JUAN: A more challenging situation but also it portends poor prognosis. Sodium, again, the lower the sodium, the worse the prognoses come from the ESCAPE trial, also from last decade. And I will say that all of our patients that we see here in the clinic have hyponatremia. To the point that I'll tell the nurse don't even call me if the sodium is 120 or-- unless it's less than 115, then let me know, but don't call me at 4:00 in the morning when the labs get drawn to let me know that the sodium is 126. That's actually a part of chronic heart failure.
But again, lower sodiums will pretend poor prognosis. Same with low blood pressure. I mean, the lower your blood pressure is, the increase hospital mortality. And I will say that most of our patients that we see here, they run in systolics between 80 to 100. Actually, if we see a patient with higher systolics like 120s or 130s and they have a known low ejection fraction, an EF of 10%, 20%, it actually for us, it means that they have an issue with afterload. And that's why they have poor forward flow.
So we'll actually starting afterload reducing agents. There's a mantra, I think, outside in the community where if patients have systolics less than 100, then hold your medications. And we'll have a lot of people holding their meds in the morning and in the evening due to that. And I think that again, as long as your blood pressure it's low but you are asymptomatic, you're not light-headed, you're not dizzy, then you keep your medication. So we try to retrain our patients not to go by the blood pressure number but to go by symptoms. Otherwise, they'll be holding all their medications and then they are really not being optimized.
Finally, troponin levels, they usually get checked when patients get admitted. We really don't trend them or follow them. Again, when they hit the emergency department with heart failure or chest pain, they always have a troponin. But definitely having a higher troponin portends also worse prognosis.
So again, those are five things that you can take a look when patients get admitted that will give you some prediction on mortality in these patients. So, how do we evaluate and match this patient with acute decompensated heart failure? What's the hemodynamic assessment?
So a few things. You can first get a good clinical history and signs and symptoms-- again, is the company it keeps, OK? Don't go by just one number, but go that the group of these patients are bringing to the table.
Like last night, I got a call because somebody dropped their blood pressure. But they were completely asymptomatic [INAUDIBLE] All of the vital signs were normal. So you really need to focus on the company it keeps. So this is, for example, two different patients, a 60-year-old man with a long history of heart failure that comes with three weeks of gradually worsening symptoms, and they are relatively hypotensive. So they have a very delayed cardiomyopathy.
The lungs actually look pretty clear. And again, we know that they have a low ejection fraction. Compared to an 80-year-old woman with a long history of hypertension with one hour of symptoms, sudden onset of symptoms that comes hypertensive. So again, the presentation will be maybe different and the therapeutics will be different. But you need to pay attention to who is the patient person you're appointed.
And there's three hemodynamic parameters that you need to look into. And they're going to be altered. So it's either an issue with preload, so they have increased filling pressures, increased CVP, increased RA, increased pulmonary capillary wedge pressure. Or it's an issue with afterload, you have increased resistance. You have increased SVR.
Or it's an issue with contractility. So it's at least one of the three, if not the three of them. So you have to try to determine that when you see a patient. What is going on? Is this a preload issue? Is it an afterload issue? Is it a contractility issue or it's a mixture of two or three of these parameters?
So from the filling pressure perspective, from the preload perspective, you know your filling pressures, you know your usual numbers. So when you looking into filling pressures, you need to know what is normal. When you look into cardiac output, you need to know what's normal.
So here we have different measurements of output are thermodilution or Fick. And Fick is the one that you can actually calculate at the bedside if you have some information. I will go over that in a few slides. So here the cardiac index at least depending on the book, you might have different ranges which most books will take 2.2 as the normal cardiac index or above.
Again, you can have different sizes. You can have Shaquille O'Neal and Tattoo. And they're going to have maybe similar cardiac output, that's why it's so important to have an index. Because that goes into body surface area.
And then finally, you have the measurements of resistance which is either the SVR, systemic vascular resistance, or the pulmonary vascular resistance. So again, these are the three things that you want to look for in the hemodynamic perspective. Either preload with the filling pressures, the contractility with a cardiac output and index, and the afterload with the measurements of resistance.
So I think [INAUDIBLE] mentioned or showed the hemodynamic profiles for Stevenson. Profiles is from Lynne Warner Stevenson who was at the Brigham for many years. Now she's in Vanderbilt.
So there's four profiles that you can assess at the bedside. And the importance of this is if you had this, then you can decide what your therapeutic is going to be. These profiles take two things into consideration. It's not perfect, it doesn't include SVR or systemic vascular resistance, but it gives you a lot of information.
