Acute Decompensated Heart

F a i l u re
Jennifer R. Brown, MDa, Stephen S. Gottlieb, MDb,*
KEYWORDS
 Acute decompensated heart failure  Heart failure  ADHF  Heart failure hospitalization

KEY POINTS

Acute decompensated heart failure (ADHF) is characterized by the hearts inability to keep up with the
metabolic demands of the body without increasing
cardiac pressures. The clinical syndrome is characterized by the development of acute dyspnea, often
associated with the rapid accumulation of pulmonary edema. ADHF can result from systolic or
diastolic dysfunction or from changes in loading
conditions. The causes of a cardiomyopathy are
diverse, including coronary atherosclerosis, hypertension, valvular disease, idiopathic dilated cardiomyopathy, toxins, metabolic disorders, and
myocarditis; however, an acute exacerbation of
heart failure is usually a result of dietary indiscretion,
medication noncompliance, inadequate dosing of
medication, failure to seek care, or a combination
of all these.
The management of chronic heart failure is known
and well accepted. We know from multiple studies
that beta-adrenergic-blockers, angiotensin-converting enzyme (ACE) inhibitors and aldosterone
antagonists offer a survival benefit in patients with

reduced left ventricular (LV) function. We know

that diuretics make patients feel better, but offer
minimal effect on mortality. We know that patients
who go home with inotropes have worse outcomes.
We know that defibrillators reduce the incidence of
sudden cardiac death and that, in certain patients,
cardiac resynchronization therapy can improve LV
function, quality of life, and survival.
But what do we know about the management of
ADHF? The truth is, very little. And this is alarming
given that ADHF is the leading cause for cardiac
admission to the hospital, and, even more concerning, that 1 in 4 patients with heart failure is
readmitted within 30 days of being discharged.1
The economic impact that heart failure has on
our countrys health system is undeniable and
yet we have not developed a successful approach
for keeping these patients out of the hospital.
Current therapy of ADHF revolves around relief of
symptoms and amelioration of pathophysiologic
and hemodynamic imbalances; yet, data suggest
that there are ways to improve long-term

a
Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1365 Clifton Road, NE
Atlanta, GA 30322, USA; b Division of Cardiology, Department of Medicine, University of Maryland School of
Medicine, 110 North Paca Street, Baltimore, MD 21201, USA
* Corresponding author.
E-mail address: sgottlie@medicine.umaryland.edu

Cardiol Clin 30 (2012) 665671

http://dx.doi.org/10.1016/j.ccl.2012.07.006
0733-8651/12/$ see front matter Published by Elsevier Inc.

cardiology.theclinics.com

 Acute decompensated heart failure (ADHF) is the most common cause of cardiovascular hospital
admission; 1 in 4 patients with heart failure is readmitted within 30 days of being discharged, and
ADHF consumes 1% to 2% of the total health care resources.
 The most effective approach for preventing heart failure hospitalizations is a combination of
improvement in management of these patients while they are in the hospital and comprehensive
post hospitalization care.
 Decreasing the length of hospitalization can increase readmission rate, so optimization of inpatient
and outpatient care is essential, including ensuring adequate diuresis before discharge, optimization of medical treatment for heart failure during the hospitalization, thorough patient education
before discharge, and close outpatient follow-up.

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outcomes. In this article, we discuss the role, in the
acute setting, of diuretics, ultrafiltration, vasodilator therapy, neurohormonal blockade, inotropes,
and mechanical support for treatment of ADHF.
Just as importantly, we need to consider prognosis, discharge planning and optimization of
outpatient care.

