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Heart Failure Workup
Updated: Mar 02, 2021
Author: Ioana Dumitru, MD; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...

WORKUP

Approach Considerations
Careful evaluation of the patient's history and physical examination (including signs of congestion,
such as jugular venous distention) can provide important information about the underlying cardiac
abnormality in heart failure.
[3] However, other studies and/or tests may be necessary to identify
structural abnormalities or conditions that can lead to or exacerbate heart failure.
[3]

Endomyocardial biopsy is indicated only when a specific diagnosis is suspected that would
influence therapy in patients presenting with heart failure (see the image below). 

Heart Failure. Transesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve
demonstrating an increased mean gradient of 16 mm Hg consistent with severe mitral stenosis.

Routine Laboratory Tests

Laboratory studies should include a complete blood cell (CBC) count, serum electrolyte levels
(including calcium and magnesium), and renal and liver function studies. Other tests may be
indicated in specific patients. The CBC aids in the assessment of severe anemia, which may cause
or aggravate heart failure.
[64, 65] Leukocytosis may signal underlying infection. Otherwise, CBCs
are usually of little diagnostic help.

An assessment for iron deficiency should be considered; about one third of heart failure patients
are also iron deficient, which is associated with poor cardiac function and can worsen outcomes in
these individuals.
[66, 67, 68]  Iron deficiency appears to impair contractility of human
cardiomyocytes by impairing mitochondrial respiration and reducing contractility and relaxation;
these effects can be reversed by restoring intracellular iron levels.
[67]

In a study that sought to define biomarker-based iron deficiency in heart failure based on bone
marrow iron staining as the gold standard, as well as evaluate the prognostic value of the
optimized definition, investigators found that a transferrin saturation (TSAT) up to 19.8% or a
serum iron level up to 13 μmol/L had the best results in selecting patients with iron deficiency as
well as identifying heart patients with the greatest mortality risk.
[65]  These TSAT and serum iron
values not only achieved a 94% sensitivity, and a respective 84% and 88% specificity (ie,
specificity of 84% for TSAT ≤19.8% and 88% for serum iron ≤13 μmol/L), but both measures were
also independent prognostic factors for mortality.
[65]

Serum electrolyte values are generally within reference ranges in patients with mild to moderate
heart failure before treatment. In cases of severe heart failure, however, prolonged, rigid sodium
restriction, coupled with intensive diuretic therapy and the inability to excrete water, may lead to
dilutional hyponatremia, which occurs because of a substantial expansion of extracellular and
intravascular fluid volume and a normal or increased level of total body sodium.

Potassium levels are usually within reference ranges, although the prolonged administration of
diuretics may result in hypokalemia. Hyperkalemia may occur in patients with severe heart failure
who show marked reductions in glomerular filtration rate (GFR) and inadequate delivery of sodium
to the distal tubular sodium-potassium exchange sites of the kidney, particularly if they are
receiving potassium-sparing diuretics and/or angiotensin-converting enzyme inhibitors (ACEIs).

Pulmonary function testing is generally not helpful in the diagnosis of heart failure. However, such
testing may demonstrate or exclude respiratory causes of dyspnea and help in the assessment of
any pulmonary causes of dyspnea.

Renal function tests

Blood urea nitrogen (BUN) and creatinine levels can be within reference ranges in patients with
mild to moderate heart failure and normal renal function, although BUN levels and BUN/creatinine
ratios may be elevated.

Patients with severe heart failure, particularly those on large doses of diuretics for long periods,
may have elevated BUN and creatinine levels indicative of renal insufficiency owing to chronic
reductions of renal blood flow from reduced cardiac output. Diuresing this group of patients is
complex. In some individuals, diuretics will improve renal congestion and renal function, whereas in
others, overaggressive diuresis may aggravate renal insufficiency due to volume depletion.

Liver function tests

Congestive hepatomegaly and cardiac cirrhosis are often associated with impaired hepatic
function, which is characterized by abnormal values of aspartate aminotransferase (AST), alanine
aminotransferase (ALT), lactic dehydrogenase (LDH), and other liver enzymes. Hyperbilirubinemia
secondary to an increase in the directly and indirectly reacting bilirubin is common. In severe cases
of acute right ventricular (RV) or left ventricular (LV) failure, frank jaundice may occur.

