Medmastery Medical Treatment of Heart Failure

MEDICAL TREATMENT OF
HEART FAILURE
HANDBOOK
Franz Wiesbauer, MD MPH

Table of contents
Abbreviation list 4
Introduction to heart failure

Reviewing heart failure basics 7
Classifying left-sided heart failure 12
Classifying right-sided and biventricular heart failure 16
Taking a history 19
Performing a physical exam 23
Ordering laboratory tests 27
Interpreting diagnostic tests 32
Diagnosing HFpEF 37
Causes of heart failure

Identifying ischemic heart disease 43
Recognizing common underlying causes 46
Introducing cardiomyopathies 50
Managing chronic stable heart failure

Identifying stages of heart failure 54
Treating Stages A and B HFrEF 58
Treating Stage C HFrEF 61
Considering additional medications in HFrEF 65
Addressing comorbidities with HFrEF 69
Treating HFpEF 73
Handling follow-up appointments 75
Managing advanced heart failure

Identifying Stage D HFrEF 80
Recognizing acute decompensated heart failure 83
Evaluating acute decompensated heart failure 86
Using intravenous medications 90
Preparing patients for discharge 93
Exploring other treatments 95
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Appendix
Appendix 1: Drugs commonly used to treat HFrEF 98
Reference list 101

Abbreviation list
ACC American College of Cardiology
ACE angiotensin-converting enzyme
ACM arrhythmogenic cardiomyopathy
AHA American Heart Association
ARB angiotensin II receptor blocker
ARDS acute respiratory distress syndrome
ARNi angiotensin receptor-neprilysin inhibitor
ARVC arrhythmogenic right ventricular cardiomyopathy
b.i.d. twice a day
BNP B-type natriuretic peptide
bpm beats per minute
CABG coronary artery bypass graft
cath catheterization
CBC complete blood count
COPD chronic obstructive pulmonary disease
CPAP continuous positive airway pressure
CPET cardiopulmonary exercise testing
CT computed tomography
DCM dilated cardiomyopathy
ECG electrocardiogram
ECMO extracorporeal membrane oxygenation
EDV end-diastolic volume
EF ejection fraction
ESV end-systolic volume
GFR glomerular filtration rate
H2FPEF score heavy (obesity), hypertension medications, atrial fibrillation,
pulmonary hypertension, elderly, filling pressure
HCM hypertrophic cardiomyopathy
HFmrEF heart failure with mid-range ejection fraction
HFpEF heart failure with preserved ejection fraction
HFrEF heart failure with reduced ejection fraction
HIV human immunodeficiency virus
IV intravenous
JVP jugular venous pressure

LFTs liver function tests
LV left ventricular
LVADs left ventricular assist devices
LVNC left ventricular non-compaction cardiomyopathy
NT-proBNP N-terminal pro-B-type natriuretic peptide
NSAIDs nonsteroidal anti-inflammatory drugs
NYHA New York Heart Association
PCI percutaneous coronary intervention
PCWP pulmonary capillary wedge pressure
PET positron emission tomography
proBNP pro-B-type natriuretic peptide
q.d. once a day
RAAS renin-angiotensin-aldosterone system
RCM restrictive cardiomyopathy
S3 third heart sound
SARS-CoV-2 severe acute respiratory syndrome coronavirus 2
SGLT2 sodium-glucose cotransporter 2
t.i.d. three times a day
TSH thyroid-stimulating hormone

Chapter 1
INTRODUCTION TO
HEART FAILURE
www.medmastery.com
Reviewing heart failure basics
Before we dive into heart failure, you need to understand how a normal heart
works. The cardiac cycle has two phases:
1. Diastole
Ventricles relax and fill with blood from the atria.
2. Systole
Ventricles contract. The right ventricle pumps deoxygenated blood to the
lungs where it is replenished with oxygen and the left ventricle pumps
oxygenated blood from the lungs throughout the body.
What happens during heart failure?

Heart failure is a complex syndrome where the heart is not functioning properly.
The body doesn’t receive an adequate supply of blood because the heart isn’t
pumping enough, or it isn’t able to adequately fill.
Heart compensates
The heart will try to compensate by one of three methods:
1. Stretch larger
Over time, the heart becomes enlarged as it stretches to contract more
strongly and keep up with the demand to pump more blood.
2. Increase muscle mass

The second compensatory mechanism is increased muscle mass. The heart
cells get bigger. This allows the heart to pump more strongly, at least initially.
3. Pump faster
The third compensatory mechanism is to pump faster, which increases the
heart’s output.