THE ROLE OF DIURETICS

Diuresis provides a reduction of intracardiac filling
pressures, thereby reducing pulmonary pressures
and improving patients symptoms. They have
never been shown in the long-term to improve
morbidity or mortality, and, in fact, some data
suggest that diuretics may be deleterious when
used long term. Nevertheless, adequate diuresis
is clearly essential for acute improvement in symptoms. Loop diuretics are the most commonly used
in ADHF because of their superior efficacy and
rapid onset compared with other diuretics. Intravenous diuretics are usually given initially, as
patients with significant volume overload may
have intestinal edema delaying their oral absorption. It is recommended that the lowest possible
dose of diuretic thought to be effective be given
first, as the goal is to precipitate symptom relief
while minimizing potential side effects, such as
electrolyte disturbances, hypotension, and hypokalemia. Bolus doses have been the historical
standard of care. If optimal results are not seen,
the dosage, as well as the frequency, can be
increased until goal diuresis is met. Continuous
intravenous infusion can also be administered.
Studies comparing intermittent intravenous administration of furosemide compared with continuous infusion suggest that either regimen works,
with the total dose being most important.2 Nevertheless, inadequate diuresis and fear of using
necessary high doses are common problems in
clinical practice.
Individual loop diuretics differ in their pharmacokinetic properties. Furosemides bioavailability after
oral administration is variable and approximately
50%, whereas bumetanide and torsemide both
have bioavailabilities closer to 90%. In patients with
decompensated heart failure and simultaneous renal
insufficiency, higher doses of diuretics are often
needed to provoke a therapeutic response. Doses
of 200 mg of intravenous furosemide may be necessary. Combination of diuretics may also be helpful. In
some patients, renal insufficiency may improve with
diuresis because of decreased intra-abdominal
pressure. Often, however, increased diuresis may
worsen the renal insufficiency without eliciting the
needed diuretic response. Such patients may need
more aggressive therapy.

Another challenging question in the hospital

setting is when to transition to oral diuretics. This
is usually done when the symptoms of fluid overload have resolved and the patient is close to a euvolemic state. Too often patients are transitioned
to oral diuretics and discharged when they are still
considerably volume overloaded; this is likely one
reason for the high rehospitalization rate in this
patient population. When a patient is approaching
euvolemia, it is appropriate to consider switching
to oral diuretics, but the dosage must be carefully
considered. Patients should be monitored for at
least 24 hours after the transition to demonstrate
effective response to the oral regimen before
discharge, and close follow-up should be arranged to ensure rapid fluid accumulation does
not occur.

ULTRAFILTRATION
When diuretic resistance develops, ultrafiltration is
an alternative approach for effective fluid removal.
In the Ultrafiltration vs IV Diuretics for Patients
Hospitalized for Acute Decompensated CHF
(UNLOAD) trial, 200 patients hospitalized with
ADHF were randomly assigned to receive ultrafiltration or standard care (including intravenous
diuretics).3 At 48 hours, patients assigned to ultrafiltration had significantly greater fluid loss than those
in the standard care arm; however, the change in
renal function was no better, with patients often
demonstrating increased creatinine when good
fluid loss was achieved. At 90 days, patients assigned to ultrafiltration had significantly fewer heart
failure rehospitalizations than patients assigned to
standard care, perhaps because of the larger fluid
loss. Whether increased diuretic doses in the standard of care group would have achieved the same
results is unknown. Ultrafiltration is reserved for
patients who do not achieve an adequate response
to an aggressive diuretic regimen. The sickest
patients, however, may develop renal dysfunction
with the necessary fluid removal.

VASODILATOR THERAPY
In the setting of decompensated heart failure, there
may be a role for vasodilator therapy to aid with
decongestion. Vasodilators result in decreased
afterload, decreased preload, and a reduced
pulmonary capillary wedge pressure. Vasodilators
may be given orally or intravenously. In the acute
setting, intravenous agents, such as nitroglycerin,
nitroprusside, or nesiritide, are often used. Oral
agents, such as the combination of hydralazine
and isosorbide mononitrate or isosorbide dinitrate,
may also be used.

Acute Decompensated Heart Failure

Intravenous nitroglycerin is primarily a venodilator and therefore results in decreased preload and
decreased left-sided filling pressures. It may also
lower blood pressure. It is an effective agent for
the acute reduction in symptoms in the setting of
ADHF; however, dose escalation is often limited
by hypotension and headache.
Nitroprusside is another option for intravenous
vasodilation, and, in particular, should be considered when reduced afterload is needed. For this
reason, nitroprusside can be particularly useful in
the setting of ADHF secondary to hypertensive
emergency, acute aortic or mitral regurgitation, or
acute septal rupture. Nitroprusside requires continuous blood pressure monitoring, usually with an
arterial line and should not be used for more than
48 to 72 hours, as thiocyanate toxicity may
develop. Additionally, nitroprusside should be
used with extreme caution, if at all, in patients
with liver or renal disease.
Nesiritide is a third option for intravenous vasodilator therapy in ADHF. Nesiritide is recombinant Btype natriuretic peptide (BNP), and has been shown
to decrease the pulmonary capillary wedge pressure and perhaps improve acute symptoms in
patients with decompensated heart failure.4 Nesiritide has been shown to have no long-term benefit.
The Acute Study of Clinical Effectiveness of
Nesiritide in Decompensated Heart Failure Trial
(ASCEND-HF) randomized patients with ADHF to
receive standard therapy and either a continuous
intravenous infusion of nesiritide or placebo. The
results showed no significant difference in the prespecified end point of dyspnea, and at 1 month
the rate of death and hospital readmission for heart
failure was not statistically different5; however, the