Acute hepatic venous congestion can result in severe jaundice, with a bilirubin level as high as 15-
20 mg/dL, elevation of AST to more than 10 times the upper reference range limit, elevation of the
serum alkaline phosphatase level, and prolongation of the prothrombin time. The clinical and
laboratory pictures may resemble viral hepatitis, but the impairment of hepatic function is rapidly
resolved by successful treatment of heart failure. In patients with long-standing heart failure,
albumin synthesis may be impaired, leading to hypoalbuminemia and intensifying the accumulation
of fluid. Fulminant hepatic failure is an uncommon, late, and sometimes terminal complication of
cardiac cirrhosis.
Natriuretic Peptides
Clinical findings and routine diagnostic tests are not always sufficient to diagnose heart failure. In
such ambiguous cases, rapid measurement of B-type natriuretic peptide (BNP) or N-terminal
proBNP (NT-proBNP) levels can aid clinicians in differentiating between cardiac and noncardiac
causes of dyspnea.
[3, 4, 5, 61, 62, 69, 70] That is, BNP is mostly limited to the differentiation of heart
failure versus other causes of dyspnea in patients with an atypical presentation.

BNP is a 32-amino-acid polypeptide containing a 17-amino-acid ring structure common to all

natriuretic peptides. The major source of plasma BNP is the cardiac ventricles, and the release of
BNP appears to be in direct proportion to ventricular volume and pressure overload. BNP is an
independent predictor of high LV end-diastolic pressure, and it is more useful than atrial natriuretic
peptide (ANP) or norepinephrine levels for assessing mortality risk in patients with heart failure.
[71,
72, 73, 74]

Although BNP has been determined to be the strongest predictor of systolic versus nonsystolic
heart failure (followed by oxygen saturation, history of myocardial infarction, and heart rate), BNP
does not reliably differentiate between heart failure with preserved ejection fraction and heart
failure with reduced ejection fraction.
[69] Increased NT-proBNP was found to be the strongest
independent predictor of a final diagnosis of acute heart failure.
[75, 76, 77]

Measurement of BNP and its precursor NT-proBNP in the urgent care setting can be used to
establish the diagnosis of heart failure when the clinical presentation is ambiguous or when
confounding comorbidities are present.
[3, 4, 5] BNP and NT-proBNP assays have different cutoff
values for ruling in and ruling out heart failure.
[57, 59, 78, 79, 80]

BNP levels correlate closely with the New York Heart Association (NYHA) classification of heart
failure.
[81, 82] BNP levels greater than 100 pg/mL have a specificity greater than 95% and a
sensitivity greater than 98% when comparing patients without heart failure to all patients with heart
failure.
[83] Even BNP levels greater than 80 pg/mL have a specificity greater than 95% and a
sensitivity greater than 98% in the diagnosis of heart failure.
[78]

Table of cutoff values

Table 4, below, summarizes the evidence-based cutoff values of BNP and NT-proBNP for ruling in
and ruling out the diagnosis of heart failure in the dyspneic patient presenting to the emergency
department.

Table 4. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF (Open Table in a
new window)

BNP, pg/mL NT-proBNP, pg/mL

Criterion
HF Unlikely HF Likely HF Unlikely HF Likely
(LR-Negative) (LR-Positive) (LR-Negative) (LR-Positive)

Age, y >17 < 100 (0.13)* >500 (8.1)* - -

 >21 - - < 300 (0.02)† -

21-50 - - - >450 (14)†

50-75 - - - >900 (5.0)†

>75 - - - >1800 (3.1)†

Estimated GFR,
< 60 mL/min < 200 (0.13)‡ >500 (9.3)‡ - -

BNP = B-type natriuretic peptide; GRF = glomerular filtration rate; HF = heart failure; LR =
likelihood ratio; NPV = negative predictive value; NT-pro-BNP = N-terminal proBNP; PPV =
positive predictive value; – = not specifically defined.
*Derived from Breathing Not Properly data (1586 emergency department [ED] patients,
prevalence of HF = 47%).
[61]

† Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%).

[62, 70]

‡Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF =
49%).
[69]

BNP and NT-proBNP levels are higher in older patients,

[84] women,
[84] and patients with renal
dysfunction
[85] or sepsis. Atrial fibrillation has also been associated with increased BNP levels in
the absence of acute heart failure. However, BNP levels may be disproportionately lower in
patients who are obese due to fat metabolism or who have hypothyroidism or advanced end-stage
heart failure (the latter due to increased fibrosis). NT-proBNP plasma levels are also lower in obese
heart failure patients relative to nonobese patients with heart failure, regardless of whether the
etiology is ischemic or nonischaemic.
[86]

However, NT-proBNP may be elevated in severely obese patients (BMI >40 kg/m2) owing to an
increased cardiac burden in these individuals.
[87] NT-pro-BNP may be a better marker for
detecting cardiac dysfunction than BNP, because its chemical stability is better in circulating blood
than that of BNP, and it is a sensitive marker of cardiac function even in early cardiac
decompensation.
[88]