Stretch larger Increase muscle mass Pump faster
Body compensates
The body also tries to compensate for the decreased blood flow it is receiving.
1. Narrow vessels
The blood vessels narrow to keep blood pressure up and make up for the
heart’s loss of pumping power.
2. Divert flow
The body diverts blood flow away from less important tissues and organs to
the heart and brain.
These temporary measures mask heart failure but it continues to worsen

until these compensatory processes no longer work and the patient develops
characteristic symptoms of heart failure.
How does heart failure develop?

We often talk about heart failure as being either acute or chronic.
• Acute
- occurs suddenly, such as after a heart attack or after an arrhythmia develops
- often requires hospitalization and immediate treatment with diuretics or
other agents
• Chronic
- develops gradually from longstanding issues, such as hypertension
- often well compensated by the heart and body, at least for a while

Less common causes of heart failure include:
• Genetic or hereditary causes:

- hypertrophic cardiomyopathy (HCM)
- arrhythmogenic right ventricular cardiomyopathy (ARVC)
- left ventricular (LV) non-compaction cardiomyopathy
- hemochromatosis
• Infiltrative causes:
- amyloidosis
- glycogen storage disease
- Fabry ’s disease
• Inflammatory / infectious immune causes:
- myocarditis
- pericarditis
- sarcoidosis
- autoimmune diseases (e.g., systemic lupus erythematosus, scleroderma)
• Metabolic causes:
- diabetes
- thyroid disease
- adrenal insufficiency
- Cushing’s disease
- pheochromocytoma
• Pregnancy-related causes:
- postpartum cardiomyopathy
- pre-eclampsia
- gestational diabetes
• Toxic agent-related causes:
- alcohol
- amphetamines
- cocaine
- steroids
- chemotherapy
- radiation
- heavy metals

• Nutritional causes:
- thiamine deficiency
- selenium deficiency
- obesity
- malnutrition
Note that heart failure affects both males and females equally, but seems to
appear in males at a younger age.
How do we describe heart function?

The following terms will help you when discussing heart function:
• Stroke volume
- volume of blood pumped out by the left ventricle in one contraction
- calculated as the difference between the volume at the end of ventricular
filling (end-diastolic volume, EDV) and the volume at the end of ventricular
contraction (end-systolic volume, ESV)
Stroke volume = end-diastolic volume – end-systolic volume
• Cardiac output
- volume of blood the heart pumps through the circulatory system in 1 minute
- stroke volume multiplied by the heart rate
- normal adult at rest has a cardiac output of 4.7 L of blood / minute
There are two other factors that will affect cardiac output:
• Preload
Preload is the initial stretching of the cardiac muscle cells before contraction.
It is related to ventricular volume and the end-diastolic pressure in the

ventricle. Increased preload will increase the cardiac output and decreased
preload will decrease cardiac output.
Preload
• Afterload
Afterload is the pressure against which the heart must contract to eject blood
during systole. It is proportional to the mean systolic blood pressure, so
hypertension will increase the afterload. On the other hand, vasodilation will
reduce the afterload by reducing the systemic vascular resistance in the
blood vessels.
Afterload
In a dilated heart, which occurs in some types of heart failure, afterload will be
increased and cardiac output will be decreased.
In the upcoming lessons, you will learn how to recognize the different types of
heart failure.
Return to table of contents.

Classifying left-sided heart failure
Heart failure can involve the left side, right side, or both sides of the heart.
What causes left-sided heart failure?

Left-sided heart failure can be caused by the following:
• Left ventricular dysfunction (most common)
• Mitral or aortic valve dysfunction
• Cardiomyopathies
• Congenital heart disease
How do we classify left-sided heart failure?

