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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
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
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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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.
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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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
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.
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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
REFERENCES
1. Ross JS, Chen J, Lin ZQ, et al. Recent national
trends in readmission rates after heart failure hospitalization. Circ Heart Fail 2010;3(1):97103.
2. Felker MG, Lee KL, Bull DA, et al. Diuretic strategies
in patients with acute decompensated heart failure.
N Engl J Med 2011;364:797805.
3. Costanzo MR, Guglin ME, Saltzberg MT, et al,
UNLOAD Trial Investigators. Ultrafiltration versus
intravenous diuretics for patients hospitalized for
acute decompensated heart failure. J Am Coll Cardiol 2007;49:67583.
4. Young JB, Abraham WT, Warner-Stevenson L, et al.
Results of the VMAC trial: vasodilation in the
management of acute congestive heart failure.
Circulation 2000;102:2794.
5. OConnor CM, Starling RC, Hernandez AF, et al.
Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med 2011;365:
3243.
6. 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.
7. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure:
results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med
1987;316:142935.
8. Zannad F, McMurray JJ, Krum H, et al. Eplerenone in
patients with systolic heart failure and mild symptoms. N Engl J Med 2011;364:1121.
9. Levy D, Kenchaiah S, Larson MG, et al. Long-term
trends in the incidence of and survival with heart
failure. N Engl J Med 2002;347:1397.
10. Tsuyuki RT, Shibata MC, Nilsson C, et al. Contemporary burden of illness of congestive heart failure in
Canada. Can J Cardiol 2003;19:4368.
11. 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.
12. McAlister F, Stewart S, Ferrua S, et al. Multidisciplinary strategies for the management of heart
failure patients at high risk for admission. A systematic review of randomized trials. J Am Coll Cardiol
2004;44:8109.
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