BNP measurement not indicated with nesiritide therapy

Nesiritide is a synthetic BNP analogue; therefore, the measurement of BNP is not indicated in
patients who are receiving nesiritide. If BNP is used as a diagnostic marker to rule in heart failure,
the level must be determined before nesiritide therapy is started.
[89, 90, 91, 92]

In a study by Miller et al, levels of NT-proBNP and BNP decreased in patients with advanced heart
failure after therapy with nesiritide, but the majority of the patients did not have biochemically
significant decreases in these markers even with a clinical response.
[93] The investigators were
unable to give a definitive reason for their results, and they indicated that nesiritide therapy should
not be guided by the use of levels of both markers.
[93] Fitzgerald et al also found decreased levels
of both natriuretic peptides following nesiritide therapy in patients with decompensated heart
failure.
[94]

For more information, see the Medscape Drugs & Diseases article Natriuretic Peptides in
Congestive Heart Failure.

Genetic Testing
Cardiomyopathy phenotypes that have known genetic cause(s) include hypertrophic (HCM),
dilated (DCM), restrictive (RCM), arrhythmogenic right ventricular dysplasia/cardiomyopathy
(ARVD/C), and left ventricular noncompaction (LVNC). Because most cases of cardiomyopathy are
treatable—which is not the case in many genetic diseases—and screening for genetic risk of
cardiomyopathy before the onset of disease can guide the recommendations for early detection of
disease and therapy (see Presentation, History),
[5, 30] it is recommended that consideration be
given for patients with cardiomyopathy to be referred to centers with expertise in these matters and
in family-based management.
[5] These specialized centers will have a better understanding of the
complexities involved in genetic evaluation, testing, and counseling of patients with
cardiomyopathy.

To establish specific gene testing and laboratories offering tests, please see www.genetests.org for
further information and larger reviews.

Genetic testing has the highest yield in three types of cardiomyopathy: DCM, HCM, and autosomal
dominant ARVD/C. The diagnosis must be established using the specific criteria for each type of
cardiomyopathy, as the genetic testing is different for each type.

Dilated cardiomyopathy
It is thought that approximately 20-50% of idiopathic dilated cardiomyopathy (IDC) may have a
genetic basis. Screening first-degree relatives of a proband with IDC by echocardiography and
electrocardiography (ECG) reveals that 20-48% of probands have affected relatives, consistent
with a diagnosis of familial dilated cardiomyopathy (FDC).
[95, 96, 97]

Molecular genetic testing of the proband for an LMNA mutation is probably indicated, particularly if
significant conduction system disease is present in the family. It should be noted that although the
analytical sensitivity for detecting LMNA gene mutations is quite high, the clinical sensitivity
(likelihood of identifying a mutation in a person with the disorder) is approximately 8% for FDC.
Because molecular genetic testing for MYH7 has comparable clinical sensitivity, testing for
mutations in MHY7 may also be considered.

Hypertrophic cardiomyopathy

HCM, caused by mutation in one of the genes currently known to encode different components of
the sarcomere, is characterized by left ventricular (LV) hypertrophy (LVH) in the absence of
predisposing cardiac conditions (eg, aortic stenosis) or cardiovascular conditions (eg, long-
standing hypertension). Most often, the LVH of HCM becomes apparent during adolescence or
young adulthood, although it may also develop late in life, in infancy, or in childhood.

Molecular genetic testing of any of the 14 genes currently known to encode different components
of the sarcomere is clinically available. A detailed 3- to 4-generation family history should be
obtained from relatives to assess the possibility of familial HCM. Attention should be directed to a
history of any of the following in relatives: heart failure, HCM, cardiac transplantation, unexplained
sudden death, unexplained cardiac conduction system disease and/or arrhythmia, or unexplained
stroke or other thromboembolic disease.

Autosomal dominant arrhythmogenic right ventricular

dysplasia/cardiomyopathy
ARVD/C is characterized by progressive fibrofatty replacement of the myocardium that
predisposes to ventricular tachycardia and sudden death in young individuals and athletes. It
primarily affects the RV; with time, it may also involve the LV. The presentation of disease is highly
variable even within families, and affected individuals may not meet the established clinical criteria.
The mean age at diagnosis is 31 years (±13 y; range, 4-64 y).

