I. Acute Heart Failure: What every physician needs to know.

Acute heart failure (AHF), also known as acute decompensated heart failure or cardiac
failure, is not a single disease entity, but rather a syndrome of the worsening of signs and
symptoms reflecting an inability of the heart to pump blood at a rate commensurate to the
needs of the body at normal filling pressure. AHF is often not acute in onset, typically
developing gradually over the course of days to weeks, where the acuity is a function of the
need for urgent or emergent therapy due to the severity of these signs or symptoms.

AHF may be the result of a primary disturbance in the systolic or diastolic function of the
heart or of abnormal venous or arterial vasoconstriction, but generally represents an
interaction of multiple factors, including volume overload. The majority of patients have
decompensation of chronic heart failure (CHF) and consequently much of the discussion of
the pathophysiology, presentation, and diagnosis of CHF is directly relevant to an
understanding of AHF.

II. Diagnostic Confirmation: Are you sure your patient has Acute Heart
Failure?
N/A

A. History Part I: Pattern Recognition:

A patient with AHF typically presents with some combination of increased congestion and,
less frequently, decreased peripheral perfusion. In addition to disturbances in oxygenation
due to pulmonary edema, renal dysfunction is a frequent manifestation of AHF and reflects
the multisystem nature of this disease.

The mean age of patients with AHF is in the mid-70s, with about half of each sex and the
majority with normal or elevated blood pressure.

Most frequent symptoms at presentation:

• Dyspnea (including increasing dyspnea on exertion, dyspnea at rest, orthopnea, and

paroxysmal nocturnal dyspnea)

• Fatigue (including confusion)

• Cough

• Abdominal discomfort (including early satiety, bloating, anorexia)

• Leg pain (secondary to tense peripheral edema)

• Sleep disturbances
The typical patient presents with signs and symptoms of congestion, usually with some
combination of lower extremity edema and pulmonary congestion, normal or elevated blood
pressure and heart rate, and compromised oxygenation proportional to the extent of the
pulmonary edema. A significant minority of patients may manifest worsening of their heart
failure with predominantly abdominal congestion symptoms and signs, rather than lower
extremity edema.

Other patients, often elderly with hypertension, can present with rapid, if not fulminant,
pulmonary edema with no or mild increase in total body fluid. Patients with recurrent heart
failure exacerbations tend to recapitulate their clinical presentations in subsequent
episodes, so obtaining a history of the time course, triggers, signs and symptoms, and
response to therapy of prior events can increase the sensitivity to early decompensation.

B. History Part 2: Prevalence:

In the United States, there are approximately 1 million admissions for heart failure and 3
million admissions where heart failure is a secondary diagnosis. It is the leading cause of
hospitalization in patients over 65 years of age.

In Europe, heart failure (HF) is the cause of 5% of acute hospital admissions, is present in
10% of patients in hospital beds, and accounts for 2% of the national expenditure on health,
mostly due to the cost of hospital admissions.

Patients with a substrate of cardiovascular disease are most at risk for developing AHF,
including those with decreased systolic function (typically due to either ischemic or
nonischemic cardiomyopathy), diastolic dysfunction (usually patients with a history of
hypertension and/or left ventricular hypertrophy), other forms of cardiac disease (such as
severe valvular heart disease), and patients with abnormal vasculature (typically elderly,
hypertensive patients).

Common precipitants of decompensation include one or multiple factors, such as

medication noncompliance, dietary indiscretion with salt and/or fluid intake, myocardial
ischemia, hypertensive episode, and arrhythmias (e.g., atrial fibrillation). The advent and
widespread use of troponin assays has revealed that many patients who present with AHF
have evidence of myocardial necrosis, suggesting that this event represents a medical
condition with ongoing end organ damage, deserving of emergent treatment.

