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Clinical manifestations and diagnosis of advanced heart


failure
Authors: Wilson S Colucci, MD, Shannon M Dunlay, MD, MS
Section Editor: Donna Mancini, MD
Deputy Editor: Todd F Dardas, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Mar 2022. | This topic last updated: Apr 07, 2022.

INTRODUCTION

Advanced heart failure (HF) occurs when patients with HF experience persistent severe
symptoms that interfere with daily life despite maximum evidence-based medical therapy.
Patients with advanced HF have alternatively been described as having "refractory," "end-
stage," or "American College of Cardiology/American Heart Association stage D" HF [1,2]. (See
"Determining the etiology and severity of heart failure or cardiomyopathy", section on 'Stages
in the development of HF'.)

An overview of the clinical manifestations and diagnosis of advanced HF will be presented here.
The management of advanced HF, diagnosis and management of patients with suspected HF,
and management of acute decompensated HF will be discussed separately. (See "Management
of refractory heart failure with reduced ejection fraction" and "Treatment of acute
decompensated heart failure: Specific therapies" and "Treatment of acute decompensated
heart failure: General considerations" and "Epidemiology and causes of heart failure" and
"Overview of the management of heart failure with reduced ejection fraction in adults".)

CLINICAL MANIFESTATIONS

Symptoms and signs — While signs and symptoms of advanced HF are variable, common
manifestations of advanced HF include exercise intolerance, unintentional weight loss,
refractory volume overload, recurrent ventricular arrhythmias, as well as hypotension and signs
of inadequate perfusion (eg, low pulse pressure). These signs and symptoms occur on optimal
(maximum tolerated doses up to target) evidence-based medical therapy, following insertion of
all appropriate devices (eg, cardiac synchronization therapy) and with all reversible causes of HF
addressed.

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Mortality risk increases with each subsequent HF hospitalization [3,4]. The presence of repeated
hospitalizations, unplanned acute visits for HF decompensation, or complicated hospitalizations
(eg, requiring intensive care unit care or inotropes) can suggest advanced HF [2].

Dyspnea, fatigue, and exercise intolerance — As HF progresses, patients frequently develop


symptoms such as dyspnea, lightheadedness, or fatigue at rest or with minimal exertion that
limits exercise capacity. Patients with advanced HF generally exhibit New York Heart Association
(NYHA) functional class III (symptoms with minimal exertion) or IV (symptoms at rest or with
any activity) symptoms ( table 1). Since normal exercise capacity varies based on individual
factors, such as age and activity level, standard benchmarks for exercise capacity may not be
suitable for individual patients. Thus, a patient’s report of decline in exercise capacity over time
can be most informative in signaling a significant change in exercise capacity. However, exercise
limitation that is worrisome for advanced HF includes inability to walk a city block or perform
activities of daily living such as bathing or dressing without limiting symptoms [1]. Many
patients will progress to have dyspnea at rest, including at night (orthopnea, paroxysmal
nocturnal dyspnea). Poor functional status is an adverse prognostic indicator in patients with
HF. (See "Predictors of survival in heart failure with reduced ejection fraction".)

The role of objective assessment of exercise tolerance is discussed below. (See 'Exercise testing'
below.)

Unintentional weight loss — Unintentional weight loss sometimes leading to cachexia is a


common complication of advanced HF. It is characterized by body wasting, including loss of
lean tissue (ie, muscle) and fat [5]. While often accompanied by anorexia (loss of appetite), it can
occur despite adequate caloric intake, due to catabolic/anabolic imbalances.

Refractory volume overload — Patients with advanced HF often present with refractory
volume overload despite escalating doses of diuretics. Volume overload can manifest as
pulmonary congestion, peripheral edema, ascites, and elevated jugular venous pressure. A
requirement of very high doses of loop diuretics, such as furosemide ≥160 mg/day or
equivalent, or frequent use of metolazone is common in advanced HF. Worsening renal function
and inadequate diuresis despite escalating doses of diuretics is also frequently observed.
Volume assessment in HF is discussed in more detail separately. (See "Heart failure: Clinical
manifestations and diagnosis in adults" and "Examination of the jugular venous pulse".)