Genetic testing should be considered in individuals who have a clinical diagnosis of ARVD based
on the diagnostic criteria. A case can be made to offer genetic testing to all with a clinical diagnosis
of ARVD with a negative family history based on the high rate of reduced penetrance thus far
identified with the ARVD genes. Molecular genetic testing is available on a clinical basis for
TGFB3, RYR2, TMEM43, DSP, PKP2, DSG2, DSC2, and JUP.
[98]

For more information regarding genetic testing and cardiomyopathy, please see HFSA Guideline
Approach to Medical Evidence for Genetic Evaluation of Cardiomyopathy, as well as Murphy RT,
Starling RC. Genetics and cardiomyopathy: where are we now? Cleve Clin J Med. Jun
2005;72(6):465-6, 469-70, 472-3 passim.
[30]

Assessment of Hypoxemia
Arterial and venous blood gases

Although arterial blood gas (ABG) measurement is more accurate than pulse oximetry for
measuring oxygen saturation, it is unclear if ABG results add any clinical utility to pulse oximetry. In
the setting of acute heart failure, ABG measurement is rarely performed. Indications include severe
respiratory distress, documented hypoxemia by pulse oximetry not responsive to supplemental
oxygen, and evidence of acidosis by serum chemistry findings or elevated lactate levels.

In general, heart failure patients who do not have comorbid lung disease do not manifest
hypoxemia except in severe acute decompensation. Patients with severe heart failure may have
signs and symptoms ranging from severe hypoxemia, or even hypoxia, along with hypercapnia, to
decreased vital capacity and poor ventilation.

ABG measurement helps assess the presence of hypercapnia, a potential early marker for
impending respiratory failure. Hypoxemia and hypocapnia occur in stages 1 and 2 of pulmonary
edema because of a ventilation/perfusion (V/Q) mismatch. In stage 3 of pulmonary edema, right-to-
left intrapulmonary shunt develops secondary to alveolar flooding and further contributes to
hypoxemia. In more severe cases, hypercapnia and respiratory acidosis are usually observed. The
decision regarding intubation and the use of mechanical ventilation is frequently based on many
clinical parameters, including oxygenation, ventilation, and mental status. ABG values in isolation
are rarely useful, but they may add to the entire clinical picture.
Mixed venous oxygen saturation (obtained from the main pulmonary artery in the absence of an
intracardiac shunt) is a good marker of the blood circulation time and thus of the cardiac output and
cardiac performance. Patients who have advanced heart failure have low cardiac output and
slower circulation time, which translate into an increased oxygen extraction by the tissues and
therefore lower oxygen (< 60% saturation).

Pulse oximetry
Pulse oximetry is highly accurate at assessing the presence of hypoxemia and, therefore, the
severity of acute heart failure presentations. Patients with mild to moderate acute heart failure may
show modest reductions in oxygen saturation, whereas patients with severe heart failure may have
severe oxygen desaturation, even at rest. Pulse oximetry is also useful for monitoring the patient's
response to supplemental oxygen and other therapies.

Patients with mild to moderate heart failure may have normal oxygen saturations at rest, but they
may exhibit marked reductions in oxygen saturations during physical exertion or recumbency. In
general, arterial desaturation during exercise is not expected in heart failure and suggests the
presence of comorbid lung disease. The use of continuous oxygen may be needed until
compensation returns oxygen saturation to normal during exertion and recumbency or on a
permanent basis if oxygen desaturation during exertion and/or recumbency exists during
compensated severe chronic heart failure.

Electrocardiography
A screening electrocardiogram (ECG) is reasonable in patients with symptoms suggestive of heart
failure. The presence of left atrial enlargement and left ventricular (LV) hypertrophy (LVH) is
sensitive (although nonspecific) for chronic LV dysfunction. It is unlikely that an ECG would be
completely normal in the presence of heart failure; therefore, an alternative diagnosis should be
sought in such cases.
[4, 5]

Electrocardiography may suggest an acute tachyarrhythmia or bradyarrhythmia as the cause of

heart failure. It may also aid in the diagnosis of acute myocardial ischemia or infarction as the
cause of heart failure, or it may suggest the likelihood of a prior myocardial infarction or the
presence of coronary artery disease as the cause of heart failure.
[3, 5]

Heart failure can have multiple and diverse presentations on ECGs (see the images below).

Heart Failure. This electrocardiogram (ECG) is from a 32-year-old female with recent-onset congestive heart failure and
syncope. The ECG demonstrates a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing
whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular
tachycardia [VT]). At first glance, sinus tachycardia in this ECG might be considered with severe conduction disease
manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely, ECG
morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the precordial
leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated
cardiomyopathy.