C. History Part 3: Competing diagnoses that can mimic Acute Heart Failure.
Since acute heart failure is manifest by many nonspecific symptoms, there are multiple
competing diagnoses, including:

• Chronic obstructive pulmonary disease (COPD) exacerbation

• Pneumonia
 • Pulmonary embolism

• Venous insufficiency

• Drug-induced peripheral edema (i.e., calcium channel blockers, thiazolidinediones)

• Acute coronary syndromes, including acute myocardial infarction

• Severe cardiac valvular disease, especially acute mitral or tricuspid regurgitation

(consider endocarditis) or severe mitral or aortic stenosis

• Sepsis

• Other forms of noncardiogenic shock, including pseudosepsis due to excessive

therapeutic vasodilator use

• Noncardiac forms of acute kidney injury/renal insufficiency, including overdiuresis

D. Physical Examination Findings.

Most frequent signs at presentation:

• Edema (legs, abdomen, sacral)

• Pulmonary rales, pleural effusion

• Elevated jugular venous pressure

• Positive abdominojugular reflux (hepatojugular reflux)

• Increased body weight

• Increased abdominal girth

• Normal or elevated blood pressure

• Tachypnea

• Increased heart rate

• Third heart sound

Less common signs at presentation, suggestive of low cardiac output:

• Cool extremities

• Hypotension

• Narrow pulse pressure

• Pulsus alternans
 • Impaired end organ function, such as decreased urine output

There are no physical exam findings that individually establish a definitive diagnosis of AHF,
but relevant findings may be considered in two main categories. First, there are findings that
suggest the presence of underlying cardiac dysfunction that provides the substrate for the
AHF episode.

These findings include evidence of left ventricular systolic dysfunction (laterally displaced
and/or diffuse PMI, S3, decreased stroke volume on carotid pulse), diastolic dysfunction
(S4), or both.

Second, physical exam signs can support the diagnosis of AHF by suggesting the
predominant pathophysiologic process involved in the decompensation, such as volume
overload (peripheral edema, pleural effusions, rales, ascites, elevated jugular venous
pressure, hepatojugular reflux), vascular redistribution (elevated jugular venous pressure,
hepatojugular reflux, often elevated blood pressure), or low cardiac output (cool extremities,
low blood pressure, often narrow pulse pressure, pulsus alternans).

Note that patients with chronic heart failure may have markedly elevated pulmonary venous
pressure causing significant dyspnea with relatively mild rales. Patients with AHF due to
vascular redistribution frequently have rapid onset of symptoms that can occur in the
absence of signs of marked volume overload.

E. What diagnostic tests should be performed?

N/A

1. What laboratory studies (if any) should be ordered to help establish the
diagnosis? How should the results be interpreted?
As with physical exam findings, laboratory tests can provide insight into the diagnosis of
AHF.

BNP/ NT-proBNP: Plasma concentrations of B-type natriuretic peptide (BNP) and its by-
product, N-terminal-proBNP (NT-proBNP), are increased in the presence of elevated
ventricular (both left and right) pressure and volume, and have been demonstrated to assist
in the diagnosis of AHF in patients with dyspnea.

While there is no absolute “diagnostic level” of these biomarkers for AHF, most assays have
three ranges. For example, for the typical BNP assay, a BNP less than or equal to 100
pg/mL is strongly suggestive of non–heart failure etiology for the dyspnea, BNP 100 to 400
pg/mL is indeterminate, and BNP greater than 400 pg/mL is strongly supportive of AHF.

As with all laboratory tests, BNP concentrations need to be interpreted in the context of the
individual patient, and some assays provide different diagnostic ranges based upon a
patient’s gender, age, and renal function. In addition, there are known factors other than
CHF that can result in high BNP levels (e.g., age, renal dysfunction, myocardial infarction,
acute pulmonary embolism, and high output states such as cirrhosis) and in lower than
expected BNP levels (e.g., obesity, within 1 hour of flash pulmonary edema, acute mitral
regurgitation, and mitral stenosis).

Note specifically that elevated BNP levels can occur with right-sided heart failure, and may
be present in acute pulmonary embolus.

Electrolytes: Measurement of serum electrolytes can also often assist in the diagnosis of
AHF and are reflective of the patient’s clinical course prior to presentation. Hyponatremia
may be suggestive of neurohormonal imbalance due to advanced or undertreated chronic
heart failure or iatrogenic from diuretics (particularly thiazides).

Hyperkalemia often suggests acute renal insufficiency due to worsening heart failure, but
may also be due to recent initiation of a mineralocorticoid receptor antagonist
(spironolactone or eplerenone), ACE inhibitor, or angiotensin receptor blocker while
hypokalemia is frequently seen in the presence of increased diuretics with insufficient
potassium repletion.

Hypomagnesemia may accompany hypokalemia, especially if diuretic-related, and should

be assessed. Hyperchloremia may be associated with excessive diuresis and volume
depletion.