Hypotension and signs of inadequate perfusion — On physical examination, patients with


low cardiac output may have signs of poor perfusion, including narrowed pulse pressure, cool
extremities, hypotension, and mental status changes.

Although many patients with HF (particularly those with HF with reduced ejection fraction) have
low blood pressure as a result of the combined effect of medical therapy and cardiac
dysfunction, hypotension (systolic blood pressure <90 mmHg) accompanied by symptoms such
as lightheadedness and/or signs of organ dysfunction (eg, worsening renal function) can be

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indicative of advanced HF. Low blood pressure has been associated with increased mortality in
patients with HF [6-8]. In particular, intolerance or the need to cut back doses of
neurohormonal antagonists such as angiotensin converting enzyme inhibitors and beta
blockers due to symptomatic hypotension is suggestive of poor prognosis and advanced HF
[9,10].

Initial tests — Initial laboratory testing that may reveal signs of advanced HF includes blood
tests, a chest radiograph, and an electrocardiogram (ECG).

Blood tests — While there are a multitude of blood tests that have been associated with
prognosis in HF, the following are the most common blood test findings in patients with
advanced HF.

Poor or worsening renal function — Impaired renal function is defined by a reduction in


glomerular filtration rate (GFR), which is most often estimated using serum creatinine
concentration. A variety of factors can contribute to a reduction in GFR in patients with HF,
including neurohormonal adaptations, reduced renal perfusion, increased renal venous
pressure, and right ventricular dysfunction. Both lower GFR and higher blood urea nitrogen
(BUN) have been associated with increased mortality in HF [7,11-13]. In addition, worsening
renal function, as evidenced by increase in BUN or creatinine over time, is associated with
worse prognosis [14,15]. Advanced HF is often characterized by worsening renal function, often
in response to diuresis for refractory volume overload. (See "Cardiorenal syndrome: Definition,
prevalence, diagnosis, and pathophysiology".)

Hyponatremia — Advanced HF is a cause of hyponatremia. Hyponatremia is associated


with worse outcomes in patients with HF. The prognostic significance, pathogenesis, and
management of hyponatremia in HF are discussed in detail elsewhere. (See "Hyponatremia in
patients with heart failure".)

Hypoalbuminemia — Hypoalbuminemia (serum albumin ≤3.4 mg/dL) is common in HF


and associated with worse prognosis [16,17]. It results from a multitude of factors including
decreased liver synthesis, increased vascular permeability, increased degradation, and renal
and gastrointestinal loss [18].

Congestive hepatopathy — Right-sided HF (which often accompanies left-sided HF) can


result in hepatic congestion, which is often suggested by abnormal liver biochemical tests. A
mild elevation in serum bilirubin (total bilirubin <3 mg/dL) is most common, though serum
aminotransferase levels are elevated in a subset of patients. Serum alkaline phosphatase is
usually normal or only mildly elevated. Elevated total bilirubin is associated with increased risk
of death in HF [19]. (See "Congestive hepatopathy".)

Elevated serum natriuretic peptide levels — While persistent elevation in B-type


natriuretic peptide (BNP) and/or N-terminal pro-BNP is usually present in patients with

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advanced HF, there is no specific value that indicates that a patient has advanced HF. (See
"Natriuretic peptide measurement in heart failure".)

Chest radiograph — Advanced HF is often characterized by episodes of fluid retention, which


may manifest as pulmonary edema, pleural effusions, and/or pulmonary vascular congestion
on chest radiograph, although when HF has been chronic, the radiographic signs of pulmonary
congestion may be absent or mild due to increased pulmonary lymphatic drainage.

Electrocardiogram — ECG abnormalities are common in patients with advanced HF (eg, Q


waves, ST and T wave abnormalities in patients with prior myocardial infarction or with
cardiomyopathy). However, there is no ECG finding that is specific for advanced HF. Increased
frequency or new onset atrial (eg, atrial fibrillation) and ventricular (eg, ventricular tachycardia)
arrhythmias can contribute to the development of advanced HF symptoms and should be
assessed.