So either you are congested or not. And that's with an estimated wedge of 22. Or you are well or not perfused. So either you're dry or wet, or either you're warm or cold. So the ideal circumstance, the ideal hemodynamic profile is profile A. That means you're warm and you're dry.
The most common garden variety presentation you're going see in the clinic is profile D, you're warm and wet, so you have increased filling pressures. The profile Cs the one that we see here a fair amount which is cold and wet. So you have low cardiac index and that makes you cold, and then you're congested, that make you wet.
And then finally, the worst of the profiles, which is profile L, which is cold and dry. You only have low cardiac index, but also your filling pressure is actually normal. So if you know those hemodynamic profiles, you will actually know what therapeutics you'll need to get to a profile A. So if you're a warm and wet, usually-- again, patients come with decompensated heart failure.
They look warm or they look wet, they went up on their weight by 5 pounds, 10 pounds. They kind of lay flat in bed. They have orthopnea, et cetera. Then you need to dry them as long as they're warm, meaning that they have normal cardiac index.
If you have the profile Cs or L, they usually are associated with cardiogenic shock where you need to not only to dry them but you also need to warm that. So you need to make them from cold to warm and you need to make them from wet to dry. So most of these patients if you can assess that at the bedside, then they not only need diuretics, they also need either inotropes or vasodilator therapy.
So I think this is the slide that you saw from [INAUDIBLE] a few talks before. So this, again, this gives you the four hemodynamic profiles. The one thing that is not included is the SVR, the systemic vascular resistance. And the tip for this is really those patients who have higher blood pressure than what is expected.
So you have someone with an ejection fraction of 10% or 20% and their blood pressure is 120s, 130s, 140s, so that will give you a clue that their SVR is high. So the way I explain this to patients is that if you have a small straw and you have to blow through it, it's very hard to blow through. You have to put a lot of pressure compared to how a bigger straw which you can blow with less resistance.
So when you have a high resistance, you pump your heart, you won't be able to pump against a high resistance. So you need to lower that resistance. And that's why you use afterload reducing agents. So profile A is what we want to have. We have patients warm and dry.
Profile B, the most common profile you're going to see in the community, you have patients with normal or low cardiac output. They might have normal or high systemic vascular resistance but definitely have increased filing pressures. Profile C, these are patients that you can see they're in cardiogenic shock. They have low cardiac output. They Have increased filing pressures and they might have increased systemic vascular resistance.
And finally, profile L, which is the most sick of them, they definitely have low cardiac output. They have increased or normal systemic vascular resistance but their filling pressures are normal. And these are the patients that we tend to see most commonly in the [INAUDIBLE] clinic. And again, we have a profile B minus that we kind of created here that it's those patients who are kind of lukewarm. Their cardiac output is slow, but definitely their systemic vascular resistance is high.
Usually, they'll present with higher blood pressure than what you expect. And definitely, they have increased filling pressure. So those are patients that will benefit from therapies in these two profiles. So if you know the hemodynamic profile, you know exactly how to treat them. So if you call me saying I have a patient with acute and chronic biventricular heart failure with reduced ejection fraction and they have a profile B or profile C, I know exactly what kind of patient you're talking about.
You don't need to give me the whole picture of oh yeah, they have leg swelling, and they have orthopnea, and they have liver congestion. Again, you tell me the profile, and I know exactly what kind of therapeutics they need.
ROHAN: Hey, Juan, this is Rohan. If you go back to the slide for the audience, how do people transition from A to B to C to L? Is it one to one or can somebody go A to C or B to L? How does that work for the public?
JUAN: Yeah, so actually I have a slide on that in a little bit. But in general, again, this is where you want to go, where you will be, profile A. So you want to be warm and you want to be dry. So most patients are going to present with profile B, so they're wet, but they're warm, meaning that they have enough perfusion to their vital organs.
So in this patient, you should see normal kidney function or ideally, you should see normal kidney function. You shouldn't see any signs of end-organ perfusion issues, no liver congestion or liver failure. You should see these patients actually in general with good mentation, they're just wet. So these are patients that you can just dry.
You can give diuretics and you can get from a profile B to a profile A. Profile C, again, they're cold and wet. So you cannot just dry them. If you put up 200 milligrams of Lasix in the IV, peripherally, it's going to stay there. There's no circulation.