Renal function markers: Blood urea nitrogen (BUN) and creatinine serve as markers of
renal function. Chronic renal insufficiency is a frequent comorbidity in patients with heart
failure and AHF episodes are often accompanied by acute on chronic renal failure.

This renal insufficiency is usually due to increased central venous pressure (increased
“afterload” on the kidney), rather than decreased renal perfusion form decreased cardiac
output. Cystatin-C is another marker of renal function with the putative advantage of
responding more rapidly to acute changes in renal function. Other markers to assess acute
kidney injury are in development and should assist the evaluation and treatment of these
patients.

Troponin: Increased troponins above the upper limit of normal occur in 15% to 70% of
patients with AHF, depending upon the series and the assay used. Acute coronary
syndromes (ACS) may precipitate AHF, but much more frequently, AHF is accompanied by
mild-to-moderate troponin elevations, suggestive of myocardial damage from the AHF itself.
Distinguishing the “troponinemia” of heart failure from that of ACS or myocardial infarction
can often be challenging and requires synthesis of symptoms, clinical context, and other
diagnostic tests.

2. What imaging studies (if any) should be ordered to help establish the
diagnosis? How should the results be interpreted?
Electrocardiogram (ECG): The ECG can assist in the evaluation of myocardial ischemia, left
ventricular hypertrophy, arrhythmias, and electrolyte disorders as contributing factors to
AHF.
Chest radiography: The chest x-ray (CXR) is useful in assessing the presence and extent of
pulmonary congestion, although it may underestimate the extent of congestion and
pulmonary venous hypertension in patients with chronic heart failure. Pleural effusions may
be detected, as well as evidence of pneumonia, a common confounding differential
diagnosis, comorbidity, or exacerbating factor. Changes in cardiac silhouette, suggestive of
pericardial effusion, or aortic contour (e.g., aortic dissection) should also be examined.

Echocardiogram: In patients with no prior echocardiogram, this test is probably the most
useful noninvasive imaging study, given that it provides information on size, structure, and
function of all cardiac chambers and valves, potential wall motion abnormalities, and
estimates of hemodynamics, including central venous and left ventricular filling pressure.

However, most patients do not require an emergent or urgent echo to guide early therapy,
and a full, more detailed, higher quality, and clinically relevant echocardiographic
examination can be performed after compensation is reestablished. One study
demonstrated no significant difference in left ventricular ejection fraction upon presentation
with AHF compared to later in the hospitalization.

Pulmonary artery catheterization: The PA catheter is an essential and very useful diagnostic
tool in properly selected patients. In patients with evidence of shock in whom it is unclear
whether the etiology is cardiogenic or noncardiogenic, invasive assessment of central
venous pressure, pulmonary arterial (PAP) and pulmonary capillary wedge pressures
(PCWP), cardiac output, and vascular resistances can provide crucial information to guide
appropriate selection of and evaluate response to therapy.

A PA catheter should not be routinely used in most patients with AHF, given the small, but
finite, risk of infection, vascular injury, and other associated complications. One of the
greatest problems with the use of the PA catheter is that members of the medical team may
lack familiarity with wave forms and have limited experience in distinguishing artefact and
recognizing other problems (e.g., migration of the right atrial port into the RV or into
permanent wedge position, setting the pressure transducer to the appropriate height).

Vigilance in assessing data obtained from the PA catheter and interpretation in the context
of other data from the patient is essential to ensure that information used to guide clinical
decisions is correct. Other diagnostic tests, such as noninvasive cardiac stress testing or
cardiac catheterization with coronary angiography, should also be considered in selected
patients.

III. Management.
N/A

A. Immediate management.
The first step in management of the patient with AHF is to address life-threatening issues,
including, but not limited to:
Respiratory failure: The most common presenting symptom of subjects with AHF is dyspnea
and respiratory failure is the most frequent life-threatening condition for these patients.
Immediate administration of the following is recommended:

Reposition the patient: If it is safe to do so, support the patient in assuming an upright,
sitting posture. Many patients will do this on their own to optimize their ventilator efficiency

Oxygen: Although no randomized study has been performed, immediate administration of

supplemental oxygen is the most readily available means to increase end organ oxygen
delivery.