investigators also found no evidence of an increase

in mortality or renal injury.
Careful consideration must be taken before
starting these agents and, in particular, close
attention to blood pressure is needed. Hypotension must be avoided to ensure that adequate
renal perfusion is maintained. The effects of
a vasodilator on blood pressure are unpredictable,
with increased cardiac output often minimizing the
blood pressure effects. Although vasodilators
improve hemodynamics in the short term, there
is no good evidence to suggest they provide any
long-term benefit. Retrospective studies suggest
improved outcomes in patients who receive vasodilators as compared with inotropes, but this may
be because of selection bias or adverse effects of
inotropes.

INOTROPIC THERAPY
Inotropic agents increase cardiac contractility,
thereby improving cardiac output and may be indicated in ADHF when low output and poor organ
perfusion are suspected; however, whereas inotropes may be beneficial in improving hemodynamics in ADHF, the use of inotropes is
associated with a number of adverse cardiovascular events, and may worsen patient outcomes
in the long term (Fig. 1).6 Limitations and adverse
effects of inotropic therapy include tachyarrhythmias, ischemia, hypotension, and, with chronic
use, increased pathologic ventricular remodeling.
Intravenous inotropes should therefore be
considered only in the management of ADHF
when other therapies, such as diuretics and vasodilators, have been ineffective. Whenever possible,

Fig. 1. In OPTIME-HF, patients receiving milrinone were found to have a significantly increased adverse event rate
by 48 hours as compared with placebo. (Data from Cuffe MS, Califf RM, Adams KF Jr, et al. Outcomes of a Prospective
Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term
intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA
2002;287(12):15417.)

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inotropic support should be short term, although
inotropes may need to be continued in patients
with severe advanced heart failure who are awaiting heart transplantation or are being considered
for mechanical circulatory support. Despite their
limitations and no controlled studies, inotropes still
play an essential role in the resuscitation of a select
patient population.

NEUROHORMONAL BLOCKADE
A decline in cardiac output leads to activation
of various neurohormonal cascades as compensatory processes. This includes activation of the
sympathetic nervous system and the reninangiotensin-aldosterone axis. Increased concentrations of catecholamines, angiotensin II, vasopressin,
atrial/brain natriuretic peptides, and endothelin are
seen. Although the short-term results of these
processes often are helpful, the long-term consequences are more problematic. The proper use of
neurohormonal blocking agents in the acute setting
is thus difficult, with need to consider both shortterm and long-term consequences.
There are minimal data about how to manage
beta-blockers in patients with ADHF. Discontinuing
beta-blockers in these patients may improve hemodynamics in the short term, but the withdrawal
of beta-blocker therapy may permit more rapid
ventricular remodeling and worsen long-term
prognosis. The goal should therefore be to continue
as much beta-blocker as possible while stabilizing
the patient as rapidly as possible.
Thus, patients who come into the hospital with
ADHF should remain on some dosage of betablocker if they are not in cardiogenic shock. If the
exacerbation is mild, with fluid overload being
the main issue, the home dosage of beta blocker
can be maintained. (However, make sure that the
patient is truly taking the prescribed dosage at
home!) If the exacerbation is more severe, then it
is reasonable to consider cutting the dosage in
half until perfusion is improved. The sickest
patients may need withdrawal of beta blockade.
Patients with ADHF, who have either not been on
beta-blocker therapy or who have not been
compliant with beta-blockers, should not be restarted on beta-blocker therapy acutely. Lowdose initiation may be considered just before
discharge in stable reliable patients.
Long-term use of any medication is improved if
started in the hospital. For this reason, once the
patient has been optimized from a hemodynamic
standpoint, beta-blockers can be started at a low
dose and titrated up very slowly (usually every 2
weeks), as an outpatient. Obviously more caution
should be used in patients requiring inotropic

