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Acute Decompensated Heart Failure
Gabriel Sayer* and Sean P. Pinney
Key Pearls
• Acute decompensated heart failure can occur in patients with preserved
or impaired left ventricular systolic function, and is associated with an
increased risk of subsequent rehospitalization and mortality.
• The initial patient evaluation should include an assessment of volume
status, adequacy of perfusion and triggers that led to decompensation.
• Management can be guided by physical examination and rarely
requires pulmonary artery catheterization.
• Diuretics are the mainstay of therapy alleviating symptoms of congestion, and inotropes are reserved for the minority of patients who
present with hypotension and low cardiac output.
• Prior to home discharge all patients should be educated about their
medications, dietary restrictions, weight monitoring and followup
appointments.
Introduction
Heart failure hospitalizations significantly burden the healthcare system.
They account for more than one million admissions yearly in the United
States, often with high levels of in-hospital morbidity and mortality, particularly among the elderly.
1
They signify a deleterious turn in an individual’s
205
20
Chapter
*Massachusetts General Hospital, Boston, MA, USA.
†
Mount Sinai School of Medicine, New York, NY, USA.
natural history of chronic heart failure. Nearly half of all patients hospitalized
with acute decompensated heart failure will be rehospitalized within six
months of discharge. One quarter to one third of patients will die from heart
failure within one year of discharge.
2,3
This chapter will outline the diagnostic and therapeutic approaches to managing hospitalized heart failure patients,
and will discuss the important transition back to the outpatient setting.
Clinical Profiles
There are three general profiles that describe patients with decompensated
heart failure (Fig. 1).
4
The first is characterized by volume overload with
pulmonary and/or peripheral congestion usually associated with systemic
hypertension, so-called “warm and wet.” The second profile refers to
patients who are “cold and wet.” They show signs of hypoperfusion with
diminished pulses, cool skin and congestion with a normal or reduced
blood pressure. The third profile is that of a profoundly reduced cardiac
output with renal failure, poor mentation, hypotension and other signs of
cardiogenic shock. These patients are referred to as “cold and dry.” These
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G. Sayer and S. Pinney
based on evidence of congestion and perfusion on physical examination. Adapted, with
permission, from Stevenson.
4
Congestionat rest
No Yes
Signs/symptoms
of congestion
Low
No Warm and Dry Warm and Wet
perfusion
at rest
Yes Cold and Dry Cold and Wet
Possible evidence of low perfusion
• Narrow pulse pressure
• Sleepy/obtunded
• Low serum sodium
• Cool extremities
• Hypotension with ACE inhibitor
• Renal dysfunction (one cause)
• Orthopnea
• Paroxysmal
nocturnal dyspnea
• Jugular vein
distension
• Ascites
• Edema
• Rales (rare in CHF)
clinical profiles are present in all forms of heart failure and occur in
patients regardless of their systolic function. However, cardiogenic shock
is more commonly seen in patients with decreased systolic function.
The understanding of the demographic and clinical characteristics has
been informed by two large clinical registries of patients hospitalized with
heart failure (Table 1).
5
In general, these patients are of advanced age and suffer from other chronic medical conditions, such as hypertension, coronary
artery disease, diabetes and chronic kidney disease. About half have a normal
or near-normal ejection fraction. Men and women are affected in nearly equal
numbers. The most common presenting complaint is dyspnea, and most
patients have pulmonary vascular congestion or peripheral edema. Typically,
the systolic blood pressure is elevated. Overt cardiogenic shock is rare.
Diagnostic Strategies
The initial approach when encountering a patient with acute heart failure
is to quickly ascertain volume status, adequacy of perfusion, and triggers
that led to decompensation.
207
Acute Decompensated Heart Failure
Mean Age 74 Years
Men 48%
Coronary artery disease 55%
Hypertension 72%
Diabetes 43%
Atrial fibrillation 31%
Renal insufficiency 30%
COPD 30%
Hyponatremia 25%
Mean systolic blood pressure 143 mmHg
Dyspnea at rest 40%
Rales 65%
Peripheral edema 66%
Heart failure is a condition typified by expansion of extracellular
volume. Signs and symptoms of volume overload are present in most
patients with acute heart failure. Typically, hospitalized patients will
report recently experiencing exertional dyspnea, orthopnea, paroxysmal
nocturnal dyspnea or lower extremity edema. Signs of congestion that
may be present on exam include an elevation of the jugular venous waveform, inspiratory crackles, palpable hepatomegaly, ascites or peripheral
edema. Occasionally, pulmonary edema may be present in a chest radiograph, but not appreciated when auscultating the lungs. The reason for
this apparent paradox is a result of enhanced lymphatic drainage of the
lung. The presence of Kerley B lines, the horizontal densities present at
the periphery of the lung bases on a chest radiograph, is a reflection of
increased fluid in the lymphatic system. Chest radiographs are also helpful in identifying cardiomegaly and pleural effusions, typically more
common on the right side than the left. While not exclusively a sign of
volume overload, a third heart sound (S3 gallop) is a specific finding for
decompensated heart failure which often identifies those patients at higher
risk of further hemodynamic compromise.