Ventilatory support: If the above measures remain inadequate, rapid application of

noninvasive ventilatory support (CPAP or NIPPV) has been shown to be very effective in
rapidly improving symptoms, hemodynamics, and metabolic abnormalities associated with
AHF. If noninvasive measures are insufficient, rapid intubation with mechanical positive
pressure ventilation should be employed.

Nitrates: Sublingual or intravenous nitrates can be very effective as vasodilators, decreasing

pulmonary venous pressure and relieving dyspnea. Rapid administration of intravenous
nitrates in patients with severe pulmonary edema decreased the need for mechanical
ventilation and myocardial infarction compared to a high-dose furosemide strategy in a
randomized study.

Diuretic: Most patients will also have significant volume overload contributing to the
respiratory insufficiency, so if there is evidence of volume overload (as opposed to volume
redistribution), rapid administration of intravenous loop diuretics is recommended. Although
it has remained controversial, one early study suggested that furosemide also directly
dilates pulmonary veins.

Opiates (morphine) in the setting of AHF have been associated with increased rates of
mechanical intubation, prolonged hospitalization, more frequent ICU admissions, and higher
mortality. While this association may be reflective of the greater disease severity of patients
receiving morphine, these findings argue against routine use of morphine in patients with
dyspnea, as well as for careful monitoring in the select patients who receive opiates.

Circulatory failure: Surprisingly few (approximately 5%) patients present with low output
syndromes in the general HF population, but these patients require aggressive
management of their shock to mitigate or prevent the related end organ damage.

Positive inotropes: To date, there are no “pure” inotropes, since all of the currently available
agents also have some vascular effects, and the selection of the specific agent should
account for these differences. All of these agents increase cAMP and intracellular calcium,
with the related increases in heart rate, myocardial oxygen consumption, and arrhythmias,
potentially resulting in myocardial ischemia, infarction, or death.

Monitoring of response to these therapies depends upon the initial derangements, including
blood pressure, peripheral perfusion, respiratory status, urine output, mental status, and
other end organ function.
Catecholamines such as dobutamine, epinephrine, and norepinephrine have been used to
improve myocardial contractility and increase the heart rate in the setting of AHF.
Dobutamine is a predominant beta-1adrenergic receptor agonist with mild vasodilating
properties.

Recent practice has used lower doses of dobutamine (2 to 5 µg/kg/min) for positive
inotropic effect than previously (10 to 20 µg/kg/min), and due to the potential adverse
effects, the lowest effective dose should be used. Low doses of dobutamine are also
associated with mild vasodilation, while higher doses can cause vasoconstriction.

Dopamine has multiple dose-related effects with mid-range doses (approximately 3 to 5

µg/kg/min) providing increased contractility and higher doses (approximately >5 µg/kg/min)
giving increasing amounts of vasoconstriction in addition to augmenting inotropy.

Phosphodiesterasetype III inhibitors, such as milrinone (in U.S. and Europe) andenoximone
(in Europe), increase cardiac contractility, as well as acting as peripheral arterial
vasodilators. Many clinicians no longer use a bolus loading dose of these agents, so as to
avoid significant hypotension, but a bolus may be used in selected situations. Hypotension,
tachycardia, atrial, and ventricular arrhythmias, increased myocardial ischemia, and other
adverse effects, including suggestions of increased mortality in patients with ischemic heart
disease, may occur and patients should be carefully monitored.

Levosimendan (available in Europe and other non-US countries) is an ATP-dependent

potassium channel activator with myocardial calcium sensitizing effects (and possible PDE
III inhibitor effects), and acts as a vasodilator and inotrope. Many clinicians no longer use a
bolus loading dose, so as to avoid significant hypotension, but a bolus may be used in
selected situations. Hypotension, tachycardia, atrial and ventricular arrhythmias, and other
adverse effects may occur, and patients should be carefully monitored.

Mechanical support: Intraaortic balloon pumps (IABP) can be used at many centers in the
setting of severe cardiac compromise and provide a rapid decrease in ventricular afterload
with some augmentation of forward flow. Its use is contraindicated in the setting of
moderate-to-severe aortic insufficiency and aortic aneurysms/dissections, as well as limited
by vascular access issues and complications.

Other mechanical support devices may be used at specialized centers, including ventricular
assist devices (VADs) and extracorporeal membrane oxygenation (ECMO).