So you need to increase the circulation. You need to increase the forward flow. But you need to get them from profile C to profile B. And how do you do that?
Well, you will need inotropes. You need to warm them up. You need to increase the circulation. And concomitant, you can do diuretics, but you have to warm them up. Otherwise, whatever diuretic you're giving is going to stay in the-- it's not going to circulate.
And then profile, L, actually those are the most sick ones. Usually, you need to get them from being cold to be warm. And sometimes, actually, you need to give fluids, because they're dry. But you need to be very gentle doing that.
And again, these two profiles down here, those are profiles that you might need to start considering mechanical support, temporary mechanical support. Those are [INAUDIBLE] and cardiogenic shock. So again, when patients come here or come to your clinic and they already have symptoms of heart failure, you are only seeing the tip of the iceberg. You're not seeing what has happened previously in the past few days to weeks.
And that's why some of these new devices or hemodynamic monitors that we have remotely, they can help to discern when that-- or part of that iceberg that you're only see the tip of it. So why do people have acute decompensated heart failure?
Well, most of the time, it's noncompliance. They don't take their medications. Sometimes they again, have dietary indiscretions, and that's very common with a lot of patients in terms of fluid and salt restriction. So it's not uncommon that once we fix that, they stop having visits to the emergency.
So we talk about salt restriction, no more than 2000 milligrams of salt a day. And fluid restriction, no more than 50 ounces. And many patients will come here saying, well, my doctor told me I need to flush my kidneys. Or I need to take at least a glass of water a day. Well, that's for a normal heart.
If you have heart failure, you have to have a fluid restriction. How much? Well, it depends on your physical activity, depends on your size. You cannot have the same food restriction for Tattoo than for Shaquille O'Neal, but there has to be some sort of limit. So we usually say 50 ounces. Some patients may need 60 or even 70 ounces, but there has to be some restriction.
Purely control hypertension-- again, ischemic event or ACS. I just have a patient that was very stable with an ejection fraction of 20% for four years, pretty functional and NYHA functional class I or II. And he had AFib last week and he kind of went down the drain.
So now we have one in [INAUDIBLE] and we had to do a lot of therapy. So patients can be stable and a reading can really push you over the edge. Infection is the same issue. It's physiological stress, [INAUDIBLE] and of course, worsening renal function. So why do-- again, people get readmitted for heart failure? Again, diet noncompliance and medication noncompliance are the most-- we put them together-- the most common reasons.
And then you will hear a lot about cardiorenal syndrome in heart failure. Again, these are patients who it's not uncommon that you try to dry patients, you're giving the right amount of diuretics and they still are not pulling through. They still have signs of decreased cardiac output.
And then when they come for your next visit, their kidney function is worse. So in general, those patients have decreased cardiac output due to neurohormonal activation and diminished blood flow to the kidneys. So that means decreased renal perfusion.
So, what does that entail? It's impaired renal function, increase water and sodium retention, and decreased cardiac performance. So we see a fair amount of these patients. And once you warm them up or you are using the right amount of medications, a afterload reducing agent, et cetera, then the kidney function starts getting better.
So we talked about the three hemodynamic parameters in terms of what to look for, but what are the symptoms and signs you're looking for? Well, high filling pressures. So how do you know that at the bedside?
Well, again, the company keeps-- now patients are telling you they have dyspnea on exertion, they have PND. They lay flat in bed, and they have to wake up 3, 4 hours later and have to kind of go in a tripod position or open their windows and get a full breath of air. They have orthopnea, they have leg swelling, abdominal fullness. Some of them actually come with nausea and vomiting.
And the first reaction when they come to the emergency is to give them fluids because they're dry. But if you examine the patient, actually, they're wet. So they have abdominal distention, they have gastric congestion, and that's why they feel nauseous.
And weight gain, again, always look at trends. So if someone has a weight of 150 pounds and suddenly they have 160, 170, even if their blood pressure is low, again, examine the patient. They may actually be volume overloaded. Again, they're going to be tachypneic or hypoxic. Cardiac-wise on exam, they may have tachycardia, S3, of course, elevated JVP, hepatojugular reflux or pulsatile liver, so make sure you touch the-- that you examine the abdomen and look for that liver.
From pulmonary perspective, crackles or decreased breath sounds. But I'll show an example that sometimes the lung exam is completely normal. And then of course, abdominal or lower extremity swelling.