We classify left-sided heart failure based on how the ejection fraction (EF) has
changed. EF describes the pumping ability of the left ventricle. It measures the
percentage of blood pumped out of the left ventricle with each contraction.
Ejection fraction
To calculate EF, we divide the left ventricular stroke volume by the end-diastolic
volume, then multiply by 100.
EF (%) = (stroke volume / end-diastolic volume) x 100
The ejection fraction in a normal heart ranges from 55–70%. If the pumping
ability of the heart is impaired, the ejection fraction decreases. Echocardiograms
are used to assess EF and the pumping abilities of the left and right ventricles of
the heart.

There are three types of left-sided heart failure:
1. Heart failure with reduced ejection fraction (HFrEF)
2. Heart failure with preserved ejection fraction (HFpEF)
3. Heart failure with mid-range ejection fraction (HFmrEF)
≤ 40% ≥ 50% 41–49%
Heart failure with reduced ejection fraction

HFrEF is also known as systolic heart failure. It is defined by an ejection fraction
of 40% or less. The most common causes of HFrEF include the following:
• Coronary artery disease
• Idiopathic dilated cardiomyopathy
• Hypertension
• Valvular disease
We’ll talk about these in more detail in a later lesson.
In HFrEF, the left ventricle is dilated and the heart muscle is weakened, so the left
ventricle does not contract effectively and less blood is pumped out to the body.
As a result, oxygenated blood coming back from the lungs builds up in the
pulmonary veins, and fluid backs up in the lungs causing pulmonary edema.
Systolic heart failure

Left ventricle is dilated and weakened

Pulmonary edema presents with the following symptoms:
• Shortness of breath, also called dyspnea
• Coughing
• Fatigue
Dyspnea often occurs when the patient is exerting

themselves, or when they are lying down, in which
case it is called orthopnea.
If not treated promptly, pulmonary edema can lead to respiratory distress.
Heart failure with preserved ejection fraction

HFpEF is also known as diastolic heart failure. It is defined by a normal or
preserved ejection fraction of 50% or higher. The most common causes of HFpEF
include the following:
• Hypertension
• Coronary artery disease
• Diabetes
• Hypertrophic obstructive cardiomyopathy
• Restrictive cardiomyopathy
HFpEF develops when the wall of the left ventricle becomes stiff and thickened.
It can no longer fully relax during diastole. So, the amount of blood filling the left
ventricle is smaller than normal.
Diastolic heart failure

Left ventricle stiff and thickened
Even though the heart muscle cannot relax as it should, the left ventricle is still
contracting normally, so the ejection fraction—the percentage of blood pumped

in each contraction—is preserved. But the absolute volume of blood per beat is
decreased, meaning the heart is unable to meet the body’s needs.
HFpEF is more difficult to diagnose than HFrEF. HFpEF is most common

in females and in older people with comorbidities so keep it in mind when
evaluating these patients. We will further discuss diagnosing HFpEF in Lesson 4.
Heart failure with mid-range ejection fraction

HFmrEF is a newer classification. This encompasses heart failure with an
ejection fraction of 41–49% and it has characteristics of both HFrEF and HFpEF.
In the next lesson, we’ll talk about classifying patients with right-sided and
biventricular heart failure.

Classifying right-sided and biventricular
heart failure
In the previous lesson, we covered left-sided heart failure. Heart failure can
also involve the right side or both sides of the heart, which we will look at in
this lesson.
How does right-sided heart failure develop?

Right-sided heart failure is caused by conditions such as the following:
• Pulmonary hypertension
• Right ventricular dysfunction
• Pulmonic or tricuspid valve dysfunction
• Pulmonary embolism
• Lung diseases like chronic obstructive pulmonary disease (COPD)
If the right side of the heart cannot pump effectively, blood backs up in the veins.
The increased pressure inside the veins can push fluid out of the veins into the
surrounding tissue. The fluid build-up in the tissues results in swelling, also
known as congestion, in the ankles, legs, abdomen, or lungs. This is why heart
failure is often called congestive heart failure.
Symptoms of congestion
The symptoms of congestion can include the following:
• Peripheral edema
• Ascites
• Pulmonary edema
Peripheral edema
Swelling in the ankles and legs is known as peripheral edema.
Recall that the body compensates in response to heart failure by diverting flow
toward the heart and brain and away from other organs, such as the kidneys.
This can affect the kidneys’ ability to eliminate sodium and water, causing even
more fluid retention with worsening peripheral edema.