Heart Failure. Electrocardiogram depicting ventricular fibrillation in a patient with a left ventricular assist device (LVAD).
Ventricular fibrillation is often due to ischemic heart disease and can lead to myocardial infarction and/or sudden death.

Heart Failure. This electrocardiogram (ECG) shows evidence of severe left ventricular hypertrophy (LVH) with prominent
precordial voltage, left atrial abnormality, lateral ST-T abnormalities, and a somewhat leftward QRS axis (–15º). The
patient had malignant hypertension with acute heart failure, accounting also for the sinus tachycardia (blood pressure
initially 280/180 mmHg). The ST-T changes seen here are nonspecific and could be due to, for example, LVH alone or
coronary artery disease. However, the ECG is not consistent with extensive inferolateral myocardial infarction. Image
courtesy of http://ecg.bidmc.harvard.edu .

Heart Failure. This electrocardiogram shows an extensive acute/evolving anterolateral myocardial infarction pattern, with
ST-T changes most apparent in leads V2-V6, I, and aVL. Slow R wave progression is also present in leads V1-V3. The
rhythm is borderline sinus tachycardia with a single premature atrial complex (PAC) (4th beat). Note also the low limb lead
voltage and probable left atrial abnormality. Left ventriculography showed diffuse hypokinesis as well as akinesis of the
anterolateral and apical walls, with an ejection fraction estimated at 33%. Image courtesy of http://ecg.bidmc.harvard.edu.
Heart Failure. This electrocardiogram shows a patient is having an evolving anteroseptal myocardial infarction secondary
to cocaine. There are Q waves in leads V2-V3 with ST segment elevation in leads V2-V5 associated with T-wave
inversion. Also noted are biphasic T-waves in the inferior leads. These multiple abnormalities suggest occlusion of a large
left anterior descending artery that wraps around the apex of the heart (or multivessel coronary artery disease). Image
courtesy of http://ecg.bidmc.harvard.edu .

Electrocardiography is of limited help when an acute valvular abnormality or LV systolic dysfunction

is considered to be the cause of heart failure; however, the presence of left bundle branch block
(LBBB) on an ECG is a strong marker for diminished LV systolic function.

Chest Radiography
Chest radiographs (see the images below) are used in cases of heart failure to assess heart size,
pulmonary congestion, pulmonary or thoracic causes of dyspnea, and the proper positioning of any
implanted cardiac devices.
[3, 4, 5]  Posterior-anterior and lateral views are recommended.
[5]

Heart Failure. This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute
heart failure.
Heart Failure. A 28-year-old woman presented with acute heart failure secondary to chronic hypertension. The enlarged
cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute heart failure due to the effects of chronic
high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs (ie,
pulmonary congestion).

Although up to 50% of patients with heart failure and documented elevation of pulmonary capillary
wedge pressure (PCWP) do not manifest typical radiographic findings of pulmonary congestion,
two principal features of chest radiographs are useful in the evaluation of patients with heart failure:
(1) the size and shape of the cardiac silhouette and (2) edema at the lung bases.

Echocardiography
Two-dimensional (2-D) echocardiography is recommended in the initial evaluation of patients with
known or suspected heart failure.
[3, 4, 5] Ventricular function may be evaluated, and primary and
secondary valvular abnormalities may be accurately assessed.
[99, 100, 101, 102, 103, 104]

Doppler echocardiography, along with 2-D echocardiography, may play a valuable role in
determining diastolic function and in establishing the diagnosis of diastolic heart failure.
Approximately 30-40% of patients presenting with heart failure have normal systolic function but
abnormal diastolic relaxation. The primary finding to differentiate diastolic heart failure is the
presence of a normal ejection fraction; however, note that findings of diastolic dysfunction are
common in the elderly and may not be associated with clinical heart failure. Because the therapy
for this condition is distinctly different from that for systolic dysfunction, establishing the appropriate
etiology and diagnosis is essential.

Doppler and 2-D echocardiography may also be used to determine both systolic and diastolic left
ventricular (LV) performance, cardiac output (ejection fraction), and pulmonary artery and
ventricular filling pressures. In addition, echocardiography may be used to identify clinically
important valvular disease (see the images below).
Heart Failure. Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic
kidney failure, which can lead to heart failure. In this color Doppler and spectral Doppler ultrasonographic examination of
the left internal carotid artery (ICA) in a patient with cervicocephalic FMD, stenoses of about 70% is seen in the ICA.

