Management of Acute Decompensated Heart Failure

By Laurl Matey, M.S.N, R.N., C.H.P.N.  |  December 16, 2019  |  Emerging Medicine

Acute Decompensated Heart Failure

DeVore and colleagues’ (JAMA Cardiology, Dec 11) secondary analysis of the open-label extension of the PIONEER-HF examined the effect of switching from taking enalapril (10 mg twice daily) to sacubitril/valsartan on NT-proBNP levels. Their analyses suggest that early initiation of sacubitril/valsartan during hospitalization for stabilized patients with acute decompensated heart failure improves patient outcomes.

Review your understanding of the management of acute decompensated heart failure with Dr. Atta Behfar’s comments in K2P’s CV Updates.

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Medical Therapies for Acute Decompensated Heart Failure

Faculty: Dr. Atta Behfar.

Learning Objective

Use recent guidelines to select appropriate medical therapies for patients with decompensated heart failure.

Goals of Treatment

What are our goals of therapy and how do we get there?

We want to reduce congestion. We want these individuals to be able to ambulate and get back to a Class II or I heart failure, if possible, and we want to reduce the rate of readmission. By doing these three, we hope to extend survival in this population.

In order to treat these people appropriately, I like to break it down into four boxes: “warm & dry”, “warm & wet”, “cold & dry”, “wet & cold”

Therapeutic Intervention

So the two questions we ask are: A) are they congested and, B) are they perfusing?

We have all these hallmark markers of congestion and perfusion. Remember that, in heart failure, as we lose systolic function, so as this E-max line shrinks, the way that we fix our stroke volume is by pushing our preload.

Vasodilate & Diurese

We overfill the heart in order to compensate for the lack of stroke volume that we get with contractility. This, if it sort of goes awry and these individuals are perfusing, but they’re congested, it means that we need to likely vasodilate and diurese them.

We sacrifice a little bit of this preload in favor of dropping their afterload. Because this E max line is so shallow, the the gains you get in drop of afterload outweigh the losses you have in the preload.

Inotropes & Diurese Vasodilate

Now, what if they’re wet but they’re not perfusing?

We still want to diurese them. We still want to get that volume off. We still want to vasodilate them, get that afterload down.

But now we need inotropes. We need to improve that E-max and try to normalize it as much as possible. Because it’s not just simply a matter of having a lack of preload and afterload. The stroke volume needs are so much higher because now we have end organ perfusion deficits. And so inotropes are implemented.

Inotropes & MCSD

Now, sometimes, what we get are individuals that are both dry and non-perfusing.

This is sort of the most serious condition. In other words, this is very end stage.

We’ve done everything we can to dry these individuals out, and still we have high creatinine, poor mentation, cold digits. And in this case, the focus really is no longer on vasodilatation or diuresis. It’s purely on inotropes and a shift in focus to mechanical support.

Likely Non-cardiac

This can be offered percutaneously, so we often put temporizing measures like balloon pumps, Impellas, and ECMO devices in these individuals as a bridge to things like LVAD and transplant.

It’s also important to note that sometimes these guys don’t have acute decompensated heart failure. So if they’re perfusing well, and they’re not congested, maybe they’re in septic shock. Maybe they have pneumonia. So it’s important, using this algorithm, to also say, “This isn’t heart failure. This is something else.” So I think that those four, if you can keep them in mind, and these two questions, really will serve you well here.


So, now, let’s say we have the diagnosis at hand, what do we do?

Well, diuretics are the mainstay of therapeutic intervention here. I think when we use diuretics, we should think about some of the deleterious effects. We can get electrolyte disturbance. We do drop the preload and can diminish cardiac output. That alters GFR. And it can, in some cases, alter neurohormonal activation, just with how it influences the sympathetic feedback loops.

It’s important to do this right away. So people arrive, let’s not wait 24 hours to give them their first dose of diuretic. The first dose needs to be given, so when they say, “What’s the next best step in management?” on the question, and they’re in the ER, give them the diuretic. Right?

You’ve got to start the treatment right away. Doesn’t matter if you do continuous infusion or a bolus format. They both work the same. Sometimes, we arrange these just based on the patient’s situation and their renal function. And the goal urine output is somewhere between three and five liters per day. So when they give you the volume of urine output, know that if it’s in this range it’s likely adequate and you’re achieving your target, even if the patient remains symptomatic.

Resistant to Diuretics

All right, so if you try this and they’re resistant, obviously you keep doubling the dose every two hours. You can use distal tubule active agents such as chlorothiazide, hydrochlorothiazide, or metolazone.