Looking into low output stay, low cardiac index, you're going to have hypertension and also irregular thready pulse. Mentation is going to be affected. So these patients come stuporous, they come lethargic. They fall asleep when they're talking to you.
And you put them on inotropes and improve their cardiac output and index and suddenly, they're bright and awake. So that's a very common presentation that we see here for low output. And touch their skin, touch their legs. They look clammy, they look cool. I mean, not even cool, cold.
Touch their feet with your dorsum of your hand, and they're cold. And once you warm them up, their legs suddenly are warm. So you need to touch patients. You need to make sure that you examine them appropriately and not just go by the x-ray or the BMP because otherwise, you'll miss a lot of information. And they'll tell you, for example, that they have decreased urine output. That's another sign of low output.
And we talk about the high SVR. Again, the blood pressure is going to be relatively normal or even high for what you're expecting. Also, they may have lukewarm extremities and again, decreased urine output. Very important when you examine patients that you look at the jugular veins.
And again, you can have these examples like this that you can see that from a mile away. But the truth is that you need to examine patients. And I think 80% of the time you can really assess if somebody is wet, if someone is volume overloaded just by having a JVP. So make sure you start with the patient standing straight or sitting straight. I think most of the books will tell you that the patient needs to be at 45 degrees.
But if you have a patients at 45 degrees and their JVP is high, in now might be even higher, so you might not be able to see it. But again, the company keeps. Patient's telling you they cannot lay flat, they fill, they gain 20 pounds of weight. They stop taking their pills.
So if you put everything together, you'll expect that that JVP is going to be high. So again, most patients-- unless they're obese or they have a thick neck, you might not be able to see it-- but if you pay good attention, then you should be able to see it. And if you don't see it while standing straight up, then you start putting them down. And at some point, you're going to see it, especially if it's low. At some point when you start putting them flat on the bed, you might start seeing those neck veins kind of pop up. So you need to make sure you pay attention to that.
Again, there are some caveats, of course. Usually, the jugular venous pressure is going to reflect left sided filing pressure, but watch out for situations where it might not like lung disease, obesity, patients with pulmonary embolism or even acute MI, especially if they have RV infarct. There's a lot of practical tips when assessing JVP and you can take a look at this paper from [INAUDIBLE] from I think 2018. The reference will be in the slides.
But it is important to know that from many of the clinical findings that you can see on the patient, rales, edema, and orthopnea or even have a jugular reflux, the JVP is really the one that's going to have the most sensitivity and specificity. Also, one that is very common is bendopnea. Patients will tell you I cannot tie my shoelaces, I cannot put my socks on. And they're just telling you in front of your face I have bendopnea.
So patient's bent over like this, so you can even do the test when they're in your clinic. Just have them bend over and see if they lose their breath. Again, some of them might be obese, et cetera. But I think this is a good way to know if they have volume overload.
Again, sensitivity of other physical exam findings is poor. Rales, peripheral edema, S3, all of them might be helpful, but they might be absent. And just to give you an example, this is someone who came on July 24 and he was a transfer from another institution. And I see him, and this is his x-ray.
So if you see the x-ray, well, does it look a bit wet? Yeah. This is a 50 kilogram patient. And of course, you can see that huge cardiomegaly there. And the NTproBNP was very high but lungs were clear. So many of these patients, especially those with compensated chronic heart failure that come now decompensated, they might have a complete clear long.
So I will say it's rare for me to hear rales unless they have a new diagnosis of left sided heart failure. And this patient already came with dobutamine and milrinone. And when I touched his extremities, actually he was cold. And he had like plus 1 pitting edema. And even with that, I was able to diurese him from 57 kilograms to 50 kilograms in five days without a Swan.
How did I do that? Well, you examined the patient. You know that they have some pitting edema on the legs. But also he had a very prominent hepatojugular reflux. And the viscera in the abdomen can hold a lot of fluid, so make sure that you not only examine the JVP but also try to palpate the liver.
And if you can squeeze that liver and you say that JVP going up on their neck, they're still wet. So this is someone who I kept pressing on the abdomen every morning, and I saw that hepatojugular reflux kind of pop up on his neck, so he was volume overloaded. And we got 7 kilograms out of him without a Swan.
So make sure that you examined the patient appropriately every morning. And right now, that patient actually is waiting for a transplant. You can see here an Impella 5.5. And he's walking with Impella. We tried to put this machine's axillary with an axillary approach. And again, some patients, they may have medical management, and they can be stable. But some definitely need mechanical support.