Heart Failure. Cervicocephalic fibromuscular dysplasia (FMD) can lead to complications such as hypertension and chronic
kidney failure, which, in turn, can lead to heart failure. Nodularity in an artery is known as the string-of-beads sign, and it
can be seen this color Doppler ultrasonographic image from a 51-year-old patient with low-grade stenosing FMD of the
internal carotid artery (ICA).

Heart Failure. Echocardiogram of a patient with severe pulmonic stenosis. This image shows a parasternal short-axis
view of a thickened pulmonary valve. Pulmonic stenosis can lead to pulmonary hypertension, which can result in hepatic
congestion and in right-sided heart failure.
 0:00 / 0:24

Heart Failure. This video is an echocardiogram of a patient with severe pulmonic stenosis. The first segment shows the
parasternal short-axis view of the thickened pulmonary valve. The second segment shows the presence of moderate
pulmonary insufficiency (orange color flow). AV = aortic valve, PA = pulmonary artery, PI = pulmonary insufficiency, PV =
pulmonary valve.

The following video is from a patient with arrhythmogenic right ventricular dysplasia (ARVD), a
congenital cardiomyopathy that can lead to heart failure.

0:00 / 0:03

Heart Failure. Apical four-chamber echocardiogram in a 37-year-old man with arrhythmogenic right ventricular dysplasia
(ARVD), a congenital cardiomyopathy. Note the prominent trabeculae and abnormal wall motion of the dilated right
ventricle. ARVD can result in ventricular and supraventricular arrhythmias. The most significant of all rhythms associated
with heart failure are the life-threatening ventricular arrhythmias.
Transesophageal echocardiography

Transesophageal echocardiography (TEE) is particularly useful in patients who are on mechanical

ventilation or are morbidly obese and in patients whose transthoracic echocardiogram is
suboptimal in its imaging.
[4, 105] It is an easy and safe alternative to conventional transthoracic
echocardiography (TTE) and provides better imaging quality (see the following video).
Transesophageal echocardiography also has the potential to be a noninvasive alternative to
pulmonary artery catherization (Swan-Gantz catheterization) for hemodynamic monitoring, as it
also allows the measurement of central venous, pulmonary arterial, and pulmonary capillary wedge
pressures, as well as pulmonary and systemic vascular resistance, and stroke volume and cardiac
output.
[105]

0:00 / 0:01

Heart Failure. Transthoracic echocardiogram demonstrating severe mitral regurgitation with heavily calcified mitral valve
and prolapse of the posterior leaflet into the left atrium.

Stress echocardiography

Stress echocardiography, also known as dobutamine or exercise echocardiography, has several

uses; however, in heart failure, this technique is used mainly to assess coronary artery disease.
This imaging modality may be used to detect ventricular dysfunction caused by ischemia, evaluate
myocardial viability in the presence of marked hypokinesis or akinesis, identify myocardial stunning
and hibernation, and relate heart failure symptoms to valvular abnormalities.
[4] However, stress
echocardiography may have a lower sensitivity and specificity in heart failure patients because of
LV dilatation or because of the presence of bundle branch block.

CT Scanning and MRI

Computed tomography (CT) scanning or magnetic resonance imaging (MRI) may be useful in
evaluating cardiac chamber size and ventricular mass, cardiac function, and wall motion;
delineating congenital and valvular abnormalities; and demonstrating the presence of pericardial
disease.
[3] However, cardiac CT scanning is usually not required in the routine diagnosis and
management of heart failure, and echocardiography and MRI may provide similar information
without exposing the patient to ionizing radiation.

The benefits of cardiac MRI (cMRI) include the ability to obtain a great deal of information with a
noninvasive test. This modality provides detailed functional and morphologic information; can be
used to assess ischemic versus nonischemic disease, infiltrative disease, and hypertrophic
disease; and can be employed to determine viability. It is used principally for the delineation of
congenital cardiac abnormalities and for the assessment of valvular heart disease, and it is the
gold standard for evaluating right ventricular (RV) function (see the video below).

0:00 / 0:04

Heart Failure. Cardiac magnetic resonance image (CMRI), short-axis view. This image shows right ventricular dilatation,
trabucular derangement, aneurysm formation, and dyskinetic free wall in a patient with arrhythmogenic right ventricular
dysplasia.

MRI has become particularly useful for evaluating abnormalities in wall motion and viable
myocardium, and MRI findings can help predict the success of revascularization in patients with
low ejection fractions.
[106] However, the detailed information obtained by MRI must be balanced by
its high costs and the fact that this imaging modality cannot be performed in patients with
implantable defibrillators.