Peripheral edema
Ascites
Increased pressure in the hepatic veins will result in fluid in the abdomen, known
as ascites.
Ascites
Pulmonary edema
Also recall that when fluid collects in the lungs, it’s known as pulmonary edema,
usually present in the case of left ventricular heart failure. When right ventricular
heart failure occurs, we usually see pulmonary effusion. This is another example
of congestion.
Pulmonary edema

How does biventricular heart failure develop?
Chronic left-sided heart failure can also lead to right-sided heart failure. In fact,
most patients with right-sided heart failure have some element of left-sided
heart failure.
When the two occur together, it’s known as biventricular failure. Biventricular
heart failure can cause the same symptoms as both left-sided and right-sided
heart failure:
• Shortness of breath
• Congestion in the legs, abdomen, and / or lungs
Not everyone with heart failure will have visible congestion.

Excess fluid can hide all over the body before it becomes
readily apparent. So, keep in mind that some people will
only present with fatigue and decreased activity tolerance.

Taking a history
Taking a good history is an important first step in diagnosing your patient with
heart failure. Also, watch out for clues that may indicate the underlying cause of
heart failure.
Which symptoms are relevant to heart failure?

Heart failure symptoms may be nonspecific and / or respiratory.
Nonspecific symptoms
When you take the history, your patient with heart failure may
complain of only nonspecific symptoms:
• Dyspnea
• Fatigue
• Anorexia, weight loss, or weight gain
• Nausea
• Nocturia (waking up in the night to urinate)
• Oliguria (low urine production)
It’s important to have heart failure in your differential

diagnosis when patients present with these
nonspecific symptoms.
Respiratory symptoms
Some patients will have obvious respiratory symptoms due to
pulmonary edema:
• Dyspnea on exertion
• Cough
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Bendopnea

Paroxysmal nocturnal dyspnea is shortness of breath that awakens the
patient after 1–2 hours of sleep and sitting upright can relieve it. Bendopnea
is when the patient is very short of breath bending over and is a sign of
pulmonary hypertension.
Which clues can help identify the underlying cause of

heart failure?
Several important clues can help you identify the underlying cause of
heart failure:
• Palpitations
If a patient has palpitations, they may have an arrhythmia like atrial fibrillation
that has led to heart failure.
• Angina
Be sure to ask your patient if they have chest pain (angina) because it
can indicate coronary artery disease, one of the most common causes of
heart failure.
• Alcohol or recreational drug use

Ask about alcohol and recreational drug use as these can both cause
heart failure.
• History of radiation or chemotherapy

Radiation or chemotherapy can result in heart damage known as
cardiotoxicity. This may lead to heart failure in the days or months after
treatment, but it often develops years later.
• Family history of heart failure

Ask about a family history of heart failure. If the same cardiomyopathy
is found in two or more first-degree family members, there may be a
genetic cause.
The possible underlying causes of heart failure and the clues to identify them are
summarized in the table shown next.

Underlying cause of heart failure Clue
Arrhythmia • Tachycardia (i.e., pulse > 100 bpm at rest)

• History of atrial fibrillation
Coronary artery disease • Angina or exertional dyspnea

• Previous history of coronary artery
disease or bypass surgery
Alcoholic cardiomyopathy • Alcohol consumption
Drug-related heart disease • Recreational drug use

• Illegal use of steroids or testosterone
Cardiotoxicity • History of radiation or chemotherapy
Genetic • Family history of heart failure, sudden

cardiac death, pacemakers, or internal
cardiac defibrillators
Abbreviations: bpm, beats per minute
How do you identify heart failure with preserved

ejection fraction?
Diagnosing heart failure in a patient with a preserved ejection fraction (HFpEF)
can be more difficult. The signs and symptoms of HFpEF will be the same as
other types of heart failure, but three clues may help direct you to HFpEF:
1. Older age
HFpEF is the most common type of heart failure in patients aged 65 years
or older, especially those with comorbidities such as COPD, atrial fibrillation,
hypertension, obesity, obstructive sleep apnea, diabetes mellitus, and
chronic kidney disease.

2. Symptoms worsen on exertion
HFpEF patients may be symptomatic at rest or only
with exercise. Patients with HFpEF often complain of
exertional chest pain. Consider HFpEF as a possible
diagnosis if your patient mentions their symptoms are
worse on exertion.
3. Female
HFpEF is more common in females.