Again, we spoke about what to look for if you have an elevated right atrial pressure. Or are we looking for left side or right side heart failure, look for the symptoms. The symptoms might indicate if it's left sided only, right sided only, or biventricular failure, so look for them.
And again, the clinical examination. It's important. So assess for congestion, either right sided heart failure, left sided heart failure, or both. And assess for low cardiac output. You have cold extremities. You touch them and they're really cold or lukewarm to your hand. Or, are they warm? If they're warm, you can at least tell from the bedside that likely, they have normal cardiac index.
So again, how to manage hemodynamic abnormalities? We went over the symptoms and signs. We went over the normal values. So if you have increased preload, you need diuretics to reduce volume.
If you have afterload issues, no increased systemic vascular resistance, you can use vasodilators. And then if you have low cardiac index, you have inotropes to augment contractility. Again, this is part of what Rohan asked before. You cannot make a profile C, a profile A, meaning you cannot make someone who is cold and wet, you cannot make them warm and dry directly.
You need to go from profile C to profile A with the use of inotropic supports and sometimes vasodilators, especially if you suspect that they have increased systemic vascular resistance. If you have a Swan in, of course, you can calculate it. But I think many practices are afraid of vasodilators especially when the blood pressure is low.
And the trick for that is that if your tank is full, if your filling pressure high, you can see that JVP, you have signs of intravascular volume overload. Again, you can use these vasodilators. You have to be careful. You can, of course, start with a small dose and then up [INAUDIBLE]. But many patients that we see here, they benefit from vasodilator.
So you can use them on those patients with profile C that you feel that their SVR as high. Again, profile L usually, you need to warm them up and sometimes you need to give fluid back to help with the cardiac inputs. And profile B, in general, just IV diuretics should be sufficient, but you need to give the right amount. You cannot under-dose, and that's one of the big troubles that we see with many practices when they refer patients here.
They're giving Lasix for 40 milligrams, maybe 80 milligrams, but the truth is that they need more than that. And just to give you an idea, you can use up to 400 milligrams in one dose. We use bulimics here a lot, because they have better bioavailability, so we tend to use it.
And it's always important. If you are meeting a patient with heart failure, you need to diurese them IV not PO, unless you're transitioned to PO because you've discharged them. Sometimes if they're profile B and you want to speed up their diuresis, you could potentially add inotropes. But again, this is for profile B minus or profile C. And we talk about our profile B minus. Again, usually the SVR, it's hot.
How [INAUDIBLE]? So the main chunk is really how you can assess at the bedside what is their hemodynamic profile. Let's say that have other tools like a Swan-Ganz. Well, we use a fair amount of Swan-Ganz. I know some practice establishes placing Swan-Ganz either because of the practice are not used to it or the nursing staff is not used to it. But sometimes you really need a Swan to tell you more information, especially if they're not responding to your initial assessment at the bedside for their hemodynamic profile.
So if you cannot have a Swan, you can always also put a PICC line which is, again, peripherally inserted. And with that, you can obtain a VBG, a venous blood gas, and obtain their mixed venous oxygen saturation which is a surrogate or a poor man's way of assessing their cardiac output. Or even if they have a triple lumen catheter that was placed for central access, you can also take a venous blood gas and assess their SvO2. But if you need more information from the hemodynamic perspective, again, the Swan-Ganz is truly way to go.
Many places will have a procedure room to put it in. Sometimes they go into the ICU and have them placed there. If you have anyone going to the cath lab because they're getting a coronary angiogram because they came with chest pain and decompensated heart failure, you can always ask your interventionalist to do a right heart cath on the spot. Or even at least get an LVEDP just crossing the aortic valve. Again, that LVEDP will be helpful to have that piece of information so you can at least have some hemodynamic parameters of what do you need to do.
And once you have that, you can do your calculations, cardiac output, cardiac index, the SVR, and DVR. But even if the only thing that you have is a PICC line, you can still calculate your cardiac output if you have your venous blood gas. There's many apps. You don't need to use all these big formula. There's many apps that you can use to calculate your cardiac output at the bedside.
We spoke about the cardiac contractility. Again, you need to look beyond the EF. I have people with the EF of 10%, 20% that are very functional, NYHA function plus 1 or 2. And I have people with EF of 30%, 40% that can only walk from a few feet before they get symptomatic, OK? So again, it's part of the equation, but it's not all of it.