Nuclear Imaging
Radionuclide multiple-gated acquisition scanning

Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for the
evaluation of left ventricular (LV) and right ventricular (RV) function and wall motion abnormalities.
Because of its reliability, LV ejection fraction (LVEF), as determined by MUGA scanning, is often
used for serial assessment of postchemotherapy LV function.
[107]

Electrocardiogram-gated myocardial perfusion imaging

The high photon flux of compounds labeled with technetium-99m (99mTc) makes it feasible to
acquire myocardial perfusion images in an electrocardiogram (ECG)-gated mode. ECG-gated
single-photon emission computed tomography (SPECT) images allow for the assessment of the
global LVEF, regional wall motion, and regional wall thickening at rest in patients with documented
stress-induced wall motion and perfusion abnormalities.

In general, LVEF from gated SPECT scanning agrees well with resting LVEF determined by other
modalities. Quality assurance is important, however, because determinations of LVEF with gated
SPECT scanning may be less accurate, even invalidated, in the presence of an irregular heart rate,
low count density, intense extracardiac radiotracer uptake adjacent to the LV, or a small LV.

Combined interpretation of perfusion and function on ECG-gated images substantially increases

the confidence of the interpretation. Taillefer and associates reported that the interpretation of
stress and rest end-diastolic section, rather than summed ungated sections, may enhance the
overall sensitivity for the detection of mild coronary artery disease.
[108]

ECG-gated images are also useful for recognizing artifactual defects caused by attenuation (breast
and diaphragm) and thus are useful in the quality control of SPECT imaging. ECG-gated SPECT
imaging is considered state of the art of radionuclide myocardial perfusion imaging.

Three important practical issues need to be addressed in the evaluation of patients with presumed
ischemic dysfunction, as follows:

Assessment of the relative regional myocardial uptake of thallium-201 (

201Tl; often after rest
reinjection),
99mTc-sestamibi, or
99m Tc-tetrofosmin (often after rest administration of
nitroglycerin); when the resting uptake of radiotracer is greater than 50% of normal, expect
recovery of function after revascularization
Assessment of the presence of demonstrable ischemia (eg, partially reversible defect) in a
myocardial segment with decreased uptake, even if the resting uptake is less than 50%
Data reported in 2011 from a STICH viability substudy failed to demonstrate a significant
impact on survival based on the extent of the viable myocardium in patients with coronary
artery disease and LV dysfunction treated surgically or medically
[109]

Equilibrium radionuclide angiocardiography

Equilibrium radionuclide angiocardiography (ERNA) uses ECG events to define the temporal
relationship between the acquisition of nuclear data and the volumetric components of the cardiac
cycle. Sampling is performed repetitively over several hundred heartbeats, with physiologic
segregation of the nuclear data in accordance with their occurrence within the cardiac cycle.

Data are quantified and displayed in an endless-loop, cinegraphic format for additional qualitative
visual interpretation and analysis. Equilibrium blood-pool labeling is achieved by use of 99mTc.
Data are analyzed by use of a computer, generally with some operator interaction.

Analysis may be obtained in either the frame or list mode. Radionuclide data are collected and
segregated temporally. The process generally requires 3-10 minutes for completion of each view.
Following data acquisition, data from the several hundred individual beats are summed, processed,
and displayed as a single representative cardiac cycle.

Data from the left anterior oblique (LAO) view are also used for qualitative analysis of global LV
function. On this view, overlap of the two ventricles is minimal. In a count-based approach, LVEF
and other indices of filling and ejection are calculated from the LV radioactivity preset at various
points throughout the cardiac cycle.

Right ventricular (RV) function is best evaluated by first-pass techniques. The LAO view provides
qualitative information concerning contraction of the septal, inferoapical, and lateral walls. The
anterior view provides data concerning the regional motion of the anterior and apical segments.
The left lateral or left posterior oblique view provides optimal qualitative information concerning
contraction of the inferior wall and posterobasal segment.

ERNA may easily be combined with additional physiologic stress testing or provocation, which may
be in the form of either physiologic stress, such as exercise; pharmacologic stress, with the use of
positive inotropic agents, such as dobutamine or isoproterenol; or psychological stress. The degree
of confidence with ERNA is moderately high. False-positive and false-negative findings are
infrequent.

Radionuclide ventriculography
Radionuclide ventriculography is most often performed as part of a myocardial perfusion scan to
obtain accurate measurements of LV function and RV ejection fraction (RVEF),
[3, 4]  but it is unable
to directly assess valvular abnormalities or cardiac hypertrophy and has limited value for assessing
volumes or more subtle indices of systolic or diastolic function.