Performing a physical exam
The physical exam is the next crucial step in diagnosing your patient with heart
failure. Remember to watch out for clues that may indicate the underlying cause
of heart failure.
Step 1: Observe the patient

Start by generally observing the patient, checking for any noticeable symptoms:
• Shortness of breath
• Cyanosis
• Cachexia
Step 2: Check vital signs

Check the patient’s vital signs for the following:
• Tachycardia
• Hypertension
• Orthostatic blood pressure changes
• Pulsus alternans
Pulsus alternans is evenly spaced alternating strong and weak peripheral pulses.
It is best appreciated by applying light pressure on the peripheral arterial pulse
and can be confirmed when measuring the blood pressure. If present, pulsus
alternans is indicative of severe left ventricular systolic dysfunction.
Step 3: Examine the chest

Examine the chest, specifically the heart, jugular vein, and lungs:
• Auscultate the heart and palpate the chest
Heart auscultation may reveal soft S1, loud S2, mitral or tricuspid
regurgitation murmurs, or an abnormal third heart sound (S3 gallop). An S3 is
associated with left atrial pressures exceeding 20 mmHg and increased left
ventricular end-diastolic pressures of greater than 15 mmHg. As well, palpate

the chest for a laterally displaced point of maximal impulse, which signifies
an enlarged heart.
• Measure jugular venous pressure

Measuring the jugular venous pressure (JVP) is important for assessing
volume status and filling pressures. An elevated JVP reveals elevated right-
sided pressure, but 80% of the time it will also accurately predict the pressure
on the left side of the heart.
Elevated jugular venous pressure
• Auscultate the lungs

When auscultating the lungs, they may be clear, or you may notice the
following signs of pulmonary edema:
- pulmonary rales or crackles
- wheezing
Step 4: Examine the abdomen and limbs

Recall, excess fluid may also present peripherally. Be sure to check the limbs
and abdomen when you are considering a diagnosis of heart failure:
• Ankles and legs
- peripheral edema
• Abdomen
- ascites
- pulsatile hepatomegaly
- pain from hepatic congestion
- hepatojugular reflux

Remember, HFpEF patients are more difficult to diagnose.
They may or may not have obvious signs of heart
failure such as an elevated JVP, a third heart sound (S3),
pulmonary rales, or lower extremity edema.
Step 5: Use the Framingham Criteria

The Framingham Criteria are useful for diagnosing heart
failure. The signs and symptoms are separated into major
and minor criteria.
1. Major criteria
- orthopnea
- paroxysmal nocturnal dyspnea
- elevated JVP
- pulmonary rales
- S3 gallop
- cardiomegaly is seen on chest x-ray
- acute pulmonary edema is seen on chest x-ray
- hepatojugular reflux
Cardiomegaly Acute pulmonary edema

2. Minor criteria
- peripheral edema
- nocturnal cough
- dyspnea on ordinary exertion
- hepatomegaly
- pleural effusion
- tachycardia with a heart rate above 120 beats per minute (bpm)
3. Major or minor criterion

This criterion can be counted as either major or minor:
- weight loss ≥ 4.5 kg in 5 days of treatment with a diuretic
For a diagnosis of heart failure, a person must have a combination of criteria

present at the same time, including either of the following:
• ≥ 2 major criteria
• 1 major criterion + 2 minor criteria
After the history and physical, diagnostic tests may be necessary to measure
cardiac function and help identify any underlying cardiac abnormalities. We’ll
look at these in the next lesson.

Ordering laboratory tests
In this lesson, we’ll look at the important role that laboratory testing plays for
patients with suspected or newly diagnosed heart failure.
Step 1: Order routine tests

Routine laboratory testing includes:
• Complete blood count (CBC)
• Electrolytes
• Lipid profile
• Hemoglobin A1c
• Fasting blood glucose level
• Renal function
• Liver function tests (LFTs)
• Thyroid-stimulating hormone (TSH) level
• Urinalysis
The results of these tests help identify whether or not your patient has a
condition other than heart failure or if they have associated comorbidities such
as anemia, elevated cholesterol, diabetes, or a thyroid condition.
Renal function should be carefully monitored because worsening renal function

is associated with a poor prognosis in heart failure patients.
Step 2: Order tests specific to your suspicions

Depending on specific clinical suspicions, additional diagnostic tests may be
done, such as the following examples:
• If you suspect hemochromatosis, you should perform iron studies.
• If you suspect amyloidosis, you should perform protein electrophoresis.
• If you suspect giant cell myocarditis or your imaging study is inconclusive
and you’re convinced they have infiltrative cardiomyopathy, you might think
about an endomyocardial biopsy.