Especially you need to take into consideration not only the EF, but any associated valvulopathies, mitral regurgitation, aortic stenosis, tricuspid regurgitation. So those are things that also play a role. So people tend to fixate on the EF, but it's not the whole picture.
And again, if you can get one single piece of information on someone who gets admitted for heart failure, if you can put a PICC line or they have a triple lumen catheter in their neck, you can obtain a mixed venous oxygen saturation. And what that's going to give you is a surrogate for cardiac output. It's a poor man's way of getting an idea of the cardiac output.
So if you have [INAUDIBLE] cardiac output is low or you calculate the cardiac output is slow and your SvO2 is low, then that's low output syndrome. So you have heart failure PE hypervolemia. If you have low cardiac output where your SvO2 is high, then that could be anesthesia hyperthermia. Again, this is somewhat unusual.
If your cardiac output is actually high but your SvO2 is slow, then look into what can cause your SvO2 to be low, anemia, hypoglycemia, or high vO2. And then if you have a high cardiac output and the SvO2 is high, usually this includes sepsis. I mean, that's the thing that comes to mind, sepsis, or some high output state.
So again, four things that can cause a drop in your SvO2, you either you don't have enough cardiac output, your hemoglobin is slow to make sure that this patient might need to be transfused and their SvO2 might go high, sats are low, people have pulmonary disease, or oxygen consumption is increased without an increase in oxygen delivery, that's usually hyperdynamic states or sepsis.
One of the things you have available, CardioMEMS. Again, this is a device that it can be placed in the pulmonary artery. It helps to remotely monitor these patients. And it does reduce heart failure admissions. It does improve quality of life. It's usually indicated for people with NYHA class III. It does not improve survival, but it's a tool that it's available.
And the reason why it's helpful is because it might give you an idea about the filling pressures before patients get symptomatic. So this is a way to actually act before they have clinical symptoms, OK? The tip of the iceberg.
As you know, since July 1st, 2020, now there's coverage from Medicare to place these devices here in Florida. Other ways that you can assess their hemodynamic profile. Most patients that have HFrEF are going to have a device. Many of these devices have intrathoracic or OrptiVol. So some clinics will have a monitoring in their clinic that they can get interrogated.
Also if you know that the patient had your device interrogated a few days or a few weeks before, you can also look into the OrptiVol and it can tell you the impedance. So that will give you a fluid threshold. And also, it can give you information about the behavior of this patient from a fluid perspective.
Some clinics will have, especially heart failure clinics, will have some impedance of the devices that can measure the impedance externally. Again, we don't have them here. We just go by our physical exam and the company keeps. But definitely, there's a new set of devices like this that will measure your impedance.
If you are into point of care ultrasound focused, you can also look into the IVC. So definitely, the wider the IVC, it correlates with fluid overload. So that's another way. And again, the bigger the IVC, that also is associated with event-free survival like in this graph where these patients have a very dilated IVC compared to the other groups. So that's another way if you have an ultrasound.
And the other way that look into this, looking at the lungs, you look for those villis. And the way I interpret this is like you're in Florida, you are under in a pool, your eyes open inside the pool. And then you're looking at those rays of sun coming into the pool. That's pretty much how it looks. When you have fluid, you have these B-Lines on the lung parenchyma that represent fluid. So if you are into a point of care ultrasound, that's a way to look into it.
And this was also a nice paper published in JACC Cardiovascular Imaging a couple of years ago looking at it and looking at what windows you can get to assess for it. Not only in your bedside practice, but also there's some data on a stress echocardiography and seeing if these lines appear during stress. So again, you can define if they have right heart failure or left heart failure or they're normal.
And same as with other devices, you can have these stress B-lines to start appearing when patients are asymptomatic before the full cascade. So again, looking at the tip of the iceberg. So to finish off again, take home messages, assess your patient, get the H&P, the company it keeps, look at what else is going on with them. Clinical assessments, the beside exam, and try to assess their hemodynamic profile.
The company it keeps, make sure you use trends, look at the weight and the prior clinic visit, look at their other weight if they have recordings of their weight, because that will give you a lot of information, same with trends and labs. Don't under-dose. If your tank is full, you're full of fluid. Make sure that you diurese with the right amount. If you are uncertain about the hemodynamic profile or they're not responding, put a Swan-Ganz.
And in many of these patients, you might need temporary mechanical support. Sometimes you cannot just fix with meds. So make sure you know when to hit the button for these devices. So with that, we'll finish.