DIAGNOSIS AND EVALUATION

The approach to the patient with suspected advanced heart failure (HF) includes history,
physical examination, and diagnostic tests to help confirm the severity of HF and rule out
alternative causes of refractory symptoms.

When to suspect advanced heart failure — Advanced HF should be suspected when a patient
with HF experiences persistent severe symptoms despite optimal evidence-based therapy
(pharmacologic therapy plus cardiac resynchronization therapy, as indicated and tolerated). The
vast majority of patients presenting with advanced HF will have a known diagnosis of HF. Over
time, many will progress to advanced HF that is refractory to guideline-directed medical
therapy.

Less commonly, a patient may present with symptoms and signs of advanced HF without prior
diagnosis of HF. In such cases, the patient should undergo initial stabilization followed by
appropriately titrated evidence-based management (particularly for HF with reduced ejection
fraction). The diagnosis of advanced HF is not made unless severe symptoms persist on target
doses (or maximally tolerated doses) of evidence-based therapy including cardiac
resynchronization therapy (as indicated), with adequate time allowed for a therapeutic
response. (See "Treatment and prognosis of heart failure with preserved ejection fraction" and
"Overview of the management of heart failure with reduced ejection fraction in adults" and
"Overview of the management of heart failure with reduced ejection fraction in adults", section
on 'Pharmacologic therapy'.)

Approach to diagnosis and evaluation — We suggest the following approach to diagnosis and
evaluation of advanced HF:

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● History and physical examination to evaluate for symptoms and signs of advanced HF.
(See 'Symptoms and signs' above.)

● Initial laboratory tests include:

• Blood tests including serum electrolytes (particularly serum sodium), complete blood
count (CBC), renal function (eg, blood urea nitrogen and serum creatinine), thyroid
function tests, serum albumin, liver function tests (serum bilirubin and serum
aminotransferase levels), and serum brain natriuretic peptide (BNP) or NT-proBNP
level. (See 'Blood tests' above and 'Evaluation for reversible causes and contributing
factors' below.)

• A chest radiograph is commonly obtained in patients with dyspnea to assess for


pulmonary edema and exclude other potential causes of dyspnea. (See 'Chest
radiograph' above.)

• An electrocardiogram may be helpful to identify a factor contributing to the


development of advanced HF such as atrial or ventricular arrhythmia.

● A complete transthoracic echocardiogram should be performed in all patients suspected


of having advanced HF to evaluate for serial changes in biventricular and valvular function
that may be contributing to worsening symptoms. (See 'Echocardiography' below.)

● Exercise testing consisting of a six-minute walk test and/or a cardiopulmonary exercise


test should be performed in all patients suspected of having advanced HF that are able to
ambulate and have no other contraindications to testing. (See 'Exercise testing' below.)

● A right heart catheterization is required in patients with advanced HF undergoing


evaluation for mechanical circulatory support and cardiac transplantation. It can also be
helpful to confirm the diagnosis of advanced HF, but the decision to proceed depends
upon the patient’s eligibility for this advanced therapy and the patient’s care goals. (See
'Right heart catheterization' below.)

How to diagnose advanced heart failure — A diagnosis of advanced HF is made based upon
clinical evaluation confirming severe symptoms, episodes of refractory fluid retention and/or
hypoperfusion, evidence of severe cardiac dysfunction (on echocardiogram or right heart
catheterization), and evidence of severe impairment of functional capacity.

As there is no one single criterion for advanced HF that exists, the diagnosis is made based on
clinical judgment after compiling data from the clinical examination and diagnostic testing. We
recommend referral to an HF cardiologist when advanced HF is suspected, particularly if the
patient may be a candidate for advanced HF therapies such as mechanical circulatory support
or cardiac transplantation. We recommend use of the following criteria for diagnosis of

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advanced HF that are modified from the diagnostic criteria suggested by the European Society
of Cardiology [2].