therapy, and those with symptomatic hypotension,

bradycardia, or recent cardiogenic shock.
ACE inhibitors were the first drugs shown to
improve outcomes in patients with advanced heart
failure. They have been shown to improve survival
when started in patients hospitalized with refractory
heart failure.7 The Cooperative North Scandinavian
Enalapril Survival Study provides the basis for initiating therapy with ACE inhibitors during initial treatment of advanced heart failure while the patient is in
the hospital. Angiotensin receptor blockers (ARB)
can be used in patients who develop a cough or
angioedema with ACE inhibitors.
Agents should be initiated at a low dose in
patients with low blood pressure. In patients who
are being aggressively diuresed, there is a risk of
renal dysfunction and therefore the initiation of an
ACE inhibitor can be delayed until the patient is euvolemic. It is also important to remember when
initiating these medications that patients may experience an early rise in creatinine levels, to approximately 25% above their baseline. The serum
creatinine concentration is likely to stabilize after
4 weeks of therapy, and this rise is expected and
should not be a reason for discontinuing the drug.
Renal dysfunction may be acutely impaired in the
setting of aggressive diuresis, and if ACE inhibitors
or ARBs are held acutely, they should be restarted
when the creatinine returns to baseline.
Patients with advanced heart failure should also
be treated with aldosterone antagonists because
these agents have been shown to improve survival
in patients receiving ACE inhibitors or ARBs.8 They
have little acute hemodynamic effect, and can
safely be started early in most patients. In clinical
practice, early treatment may aid with diuresis,
prevent hypokalemia, and permit the long-term
effects to occur sooner.

Mechanical Circulatory Support

In the sickest patients, usually those presenting in
cardiogenic shock, adequate perfusion cannot be
maintained with the previously described therapies and mechanical circulatory support is
needed. Occasionally patients will present to the
hospital very unstable and in need of emergent
cardiopulmonary resuscitation. In these select
patients, an initial period of support with extracorporeal membrane oxygenation is an effective
strategy to allow triage and stabilization. As these
patients are stabilized, and the medical team gets
to know the patient a little better, the patients
prognosis can be assessed and long-term support
(such as an LV assist device) can be considered
if medical therapy is not successful. On the
other hand, patients who present in more chronic

Acute Decompensated Heart Failure

low-output heart failure and have failed medical
therapy, including diuretics and inotropes, with
refractory poor perfusion and often end-organ
failure, should be considered for a longer-term
implantable ventricular assist device, as either
destination therapy or as a bridge to transplantation. More often than not, patients are transferred to tertiary care centers for consideration of
mechanical support after they have developed
significant sequelae of chronic low-output heart
failure, making them at higher risk for surgery
and poor outcomes. Patients will likely do better
if referred earlier in these circumstances.

PROGNOSIS
Many important therapeutic tools have been implemented over the past 20 years that have
significantly improved the prognosis and quality
of life for patients with heart failure. These include
neurohormonal antagonists, implantable cardioverter-defibrillators, and cardiac resynchronization therapy, as well as advances in mechanical
support and heart transplantation. Despite these
advances, many patients with heart failure still
remain impaired with respect to functional status
and quality of life, and experience an accelerated
course until death.
Advanced chronic heart failure is still associated
with a 1-year mortality rate as high as 51%.9
Multiple biomarkers in heart failure have been
shown to be predictors of mortality in patients
with ADHF. Hospitalization for heart failure represents an important event in the life of a cardiac
patient. It is associated with a high in-hospital
mortality of 15.8%, and 32.0% are readmitted
within 1 year.10 In a pooled analysis of 1256 patients
with ADHF, a troponin of more than 0.03 was found
to be an independent predictor of mortality, with
a 3.4-fold higher risk for death at 76 days (Fig. 2).11
Worsening renal function in heart failure has also
been associated with adverse outcomes. Worsening renal function is common in decompensated
heart failure and is associated with higher mortality.
Moreover, hyponatremia, anemia, and poor nutritional status have also been associated with worse
outcomes in patients with advanced heart failure.
Recognizing higher-risk patients earlier in the
hospitalization is essential to improving outcomes
in this sick patient population.