Renal failure: Fulminant renal failure requiring emergent treatment is uncommon in patients
with AHF, but significant renal insufficiency is quite frequent. Emergent hemodialysis may
be used to treat life-threatening electrolyte abnormalities or other severe sequelae of renal
failure.

Ultrafiltration has been increasingly used to treat patients with significant volume overload.
Some centers will initiate veno-venous ultrafiltration in patients with marked fluid overload
(i.e., at least 10 kg), while others reserve this therapy for patients who fail diuretics.

Clinical trials are currently underway to provide evidence regarding these strategies. Careful
attention should be given to the filtration rate so as to not exceed the vascular refill rate.
Some clinicians will monitor for hemoconcentration, presumably to avoid excessive or too
rapid volume removal.

“Renal-dose”dopamine (<3 µg/kg/min) has been controversial, but a recent study suggests
that low-dose dopamine with furosemide provides diuresis with improved renal function and
potassium homeostasis compared to furosemide alone. Nonetheless, many clinicians do
not routinely use dopamine in the setting of mild-to-moderate renal insufficiency, and most
reserve it for patients who fail diuretics. This strategy is also being evaluated in ongoing
clinical studies.

Diuretics remain the most commonly administered agent for AHF. Intravenous furosemide
(or equivalent) can provide rapid symptom relief as well as decrease the underlying volume
overload. Diuresis can also frequently improve renal insufficiency, since the most common
cause of acute renal insufficiency in AHF patients is increased central venous pressure.

Patients receiving high-dose diuretics appear to have more rapid symptom relief with mild
transient worsening of renal function, and there does not appear to be a difference between
continuous infusion versus bolus-dosing strategies in a recent clinical study.

These findings suggest that the strategy that is most appropriate to ensure reliable diuresis
at the specific clinical setting should be implemented. While most patients present with
volume overload, there is agroup of patients with AHF due to volume redistribution, and
these patients will generally not benefit from aggressive diuresis. Electrolyte repletion is
essential in patients with hypokalemia and hypomagnesemia.

Concomitant medications: Many patients with AHF will present with a history of multiple
concomitant medications, including therapies for chronic heart failure. Depending on the
severity of the AHF episode, most of these medications can and should be continued during
their hospitalization.

Beta-blocker therapy in particular should be continued during the hospital course, unless
there is cardiogenic shock, symptomatic bradycardia, or advanced heart block. Patients in
whom beta-blocker therapy is discontinued during hospitalization have worse clinical
outcomes, even when adjusted for disease severity. ACE inhibitors and angiotensin
blockers may be held in the context of acute renal failure, but should be resumed as soon
as possible.

B. Physical Examination Tips to Guide Management.

The physical exam may be used to assess the response to therapy and guide management.

Blood pressure should be carefully followed, though with the advent of improved
noninvasive monitoring, invasive arterial lines are rarely necessary. Hypotension has been
associated with poor outcomes in the setting of AHF, and iatrogenic hypotension should be
assiduously avoided. Hypertension can be one of the major precipitants of AHF and should
be treated.
Heart rate is often a reflection rather than a cause of the AHF episode, and the initial
tachycardia often improves in conjunction with the improvement in dyspnea. However, atrial
fibrillation with rapid ventricular response is a well-known precipitant of AHF.

Tachycardia may occur due to the positive chronotropic effects of some drugs (e.g.,
dobutamine, milrinone), excessive volume depletion, or the onset/ worsening of atrial and
ventricular arrhythmias, especially atrial fibrillation. Bradycardia is less common and may be
due to excess beta-blocker therapy.

Respiratory rate is often not as carefully assessed clinically, and may not be as reliably
sensitive to therapy as other vital signs. Tachypnea may represent inadequate resolution of
the initial episode of dyspnea or a new event, such as a pulmonary embolus. Fever is
suggestive of underlying infectious process, particularly pneumonia or urinary tract
infections, both of which can instigate AHF exacerbations.

Oxygen saturation may be measured noninvasively and is useful to follow in patients with
marginal oxygenation.

Body weight is frequently overlooked in the assessment of the patient until later in their
hospital course, yet can be a very useful measure to follow the response to therapy. Body
weight should be obtained as early as practical in the hospital course. Urine output and
daily input and output measures are also useful corroborative measures, but in many
clinical practices appear to be less reliable.