Advanced HF is present when the following criteria are met despite optimum medical
management:

● Clinical evaluation confirms the presence of both of the following:

• Severe symptoms due to HF (NYHA functional class III or IV). (See 'Dyspnea, fatigue,
and exercise intolerance' above.)

• Episodes of refractory fluid retention despite intravenous diuretics, hypoperfusion


requiring intravenous inotropes or vasoactive agents, and/or recurrent malignant
ventricular arrhythmias. Hypoperfusion may be diagnosed based on physical
examination and/or laboratory testing (eg, signs of worsening renal function). (See
'Refractory volume overload' above and 'Hypotension and signs of inadequate
perfusion' above.)

● AND diagnostic testing reveals both of the following:

• Objective evidence of severe cardiac dysfunction on echocardiogram and/or right heart


catheterization, including one or more of the following:

- Left ventricular ejection fraction (≤30 percent). (See 'Echocardiography' below and
"Tests to evaluate left ventricular systolic function".)

- LV diastolic dysfunction (eg, with pseudonormal or restrictive mitral inflow pattern)


with left atrial dilation and/or pulmonary hypertension. (See "Echocardiographic
evaluation of left ventricular diastolic function in adults".)

- Right ventricular dysfunction. (See "Echocardiographic assessment of the right


heart".)

- Nonoperable severe valvular or congenital abnormalities.

- Low cardiac index (≤2.2 L/min/m2). (See 'Right heart catheterization' below.)

- High cardiac filling pressures (eg, mean pulmonary capillary wedge pressure >20
mmHg and/or right atrial pressure ≥12 mmHg). (See 'Right heart catheterization'
below.)

• Severe impairment of exercise capacity, including one or more of the following:

- Six-minute walk test distance ≤300 m.

- Peak Vo2 ≤12 kg/min or ≤50 percent predicted for age and sex. (See
"Cardiopulmonary exercise testing in cardiovascular disease".)
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- Inability to exercise due to HF.

Key tests — Tests that are helpful to confirm advanced HF include transthoracic
echocardiography, exercise testing, and right heart catheterization.

Echocardiography — Echocardiography can be useful for assessment of biventricular


function, estimating hemodynamics, and evaluation other cardiac conditions such as valve
disease, congenital abnormalities, and pericardial disease. While advanced HF can occur in
patients with HF and both preserved and reduced left ventricular ejection fraction, a drop in
ejection fraction [20] or very low ejection fraction (≤25 to 30 percent) [21] has been associated
with worse prognosis. Right ventricular dysfunction is associated with adverse prognosis in
patients with HF, regardless of ejection fraction, and should be thoroughly assessed [22-24].
Echocardiography can also provide a noninvasive assessment of hemodynamics that can be
helpful in patients with suspected or confirmed advanced HF. Variables such as cardiac output,
right atrial pressure, pulmonary capillary wedge pressure, and pulmonary artery systolic
pressure can be estimated using Doppler echocardiography and have been shown to be
reliable when assessed by experienced operators [25].

Exercise testing — Objective assessment of exercise capacity with a six-minute walk test
and/or a cardiopulmonary exercise test can confirm the presence of severely limited exercise
capacity. A cardiopulmonary exercise test can further determine whether exercise limitation is
due to cardiovascular factors.

Exercise capacity can be quantified by measuring oxygen uptake (Vo2) and other parameters
during a cardiopulmonary exercise test. The peak Vo2 provides the most objective assessment
of functional capacity in patients with HF, and lower values are associated with worse prognosis.
A peak Vo2 of ≤12 mL/kg/min (or ≤50 percent of age- and sex-predicted Vo2) is used as a
criterion for listing for cardiac transplantation [26]. The six-minute walk test measures the
distance ambulated on a level surface during six minutes, and shorter distances achieved are
consistent with more severe HF. A distance of ≤300 m has been associated with increased risk of
death [27] and correlates with peak Vo2 in some populations [28]. However, results are
generally less informative than cardiopulmonary exercise testing, and cardiopulmonary
exercise testing is favored if available, as it allows assessment of the contribution of cardiac
versus noncardiac factors that can limit exercise. Exercise testing in HF is described in more
detail elsewhere. (See "Exercise capacity and VO2 in heart failure" and "Heart transplantation in
adults: Indications and contraindications".)