These potentiate loop diuretics and make them work more aggressively. And then, make sure that these individuals aren’t drinking everything that they’re peeing, right? So if you catch them at the water fountain and they’re filling their two-gallon jug of water, that four-liter diuresis didn’t really work. So make sure that we talk about compliance.

Other things, remember vasodilators? Extremely important in augmenting stroke volume. And a right heart cath, if there’s any question in regards to cardiac output or pressures, it is extremely useful. We sometimes do consider ultrafiltration. I would have to say it’s a big stretch to get to ultrafiltration, but in some rare cases, if there’s really no other option, we do consider this.

Remember that there’s no impact on creatinine or renal function here. You’re just simply removing fluid. And this does require putting in a Mahurkar, right? So this is a big line that goes in, much like in dialysis, to do this.


Vasodilators are an extremely important component of what we do in acute decompensated heart failure.

Remember that if they’re on an oral chronic nitrate, there’s resistance that can occur with this, and it’s not really the best therapeutic management, chronically, for heart failure patients. Nitroprusside is used, but it requires invasive monitoring so that it’s titrated appropriately.

Remember that you can’t stop it abruptly; you will get rebound and could send patients back into acute decompensated heart failure. Nesiritide is sometimes utilized in the heart failure practice but has not been shown to have significant benefits over conventional therapy, but it is a tool in the tool kit. And more recently, clevidipine, which is a short-acting calcium channel blocker, is utilized as well, much like nitroprusside is utilized to treat these patients and drop their afterload, augment their stroke volume. It’s important to note that although we can get patients out of the woods using vasodilators, use of these agents has no impact on outcomes.

Inotrope Therapy

So we may be able to get them out of the hospital, potentially, a little faster or feeling better quicker, but it does not change any long-term outcomes.

Now, if the patient is not perfusing, it’s extremely important to start inotrope therapy sooner rather than later. You’re losing ground with end organ perfusion, and that means the kidney function is going to precipitously drop and may not be regained, especially if you’re thinking about things like LVAD and transplant long-term. We use this rapidly and as a bridge to either organ replacement therapy or even the decision one way or another.

Remember that this is not a good option for heart failure preserved ejection fraction. This is really utilized primarily in the reduced ejection fraction area. It almost always requires monitoring unless patients are on a chronic stable dose. Very important to think about this when patients present with shock and are not responding to the early interventions of diuretics or vasodilators.

Long-term, we either utilize this to support patients as an outpatient. You know, 85-year old with decompensated heart failure, we can’t get them out of the woods. We put them on chronic inotropes and palliate their symptoms so that they can have good quality of life. As an alternative, we can also use inotropes to bridge people to transplant and LVAD. And actually, one of the ways that people change their status on transplant listing is by having these inotropes in place.

For the boards, I think it’s important to understand how each of these inotropes work. And I would just review in your notes how it impacts a PV loop, how it impacts the forced tension, and Starling curve. You always have one or two questions. It takes two, three minutes to memorize this, and those are easy questions to then check off. Otherwise, you know, you just sort of throw your hands up.

Role of Chronic HF Maintenance Therapy

So dobutamine, primarily beta-1 action. Milrinone is a phosphodiesterase inhibitor. Dopamine, remember that in low dose it works on the kidneys, starts to become a beta agonist in medium dose, and can actually become an alpha agonist or vasoconstrictor at very high doses. When do we use them?

So Class I indication is in cardiogenic shock, and you use it early to protect end organ perfusion, thereby protecting long-term outcomes. As we learned earlier, renal dysfunction is a big risk factor for mortality.

Class II-A, bridge to transplant or palliative therapy as a Class II-B agent. And then, another Class II-B agent would be to really improve end organ perfusion in those who are already supported with mechanical support. So if you have an LVAD patient who’s still failing, primarily because of right heart failure, you can put them on inotropes to get them back to baseline. It’s important to remember, also, that dopamine’s low-dose activity on the kidneys does truly improve diuresis and it is a II-B indication.

And actually, in your practice, it’s a thing you can do on the floor that really helps things along with these patients. It’s extremely important to put them on guideline directed medical therapy, unless absolutely not tolerated. We start these both as soon as possible and titrate them both very slowly, but we don’t titrate one fully in favor of the other. We want these both to be on there. Remember that if we forget to do this, we have an independent risk factor for morbidity and mortality.

So if these individuals don’t get on guideline directed medical therapy, the risk of death goes up. So it’s extremely important that unless there’s a good reason not to, we do this.