Of similar importance to assessing volume status is determining the
adequacy of perfusion and, by extension, of cardiac output. Manifestations
of a reduced cardiac output include low blood pressure, cool extremities
with thready or absent pulses and diminished capillary refill. A cloudy sensorium or altered mental status may indicate a reduction in cerebral perfusion. Worsening renal function with elevations of BUN and creatinine is
often a sign of reduced renal perfusion. Based on this assessment of fluid
status and adequacy of perfusion, patients can be classified into the three
profiles that will help guide the treatment decisions discussed below.
4
In addition to assessing the severity and duration of symptoms, it is
also important to identify potentital etiologies that triggered decompensation (Table 2). The most common precipitants of heart failure admissions
are myocardial ischemia, pulmonary infections and failure to adhere to
medical therapy or a low sodium diet. Myocardial ischemia is frequently
present and occasionally underappreciated as a trigger of decompensation.
Increased myocardial wall stress from elevations in ventricular filling
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G. Sayer and S. Pinney
pressures leads to increased myocardial oxygen demand. This demand
may be great enough to produce ischemia even in the absence of epicardial coronary artery stenosis. Elevations in serum troponin have been
associated with an increased risk of in-hospital mortality.
6
Not all triggers
of decompensation are associated with the same risk of in-hospital mortality. For example, dietary indiscretions and medication noncompliance
are associated with a much lower risk of in-hospital mortality than worsening renal function or pneumonia.
7
Determining whether a patient is experiencing dyspnea as a result of
heart failure or from another cause, such as pulmonary disease, can be
challenging. Plasma levels of brain natriuretic peptide (BNP) are sometimes useful in these situations.
4
If a plasma BNP level is less than
50 pg/ml, the cause of dyspnea is unlikely to be related to heart failure. On
the other hand, when serum levels of BNP are elevated above 100 pg/ml,
heart failure is more likely, but other etiologies of dyspnea still need to be
considered. Serum levels of BNP may be elevated above 100 pg/ml in the
setting of advancing age, kidney disease, pulmonary embolism and pulmonary artery hypertension. For these reasons, one must rely on the history and physical examination, more than blood tests, to properly
diagnose decompensated heart failure.
209
Acute Decompensated Heart Failure
Myocardial ischemia
Arrhythmias
Uncontrolled hypertension
Pneumonia or respiratory process
Worsening renal function
Nonadherence to medications
Nonadherence to diet
Pulmonary embolus
Nonsteroidal anti-inflammatory drugs
Excessive alcohol or illicit drug use
Endocrine abnormalities (diabetes, thyroid)
Other infections
Outcomes of Acute Heart Failure
Patients hospitalized with heart failure receive treatment that improves
symptoms, but whose effect on mortality is uncertain. On average,
patients spend about four days in hospital and report feeling better by the
end of their stay. Nonetheless, 40% have residual symptoms by the time
of discharge and about 5% feel no better, or may even feel worse,
9
which
may reflect an inability to completely decongest patients. Although 70%
of hospitalized patients receive intravenous diuretics, only half will lose
more than 2 kg of weight and as many as 20% will be sent home with a
weight that is unchanged or higher than their admission weight.
9
Leaving
the hospital congested and symptomatic sets the stage for future hospitalizations. Currently, one out of every four patients will be rehospitalized
within one month of their discharge.
Admission for acute decompensated heart failure carries with it a significant risk of mortality. During hospitalization, approximately 4% of
patients will die, and 10% will die within three months of discharge.
9
Patients with systolic dysfunction experience a slightly higher rate of hospital mortality compared to those with heart failure and preserved systolic
function. Patients with systolic dysfunction are also more likely to require
intensive care unit admission and spend more days in hospital.
Predictors of increased in-hospital mortality have been identified
(Table 3).
10
They include signs of congestion, such as jugular venous distention or an elevated pulmonary capillary wedge pressure, and elevated
levels of BNP. Hyponatremia, with serum sodium less than 135 meq/L,
and a positive cardiac troponin assay are also poor prognostic signs.
6
Two
of the strongest predictors of mortality in acute heart failure are impaired
renal function and hypotension on admission. One simple clinical algorithm uses only three measurements at presentation (BUN above or below
43 mg/dL, systolic blood pressure above or below 115 mmHg and serum
creatinine above or below 2.75) to discriminate patients into low, intermediate and high risk groups in terms of in-hospital mortality.
11
Identifying at-risk subgroups helps to inform treatment decisions and,
when appropriate, facilitate discussions about advanced therapies such as
mechanical support and transplantation.