Right heart catheterization — Right heart (eg, pulmonary artery) catheterization can be
helpful to measure intracardiac pressures and determine eligibility for advanced HF therapies.
Abnormal hemodynamics are generally necessary for the diagnosis, although the precise
pattern and severity of hemodynamic dysfunction may vary greatly from patient to patient, and
abnormal hemodynamics, per se, are not sufficient for the diagnosis of advanced HF. Typically,
there is persistently elevated left- and right-sided filling pressures (pulmonary capillary wedge

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pressure >20 mmHg, right atrial pressure ≥12 mmHg) and/or decreased cardiac index (≤2.2
L/min/m2) despite optimal medical therapy is concerning for advanced HF. Right heart
catheterization is most informative when performed after volume status has been optimized.
Pulmonary artery catheterization is discussed in more detail elsewhere. (See "Cardiac
catheterization techniques: Normal hemodynamics" and "Pulmonary artery catheterization:
Interpretation of hemodynamic values and waveforms in adults" and "Pulmonary artery
catheterization: Indications, contraindications, and complications in adults".)

Evaluation for reversible causes and contributing factors — In patients diagnosed with
advanced HF, it is important to perform a thorough evaluation to ensure that there are no
potentially reversible etiologies or comorbidities causing or contributing to the patient’s signs
and symptoms of advanced HF.

Potential reversible causes of advanced HF include severe coronary artery disease, severe
operable valve stenosis or regurgitation, pericardial disease (eg, constrictive pericarditis), and a
reversible cardiomyopathy (eg, stress or takotsubo cardiomyopathy). The evaluation of the
etiology of HF is discussed separately. (See "Determining the etiology and severity of heart
failure or cardiomyopathy".)

Contributing factors include severe anemia, thyroid disease, and sleep apnea.

● Severe anemia (hemoglobin <8 mg/dL) can result in impaired oxygen delivery to tissues
and may contribute to symptoms such as dyspnea and fatigue in patients with suspected
advanced HF. Treatment of the anemia may improve symptoms. Treatment options
including blood transfusion, erythropoietin-stimulating agents, and iron supplementation
are discussed in detail elsewhere. (See "Evaluation and management of anemia and iron
deficiency in adults with heart failure".)

● Hyperthyroidism or hypothyroidism, per se, can lead to severe HF or contribute to the


severity of HF due to other common causes [29]. Therefore, thyroid function should be
assessed and corrected before classifying HF as advanced. The cardiovascular effects of
thyroid disorders are discussed in detail elsewhere. (See "Overview of the clinical
manifestations of hyperthyroidism in adults", section on 'Cardiovascular'.)

● Sleep-disordered breathing (obstructive sleep apnea [OSA] and/or central sleep apnea
with Cheyne-Stoke breathing [CSA-CSB]) is common in patients with HF. Both OSA and
CSA-CSB can impair systolic and diastolic cardiac function, and the presence of either in
patients with HF is associated with worse prognosis. Evaluation of patients with HF should
include questions about potential sleep-disordered breathing symptoms (eg, snoring,
excessive daytime somnolence, or poor sleep quality). (See "Sleep-disordered breathing in
heart failure".)

DIFFERENTIAL DIAGNOSIS
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When a diagnosis of advanced HF is suspected, it is important to exclude other potential causes


of persistent severe symptoms and signs of HF despite optimum evidence-based therapy. Two
key considerations are inadequate therapy for HF and presence of one or more concurrent
conditions (eg, lung disease) in a patient with HF (that is not advanced) that may cause signs
and symptoms like those of advanced heart failure.

In addition, reversible causes and contributing factors to HF should be excluded. (See


'Evaluation for reversible causes and contributing factors' above.)