Iobenguane scanning for cardiac risk evaluation

The scintigraphic imaging agent iobenguane I 123 injection (AdreView) is used for the evaluation of
myocardial sympathetic innervation in patients with New York Heart Association (NYHA) class 2-3
heart failure with an LVEF of 35% or less.
[6] This radionuclide tracer, which functions molecularly
as a norepinephrine analogue, can show relative levels of norepinephrine uptake in the cardiac
sympathetic nervous system and contribute to risk stratification in heart failure patients. Improved
reuptake of norepinephrine is associated with a better prognosis.
[6]

Catheterization and Angiography

In patients with a nonischemic cardiomyopathy, perfusion deficits and segmental wall-motion
abnormalities suggestive of coronary artery disease are commonly present on noninvasive
imaging.
[3] Only coronary angiography, however, can reliably demonstrate or exclude the presence
of obstructed coronary vessels (see the following image).
[3]
Heart Failure. A color-enhanced angiogram of the left heart shows a plaque-induced obstruction (top center) in a major
artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.

The procedures are frequently indicated when systolic dysfunction of unexplained cause is present
on noninvasive testing or when normal systolic function with episodic heart failure suggests
ischemically mediated left ventricular (LV) dysfunction. However, although coronary angiography
may be indicated in young patients to exclude the presence of congenital coronary anomalies, this
procedure may not be as useful in older patients, because revascularization has not been shown to
improve clinical outcomes in patients without angina.
[3] Despite this, because revascularization
may improve LV function, some experts suggest that coronary artery disease should be excluded
whenever possible, especially in patients with diabetes mellitus or other states associated with
silent myocardial ischemia.
[3] The degree of confidence is moderately high.

Right-sided heart catheterization

Right heart catheterization is useful in providing important hemodynamic information about filling
pressures, vascular resistance, and cardiac output when there is doubt about the patient's fluid
status; in heart failure refractory to initial therapy; in the presence of significant hypotension
(systolic blood pressure typically < 90 mm Hg or symptomatic low systolic blood pressure) and/or
worsening renal function during initial treatment; and when heart transplantation or placement of a
mechanical circulatory support device is being considered.
[3] However, it plays a limited role in the
diagnosis of heart failure, as studies evaluating right heart catheterization and overall improved
outcomes have been essentially neutral.
[110]

Normal right-sided hemodynamics include a right atrial pressure less than 7 mm Hg, right
ventricular (RV) pressure below 30/7 mm Hg, pulmonary pressure less than 30/18 mm Hg,
pulmonary capillary wedge pressure (PCWP) below 18 mm Hg, and cardiac index (CI) above 2.2
L/min/m2.

PCWP can be measured by using a pulmonary arterial catheter (Swan-Ganz catheter). This helps
to differentiate cardiogenic causes of decompensated heart failure from noncardiogenic causes,
such as acute respiratory distress syndrome (ARDS), which occurs secondary to injury to the
alveolar-capillary membrane rather than to alteration in Starling forces. A PCWP exceeding 18 mm
Hg in a patient not known to have chronically elevated left atrial pressure is indicative of
cardiogenic decompensated heart failure. In patients with chronic pulmonary capillary
hypertension, capillary wedge pressures exceeding 25 mm Hg are generally required to overcome
the pumping capacity of the lymphatics and produce pulmonary edema.

Large V waves may be observed in the PCWP tracing in patients with significant mitral
regurgitation because large volumes of blood regurgitate into a poorly compliant left atrium. This
raises the pulmonary venous pressure and may cause pulmonary edema.

Left-sided heart catheterization

Left-sided heart catheterization and coronary angiography should be undertaken when the etiology
of heart failure cannot be determined by clinical or noninvasive imaging methods or when the
etiology is likely to be due to acute myocardial ischemia or infarction. Coronary angiography is
particularly helpful in patients with LV systolic dysfunction and known or suspected coronary artery
disease in whom myocardial ischemia is thought to play a dominant role in the reduction of LV
systolic function and the worsening of heart failure.

Assessment of Functional Capacity

Cardiopulmonary stress testing (maximal exercise stress testing with measurement of respiratory
gas exchange) can help in the assessment of a patient’s chance of survival within the next year, as
well as determine the need for referral for either cardiac transplantation or implantation of
mechanical circulatory support.  A 6-minute walk test evaluates the distance walked, dyspnea
index on a Borg scale from 0 to 10, oxygen saturation, and heart rate response to exercise. A
normal value is walking more than 1500 feet. Patients who walk less than 600 feet have severe
cardiac dysfunction and a worse short- and long-term prognosis.
[4]

Treatment & Management

 
 

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