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G. Sayer and S. Pinney
211
Acute Decompensated Heart Failure
Systolic blood pressure Admission and early postdischarge SBP inversely
correlates with postdischarge mortality. The
higher the BP, the lower both in-hospital and
postdischarge mortality.
Renal dysfunction Associated with a two- to threefold increase in
postdischarge mortality. Worsening renal
function during hospitalization or soon after
discharge is also associated with an increase
in in-hospital and postdischarge mortality.
Coronary artery disease Extent and severity of CAD appears to be a
predictor of poor prognosis.
Elevated serum troponin level Results in a threefold increase in in-hospital
mortality, a twofold increase in postdischarge
mortality, and a threefold increase in the
rehospitalization rate.
Elevated plasma BNP Elevated natriuretic peptides associated with
increased resource utilization and
mortality.
Prolonged QRS on Increase in QRS duration occurs in
electrocardiogram approximately 40% of patients with reduced
systolic function and is a strong predictor
of early and late postdischarge mortality
and rehospitalization.
Hyponatremia Defined as serum sodium <135 mmol/L, occurs
in approximately 25% of patients, and is
associated with a two- to threefold increase
in postdischarge mortality.
Evidence of congestion An important predictor of postdischarge mortality
at discharge and morbidity.
Functional capacity at discharge Predischarge functional capacity, defined by the
6 min walk test, is emerging as an important
predictor of postdischarge outcomes.
*Adapted, with permission, from Ref. 10.
Management of Acute Heart Failure
The goals of therapy for decompensated heart failure are to:
• Alleviate symptoms;
• Improve volume status and hemodynamics;
• Optimize chronic therapy;
• Educate patients about their medicines and self-assessment;
• Initiate a disease management program when possible.
Treatment for acute heart failure should be initiated soon after arrival.
Identification and treatment of coexisting conditions, such as infections,
arrhythmias and myocardial ischemia, is essential. If an acute coronary
syndrome is present, clinicians should consider early revascularization to
prevent further deterioration of cardiac function. It is appropriate to consider reducing or temporarily discontinuing administration of ACE-I,
ARBs and/or aldosterone antagonists in the setting of worsening renal
function. This is particularly true for patients receiving intravenous diuretics, or combinations of diuretics, which may further worsen azotemia. In
the absence of cardiogenic shock, beta-blockers should be maintained at
the same outpatient dose whenever possible. Reducing the dose or eliminating beta-blockers during acute heart failure hospitalization may result
in poorer outcomes.
A pulmonary artery catheter can provide information about volume
status and response to therapy, but its routine use in clinical trials proved
to be of no benefit.
12
Placement of these catheters should be reserved for
patients with uncertain volume status and evidence of impaired perfusion
or those who may require evaluation for cardiac transplantation or
mechanical circulatory support.
Diuretics
Loop diuretics are the first agents used to treat acute heart failure. When
administered intravenously, they rapidly alleviate dyspnea, often before
producing an effective diuresis. These diuretics block the reabsorption of
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G. Sayer and S. Pinney
sodium in the thick, ascending loop of Henle. They have a relatively short
half-life and once tubular concentration falls sodium reabsorption
resumes. Patients should be treated promptly with doses sufficient to
increase urine output to optimize volume status. It is important to regularly assess a patient’s volume status and the adequacy of perfusion by
recording daily urine output, body weight and orthostatic blood pressure.
Patients should have regular blood sampling to monitor serum levels of
electrolytes, particularly potassium and magnesium, which may become
depleted.
Although loop diuretics improve symptoms of acute heart failure,
their effect on mortality is uncertain and has never been studied in a large
clinical trial. The potential to harm may be more than a theoretical side
effect. There has been a reported direct association between the daily dose
of a loop diuretic and the observed mortality. This relationship is a key
input into the Seattle Heart Failure Model, used to assess mortality risk in
heart failure patients.
12
Loop diuretics reduce plasma volume, which in
turn lowers cardiac output. The kidney senses a reduction in perfusion,
releasing renin, which subsequently increases angiotensin II. This
increase in neurohormonal activation is potentially deleterious, but
restoration of euvolemia quickly leads to sustained reductions in these
counterregulatory neurohormones.
Clinicians frequently encounter patients who inadequately respond to
diuretics. There are several potential explanations for this diuretic resistance. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the efficacy
of diuretics and when used concomitantly can precipitate acute renal failure. Excessive dietary sodium and water intake may occasionally explain
the discrepancy between increases in urine output and lack of weight loss.
Patients with chronic kidney disease have a blunted responsiveness to
diuretics and require higher initial doses. Elevations in central venous
pressure beyond 18 mmHg can lead to renal congestion and a reduction in
GFR. This is one instance where the use of loop diuretics can improve
GFR by reducing CVP to near-normal levels.
There are several strategies to overcome diuretic resistance. If urine
output is inadequate with the initial loop diuretic dose, subsequent doses
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Acute Decompensated Heart Failure