well, and this demonstrates why. Since balloon pumps are typically triggered via EKG, now there are other ways to trigger a balloon pump. There are semi-automatic ways based on pressure and other things, which can get a little more complicated, but they work best when EKG triggered. And so since balloon pumps are EKG triggered, the issue is when you're very tachycardic, even in sinus, it will miss the start of diastole often, or it will be a little bit late to inflate during diastole. And as a result, you will have poor diastolic augmentation, meaning you won't really improve their mean arterial pressure. If you have ectopy or any of the arrhythmias that was described in the earlier talk today, then we're in really another set of problems. If you have atrial fibrillation, the balloon pump's going to be a little bit confused. Where are we in systole? Where are we in diastole? And similarly, if you're having frequent ectopy. Finally, at the end of this, let's talk quickly about what we do when balloon pumps fail, because quite frankly, balloon pumps only provide 0.5 liters of support per minute for cardiac output. So most of us who take care of patients in cardiac intensive care units often reach for percutaneous matricular assist devices. In my unit, most of my patients, over 70% of my patients, have an Impella 5-5. We rarely use balloon pumps in my patients. And that's because there's a plethora of impellas available. Typically now, you'll see a CP or a 5-5. A 5-5 is inserted via an endovascular axillary artery cut down technique using fluoroscopy to put the device into the LV. It is a direct offloader of the LV, unlike a balloon pump, meaning it takes blood directly out of the LV and deposits it into the ascending aorta. The benefit of that is that you're really offloading the LV. And you can flow it at 5, 6 liters a minute. The actual controller unit in the monitor, waveforms, I've shown on the right-hand side of the screen. Those can vary a little based on which impella you use, but they all have the same information. In red, you'll see the aortic pressures. And in gray, superimposed behind it there, it will be the LV pressures. So you can see how adequately you are decompressing your left ventricle. And finally, it will demonstrate the motor current. How well is the pump even working for you? And the data we can get from that can be actually far more helpful and superior than our balloon pump tracings. So biggest take-home points for you. Balloon pumps are used in cardiogenic shock in a variety of circumstances. Most hospitals are comfortable using them, and so you'll encounter them frequently. But they only provide about 0.5 liters per minute of additional cardiac output. Timing and rhythm are primary importance. Get a chest x-ray every day. Work hard to keep the patient in sinus. Percutaneous VADs are the next move to reach for when you're not able to support a patient on a balloon pump anymore. Thank you so much. All right. Any questions? Oh, my God. Any questions? All right. Great. Thank you. Good to meet you.

IABP

PVAD

tracings

timing

abnormal tracings

positioning

leaks

Impella device

waveform tracings