Jugular venous pressure (JVP) is by far the most useful, and most challenging, physical
examination finding to monitor response to therapy in the AHF patient. Elevation of the JVP
suggests that there is persistent volume overload and additional diuresis is indicated,
whereas a low JVP suggests that there may be excessive volume depletion.

Significant tricuspid regurgitation can confound interpretation of JVP, while the elicitation of
hepatojugular reflux can augment the interpretation. Careful positioning of the patient,
optimizing the visualization of the jugular pulsation and its meniscus, is essential.

Cardiac auscultation can be useful to follow the presence and severity of extra heart sounds
(S3, S4) and murmurs. The disappearance of an S3 and reduction in the intensity of mitral
and tricuspid regurgitation murmurs are supportive of a beneficial response to therapy
through reduction of ventricular filling pressure and volume.

Lung field examination can follow the resolution of rales, rhonchi, pleural effusions, and
other signs of congestion, and reveal possible emerging zones of consolidation in the
presence of an underlying pneumonia.

Peripheral and central edema resolution should also be monitored. Perfusion of extremities
may also be followed in patients presenting with a low output syndrome.
C. Laboratory Tests to Monitor Response To, and Adjustments in,
Management.
Serial evaluation of electrolytes and renal function is important. Iatrogenic diuretic-induced
hypokalemia can result in life-threatening arrhythmias and is best prevented by adequate
supplementation, rather than treated once present. Decreases in renal function are common
during treatment of AHF. Although initially thought to be associated with poor outcomes,
transient decreases do not seem to portend a poor prognosis.

Serial BNP testing is not recommended for the routine inpatient management of patients
with AHF. Serial testing with chest radiography is usually not necessary in the absence of
new signs or symptoms.

D. Long-term management.
The long-term management of a patient admitted for AHF is directed to three main issues
(also see section on chronic heart failure):

• First, establishing the etiology of the heart failure is important, so that measures may
be taken to address potentially reversible causes. Selected patients with ischemic
cardiomyopathies may benefit from revascularization; patients with hypertensive
cardiomyopathy should have an aggressive antihypertensive regimen. Alcoholic
cardiomyopathies may resolve with cessation of alcohol consumption.

• Second, identification of precipitating factors for the AHF episode and intensive
education to avoid future hospitalizations (see later section).

• Third, optimization of therapies with demonstrated long-term benefits (see section on

Chronic heart failure). In patients with heart failure and reduced ejection fraction,
these pharmacologic therapies include beta-blockers, ACE inhibitors, possibly
angiotensin receptor blockers, mineralocorticoid receptor antagonists
(spironolactone, eplerenone), possibly isosorbide dinitrate/hydralazine, and possibly
digoxin.

It is absolutely imperative that these therapies be initiated as much as possible

during the hospitalization and not be left to the outpatient setting. In addition,
consideration and scheduling of device therapy, such as cardiac resynchronization
therapy (CRT)/biventricular pacemaker and implantable defibrillator device (ICD),
should be done while the patient is still hospitalized, if appropriate.

The hospitalization for AHF is one of the most potent “teachable moments” and care
providers are strongly encouraged to take advantage of the patient as a captive audience.

E. Common Pitfalls and Side-Effects of Management

Management of patients with AHF is complex and highly specific to the individual. However,
there are some common pitfalls:
Hypotension: Most therapies for AHF can cause hypotension, and the development of
hypotension in a number of studies has been related to poor clinical outcomes. Blood
pressure (including orthostatic measurements), central venous pressure (usually by
assessment of JVP), body weight, urine output, and renal function should be carefully
monitored to avoid hypotension. If hypotension ensues, rapidly remove inciting
pharmacologic agents (be especially aware of topical nitrates) and position the patient as
necessary to improve perfusion. In many patients, raising the legs will provide sufficient
augmentation of venous return to improve symptoms.

Worsening renal function: This problem is the most vexing for clinicians, since worsening
renal function can result from inadequate diuresis (persistent elevation of central venous
pressure) or be the result of excessive diuresis with volume depletion. In these situations, it
is very helpful to have measurements of baseline BUN and creatinine as comparators.
Ultimately, the treatment decision will be determined by the extent of volume overload as
assessed by the JVP and other clinical factors, as well as the subsequent response to
therapy. As noted above, transient decreases in renal function may not portend the poor
prognosis, as previously believed, and may just reflect the response to therapy.