Inadequate therapy — Poor adherence to medications and dietary restrictions (such as salt or
fluid restriction) or undertreatment can contribute to persistent or worsening HF symptoms
and should be assessed. Before assigning a patient a diagnosis of advanced HF, it is important
to thoroughly review the patient’s current and prior HF therapies to ensure that all evidence-
based therapies have been considered. Optimal medical management includes use of target
doses (or maximally-tolerated doses when target doses are not tolerated) of evidence-based
medications such as angiotensin converting enzyme (ACE) inhibitors and beta blockers.
Furthermore, if one medication or medication class is not tolerated, alternative agents with
similar therapeutic efficacy should have been tried. For example, if a patient does not tolerate
ACE inhibitors due to cough, an angiotensin receptor blocker should be initiated as an
alternative. Cardiac resynchronization therapy (CRT) should be added if indicated. It is also
important to ensure that the patient has been given adequate time to respond to therapy (eg,
one month after initiation of CRT). (See "Cardiac resynchronization therapy in heart failure:
Indications" and "Overview of the management of heart failure with reduced ejection fraction in
adults", section on 'Pharmacologic therapy'.)

Concurrent conditions — In a patient with HF, the presence of one or more concurrent
conditions affecting other organ systems (eg, kidney, lung, blood, thyroid, or liver) may cause
symptoms and signs similar to those with advanced HF.

● Kidney disease – There are complex interactions between the heart and the kidney, such
that worsening function in one organ impacts the performance of the other. In patients
presenting with advanced HF symptoms and renal dysfunction, it is important to
distinguish between underlying kidney disease and impaired kidney function due to
cardiorenal syndrome. (See "Cardiorenal syndrome: Definition, prevalence, diagnosis, and
pathophysiology", section on 'Diagnosis'.)

● Lung disease – Concomitant lung disease such as chronic obstructive pulmonary disease
is common in patients with HF, present in up to 40 percent of patients [30-32]. Since lung
disease and HF can both cause dyspnea, it can be challenging to sort out the relative
contribution of each to symptom burden and functional status. Cardiopulmonary exercise
testing can be helpful in distinguishing cardiac and pulmonary contributions to dyspnea in
patients presenting with suspected advanced HF. Adequate treatment of lung disease may

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improve symptom burden in advanced HF. (See "Approach to the patient with dyspnea"
and "Cardiopulmonary exercise testing in cardiovascular disease".)

● Liver disease – Cirrhosis can present with similar signs and symptoms as advanced HF,
including ascites/abdominal distension, lower extremity edema, and fatigue. The presence
of a normal jugular venous pressure on physical examination in a patient with ascites can
be helpful in attributing the ascites to a noncardiac cause. However, it is important to
recognize that longstanding right HF and elevated central venous pressure can also result
in cirrhosis, and advanced HF and cirrhosis may coexist. (See "Congestive hepatopathy".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

● When to suspect advanced heart failure – Advanced heart failure (HF) should be
suspected when a patient with HF experiences persistent severe symptoms despite
optimal evidence-based therapy (pharmacologic therapy plus cardiac resynchronization
therapy, as indicated). The vast majority of patients presenting with advanced HF will have
a known diagnosis of HF. A subgroup of patients with chronic HF will progress to develop
advanced HF refractory to guideline-directed medical therapy. (See 'When to suspect
advanced heart failure' above.)

● Symptoms and signs – While signs and symptoms of advanced HF are variable, common
manifestations of advanced HF include dyspnea, fatigue, exercise intolerance,
unintentional weight loss, refractory volume overload, hypotension, and signs of
inadequate perfusion (diminished peripheral pulses or worsening renal function). (See
'Symptoms and signs' above.)

● Initial tests – The diagnostic evaluation of patients with suspected advanced HF includes
a history, physical examination, blood tests, chest radiograph, electrocardiogram,
transthoracic echocardiogram, and exercise testing. In addition, a right heart
catheterization is required in patients with advanced HF who are undergoing evaluation
for mechanical circulatory support and cardiac transplantation. (See 'Approach to
diagnosis and evaluation' above.)