Right Heart Catheterization

Sometimes, before discharge, we do a right heart cath.

This is done either because we can’t figure out what’s going on with this person, they look like they’re diuresing but they’re just symptomatic and looking awful still, so we want to understand how to change management that tells us volume status, filling pressures, and cardiac output.

But the other reason we use right heart cath is, at the time when we’re thinking about…the patient is stable and we’re thinking about what is the next step for this individual, we want to, let’s say, initiate inotrope therapy, or we want to bridge them to advanced therapeutics. And so we do a right heart cath and actually leave the Swan in and treat these patients more chronically so that they get to their advanced care paradigm.

Cardiorenal Syndrome

Cardiorenal syndrome is a big issue in this population. And I think it needs to be carefully recognized and addressed, and the therapeutic measures that we take need to have this in mind. And I think that, often, in cardiac cachexia, creatinine may not be the best measure.

So using GFR and using other modalities of GFR sometimes is helpful here. Remember what the risk factors are for CKD, especially, you know, these are hallmark risk factors like diabetes older age.

So on a board question, it may be a renally oriented question. Remember that a lot of the reason for renal failure isn’t necessarily that the kidneys don’t see blood, but that the kidney afterload is too high.

In other words, the venous pressure that the kidney faces in the setting of congestion is very high, and so renal function diminishes and GFR diminishes. Certainly, low blood pressure, and diuretics, and things like that also drop GFR, but elevated venous pressure is a big component of that. And so if they have high JVP, you can expect that their kidneys are going to struggle.

Advanced or Refractory Heart Failure

In the setting of refractory heart failure, I think that there’s a few things to really consider. One is, if after acute management you notice that their renal function is failing, in other words, when they’re diuresed and dry, they have very high creatinine, it means that they’re not perfusing their tissues appropriately.

If they can’t be titrated on RAAS or SNS antagonism, you know that their heart’s at end stage. If these sorts of events happen as you treat these individuals, early rather than late referral for advance therapy is extremely important. And the reason I say that is that if they’re discharged to come back in two months to see one of us in transplant, then what happens is that they go into permanent renal failure, and they have liver congestion, and hepatopathy, and suddenly their medical condition becomes much more complex.

So early referral to the transplant VAD center is extremely important, and a discussion with the patient for goals of care is extremely important. What do you want as your next step? Because some people don’t want LVAD or transplant. And so to put them through a bunch of tests when that’s not their goal, I think, is a mistake. And so, discussing what they want is also extremely important for these individuals.

Risk of Recurrence

As I mentioned in the beginning of the talk, the recurrence rate of decompensated heart failure is extremely high: 1 in 4 in 30 days.

It’s very important, and especially in the aging population, to carefully manage the risks of readmission. Remember that in the Medicare population, medical literacy and cognitive function may be altered, and they have a lot more going on than just their heart failure. So the number of pills that they have to manage sometimes becomes unbearable, and the compliance rate, because of that, is hampered.

Making sure that we can simplify their medical therapeutic regimens, I think, is important. Alternative issues that were actually highlighted, also, by Dr. McKie, in tandem with alcohol use, I think, is something to be considered.

High Risk for Readmission

Again, chronic kidney disease is the number one risk factor. Aging is another big risk factor. And I’ve outlined here for you all of the different high yield risk factors that one may see for readmission in this population.

Another big issue with regards to readmission is us. If you look at this chart, the bulk of the patients that are discharged and have come in for diuresis haven’t lost a pound. So even if you’re getting to that three to five liters a day weight loss, if they’re drinking that back and no one’s tracking that, they’re going to come right back in.

A discussion with the patient as well as very careful monitoring of the patient’s weight is extremely important. You need to know what they weigh in euvolemia, and that needs to be highlighted in the chart so that when they come back, if they come back, we can go back to that target.

Goals for Dismissal by Functional Class

They need to be off all inotropes for at least 48 hours, so make sure whatever you’re doing is holding. It’s important that they’re on their oral regimen stably for a while before they’re discharged to make sure that their oral diuretics are now working.

If you take them off of IV Lasix and start torsemide at home, they may be back in two days with fluid overload. It’s important to get their community involved, their family and caretakers involved with education, and it’s really important that we see them back as soon as possible. Goals for dismissal: optimizing their medication, assessing their risk up front, looking at their readmission risks, and then transitioning them to an outpatient paradigm is extremely important. This can be done, again, as a Class I or Class II modality. And also, in the advanced heart failure, again, early referral to the heart failure transplant VAD team may be important.

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