Premature discharge: Increasing pressure to decrease hospital length of stay (LOS) has
resulted in steady declines of LOS for AHF in U.S. hospitals. Unfortunately, this decreased
LOS has also been associated with increased 30-day readmission rates. Many patients are
inadequately diuresed prior to discharge with persistent symptoms of dyspnea; some are
discharged with the plan to “complete diuresis as an outpatient.” This strategy is not
successful in many patients, who are not able to monitor all of the factors that impact the
active diuresis of AHF. Many centers are treating patients much more aggressively prior to
discharge and ensuring early outpatient follow-up to prevent early readmissions for AHF.

IV. Management with Co-Morbidities

The average age of the patient with AHF is in the 70s; therefore, these patients tend to have
multiple comorbidities in addition to the underlying cause of the heart failure. Many of these
comorbidities can both cause and exacerbate AHF. Some of the most important
comorbidities include:

Atrial fibrillation: Atrial fibrillation (AF) can be both a cause of and exacerbated by AHF.
Many patients present in atrial fibrillation (AF) with rapid ventricular response (HR >100
bpm) with AHF, but generally, therapies are initially directed to the AHF, since the
ventricular rate often decreases as the adrenergic drive resolves. However, in some
patients, the AF assumes a more primary role, often with a very rapid ventricular response
(usually >140 bpm). In these patients, rate control is important and can be challenging.

In patients with preserved ejection fraction, beta-blockers and calcium channel blockers are
often effective. Calcium channel blockers active on the atrioventricular node, such as
diltiazem and verapamil, should be avoided in patients with reduced ejection fraction, due to
their acute negative inotropic properties. Digoxin, beta-blockers, and amiodarone are often
used in the setting of AHF with reduced ejection fraction. Although one must always
consider the risk of thromboembolic events, if the patient is truly hemodynamically unstable
due to AF with rapid ventricular rate, electrical cardioversion remains an important option.
Acute coronary syndromes (ACS): From 15% to 50% of patients with AHF have troponin
levels above the established upper limit of normal and many patients have underlying
coronary artery disease. In most of these patients, the troponins decrease with the
treatment of the AHF.

In any patient presenting with AHF, it is important to consider the diagnosis of an ACS with
an ECG for the evaluation of myocardial ischemia/infarction. Therapies for ACS and AHF
can be complementary, such as nitrates (which can improve dyspnea, reduce myocardial
oxygen demand, improve coronary blood flow, and decrease platelet aggregation), or
additive, such as heparin or other anticoagulant therapies.

Chronic obstructive pulmonary disease (COPD): COPD exacerbations may present with
signs and symptoms very similar to AHF, and may also instigate an AHF episode. Although
many patients ultimately receive corticosteroid, antibiotics, and diuretics, the careful use of
diagnostic tests, such as physical examination with assessment of JVP, BNP, and chest
radiography, can reduce the necessity of such indiscriminate approaches.

Renal insufficiency: In patients who present with renal failure as evidenced by an elevated
creatinine (i.e., >3.0 mg/dL), consideration should be given to withholding ACE inhibitors,
ARBs, and mineralocorticoid receptor antagonists (spironolactone, eplerenone). Diuretic
doses need to be adjusted upward in the setting of renal failure, with doubling of initial
doses until a diuretic effect is achieved or until concerns of toxicity arise.V. Patient
Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

An episode of AHF often can be seen as representing a failure of outpatient CHF
management. It is imperative that this admission be viewed as an opportunity to prevent
future decompensations through active education; handouts and checklists without
individual instruction are rarely effective. This education should include, but not be limited
to, instruction on:

• Low-salt and weight loss diets (as appropriate)

• Daily use of a scale and a mechanism to record body weights, including directions
on the specific actions to take in the event of a change in body weight (see below)

• Self-titration of diuretics, in appropriate patients. For example, if weight increases by

3 to 5 lb above baseline, double the diuretic dose for 3 to 5 days. If body weight
returns to baseline, resume prior dose of diuretics. If symptoms of hypotension
ensue, hold diuretics, and if the symptoms of hypotension do not resolve, call care
provider. If weight does not improve or if increasing symptoms of dyspnea or other
symptoms of congestion, call a care provider.

• Chronic heart failure management programs, if available

• Exercise or rehabilitation program

• Other health-related issues such as smoking cessation