● How to diagnose advanced heart failure – A diagnosis of advanced HF is made based


upon clinical evaluation confirming severe symptoms; episodes of refractory fluid
retention, hypoperfusion, and/or recurrent malignant ventricular arrhythmias; evidence of
severe cardiac dysfunction (on echocardiogram or right heart catheterization); and
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evidence of severe impairment of exercise capacity. (See 'How to diagnose advanced heart
failure' above.)

● Evaluation for reversible causes and contributing factors – In patients diagnosed with
advanced HF, it is important to perform a thorough evaluation to ensure that there are no
potentially reversible etiologies causing or contributing to the patient’s signs and
symptoms of advanced HF. Important contributing factors including anemia, thyroid
disease, and sleep-disordered breathing. (See 'Evaluation for reversible causes and
contributing factors' above.)

● Differential diagnosis – When a diagnosis of advanced HF is suspected, it is important to


exclude other potential causes of persistent severe symptoms and signs of HF despite
optimum evidence-based therapy. Two key considerations are inadequate therapy for HF
and presence of one or more concurrent conditions (eg, lung disease) that may cause
signs and symptoms like those of advanced HF. (See 'Differential diagnosis' above.)

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GRAPHICS

NYHA and other classifications of cardiovascular disability

Canadian
NYHA functional Cardiovascular Specific activity
Class
classification[1] Society functional scale[3]
classification[2]

I Patients with cardiac Ordinary physical Patients can perform


disease but without activity, such as to completion any
resulting limitations of walking and climbing activity requiring ≥7
physical activity. stairs, does not cause metabolic equivalents
Ordinary physical angina. Angina with (ie, can carry 24 lb up 8
activity does not cause strenuous or rapid steps; do outdoor work
undue fatigue, prolonged exertion at [shovel snow, spade
palpitation, dyspnea, work or recreation. soil]; do recreational
or anginal pain. activities [skiing,
basketball, squash,
handball, jog/walk 5
mph]).

II Patients with cardiac Slight limitation of Patients can perform


disease resulting in ordinary activity. to completion any
slight limitation of Walking or climbing activity requiring ≥5
physical activity. They stairs rapidly, walking metabolic equivalents
are comfortable at uphill, walking or stair- (eg, have sexual
rest. Ordinary physical climbing after meals, in intercourse without
activity results in cold, in wind, or when stopping, garden, rake,
fatigue, palpitation, under emotional weed, roller skate,
dyspnea, or anginal stress, or only during dance foxtrot, walk at
pain. the few hours after 4 mph on level ground)
awakening. Walking but cannot and do not
more than 2 blocks on perform to completion
the level and climbing activities requiring ≥7
more than 1 flight of metabolic equivalents.
ordinary stairs at a
normal pace and in
normal conditions.

III Patients with cardiac Marked limitation of Patients can perform


disease resulting in ordinary physical to completion any
marked limitation of activity. Walking 1 to 2 activity requiring ≥2
physical activity. They blocks on the level and metabolic equivalents
are comfortable at climbing 1 flight in (eg, shower without
rest. Less-than- normal conditions. stopping, strip and
ordinary physical make bed, clean
activity causes fatigue, windows, walk 2.5
palpitation, dyspnea, mph, bowl, play golf,
or anginal pain. dress without
stopping) but cannot

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and do not perform to


completion any
activities requiring >5
metabolic equivalents.

IV Patients with cardiac Inability to carry on Patients cannot or do


disease resulting in any physical activity not perform to
inability to carry on any without discomfort. completion activities
physical activity Anginal syndrome may requiring >2 metabolic
without discomfort. be present at rest. equivalents. Cannot
Symptoms of cardiac carry out activities
insufficiency or of the listed above (specific
anginal syndrome may activity scale III).
be present even at
rest. If any physical
activity is undertaken,
discomfort is
increased.

NYHA: New York Heart Association.

References:

1. The Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the
Heart and Great Vessels, 9th ed, Little, Brown & Co, Boston 1994. p.253.
2. Campeau L. Grading of angina pectoris. Circulation 1976; 54:522.
3. Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing
cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981; 64:1227.

Graphic 52683 Version 19.0

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