DISCHARGE PLANNING AND OUTPATIENT

CARE
The most important aspect of acute care may be arranging close and careful follow-up. Thought should
be given to the cause of decompensation for each

Fig. 2. Cardiac troponin I used in conjunction with BNP

improves prognostic value. Those with higher troponin
and BNP concentrations have higher rates of mortality.
(From Horwich TB, Patel J, MacLellan WR, et al. Cardiac
troponin I is associated with impaired hemodynamics,
progressive left ventricular dysfunction, and increased
mortality rates in advanced heart failure. Circulation
2003;108:8338; with permission.)

individual patient, and a plan to avoid recurrence

should be put in place so that future hospital admissions can be prevented. Education on managing
their disease at home, medication management,
and nutrition are paramount. Patients and their families need to understand the dietary and fluid restrictions and have an opportunity to speak with
a nutritionist while in the hospital to make sure that
all of their questions have been answered. Patients
need to understand the importance of weighing
themselves daily, and keeping a written record of
these daily weights at home, to help their cardiologists keep them out of the hospital. Patients should
be counseled that if they gain more than 3 pounds in
1 day or 5 pounds in 1 week, that they should call
their cardiologist immediately for instructions
regarding diuretic titration. This close communication with patients and frequent outpatient visits are
imperative to reducing the rates of rehospitalization
in this sick population. Along these same lines, an
appointment should be made for the patient with
his or her cardiologist no more than 2 weeks after
discharge from the hospital.
Studies show that various home-monitoring
interventions can be beneficial12; however, the
aspects that are important are not clear. Patients
in such programs tend to receive more evidencebased medicines, have earlier detection of decompensation or fluid overload, and may receive
consultations from nutritionists, pharmacists, or
social workers in addition to their follow-up. The
randomized results have been uncertain and
have not clearly shown which aspects of followup care are most beneficial. Some studies have
shown improved survival, but no decrease in

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hospitalization.13,14 Negative studies are often
associated with close medical follow-up in all
patients (including the comparison group).15
Although the most important attributes of close
follow-up care are not known, there is no doubt
that close and knowledgeable follow-up care is
essential.
When seen in the outpatient setting, a continuing
effort has to be placed on medical optimization.
Patients drug regimens should be pushed to
reach target dosages. Medical care providers
may be too concerned about asymptomatic
hypotension and not titrate to proven dosages.
Similarly, patients who appear to be stable are
often not given effective dosages of medicines
that improve long-term prognosis.
These patients need to be seen frequently, so
that aggressive diuresis can continue in the outpatient setting and so that they can continue to
receive much-needed dietary counseling. It has
clearly been shown that frequent communication
between the patient and the caretaker improves
outcomes. Additionally, the patients need to
understand that if their regimens are adjusted by
physicians outside of their cardiology team, they
need to notify their cardiologist right away.
It is also very important to realize, both in the
acute setting and chronically, that patients who
are difficult to manage should be considered for
referral to a tertiary care center. There are many
options for patients with advanced heart failure,
including mechanical assist devices and transplantation, which have dramatically improved the
outcomes in these patients in the long term. These
patients should be referred before damage to the
kidneys or other organs has been prolonged. Renal
insufficiency and prolonged hepatic congestion,
leading to cirrhosis, increase the risk of mechanical
support and transplantation, so it is better to err on
the side of referring too early.

SUMMARY
Congestive heart failure is the most common cause
of cardiovascular hospital admission. Not only is
chronic heart failure a major cause of morbidity
and mortality in the general population, but it also
consumes 1% to 2% of the total health care
resources.16 The total costs for congestive heart
failure care have increased considerably over the
past 10 years. The most effective approach for preventing heart failure hospitalizations is a combination of improvement in management of these
patients while they are in the hospital and comprehensive post hospitalization care. Decreasing the
length of hospitalization can increase readmission
rate, so optimization of inpatient and outpatient

care is essential. This should include ensuring

adequate diuresis before discharge, optimization
of medical treatment for heart failure during the
hospitalization, thorough patient education before
discharge, and close outpatient follow-up.

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Acute Decompensated Heart Failure

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