Step 3: Check heart failure biomarkers
Two serum biomarkers are used in the diagnosis of heart failure:
1. B-type natriuretic peptide levels (BNP)
2. N-terminal pro-B-type natriuretic peptide levels (NT-proBNP)
In the muscle cells of the heart, proBNP is produced in response to ventricular

wall stress. In heart failure, as the heart enlarges, more proBNP is produced.
ProBNP is cleaved into two peptides:
1. Biologically active BNP
2. Biologically inactive NT-proBNP
BNP has beneficial actions in heart failure. It inhibits the renin-angiotensin-

aldosterone system (RAAS), which relaxes the blood vessels and lowers the
blood pressure. It also increases sodium and water loss through the kidneys,
which lowers blood volume.
ProBNP is cleaved into BNP and NT-proBNP;

BNP inhibits RAAS

In people without heart failure, plasma concentrations of BNP and NT-proBNP
are similar, approximately 100 pg / mL.
A BNP level below 100 pg / mL means that heart failure is unlikely while a BNP
level above 400 pg / mL suggests the patient has heart failure. In the range
between 100 and 400 pg / mL, plasma BNP concentrations are not very sensitive
or specific for detecting or excluding heart failure. Plasma BNP levels can be
used in heart failure for early detection, differential diagnosis, and prognosis.
Using BNP for the diagnosis of heart failure
BNP (pg / mL) Diagnosis of heart failure

< 100 Unlikely
100–400 Possible but other diagnoses should be considered
> 400 Very likely
As noted above, a normal value for NT-proBNP is around 100 pg / mL. Levels
below 300 pg / mL exclude a diagnosis of heart failure. An NT-proBNP of
450 pg / mL or higher indicates heart failure for patients less than 50 years old.
An NT-proBNP of 900 pg / mL or higher indicates heart failure for patients 50–75
years of age. Heart failure is diagnosed by an NT-proBNP of 1800 pg / mL or
above for patients over 75 years of age.
Using NT-proBNP for the diagnosis of heart failure
Age (years) NT-proBNP (pg / mL) Diagnosis of heart failure

Any < 300 Unlikely
< 50 > 450 Very likely
50–75 > 900 Very likely
> 75 > 1800 Very likely

Factors that affect BNP and NT-proBNP
When interpreting BNP and NT-proBNP lab results, keep in mind that the levels
increase with certain conditions or factors:
• Older age
• Female sex
• Some acute non-cardiac illnesses, such as sepsis
• Renal failure: NT-proBNP will be increased more than BNP levels
• Left ventricular dysfunction: plasma NT-proBNP will be approximately
fourfold higher than BNP
By contrast, these biomarker levels can decrease with other factors:

• Obesity
• Acute decompensated heart failure
False negatives with HFpEF

Most importantly, heart failure with a preserved ejection fraction (HFpEF) can
give false negative results for BNP and NT-proBNP. In these patients, the heart
walls are thick, and the radius of the heart is small. So, there is less cardiac wall
stress compared to an enlarged HFrEF heart, which means less stimuli for
BNP production.
Thick heart walls stimulate less BNP production
About 30% of patients who have a confirmed diagnosis of

HFpEF will have a normal BNP. Don’t be fooled by a normal
BNP in HFpEF!

As we’ve seen, laboratory tests play a useful role in the diagnosis of heart failure
and associated comorbidities but remember to interpret results in the context of
your specific patient.

Interpreting diagnostic tests
Let’s look at other tests useful for diagnosing and determining the underlying
cause of heart failure.
What can you learn from a chest x-ray?

All patients with suspected heart failure should have a chest x-ray for
two reasons:
1. To evaluate for cardiomegaly and pulmonary edema
2. To rule out other causes of dyspnea, such as pulmonary disease
Cardiomegaly Pulmonary edema
HFpEF
Note that most patients with HFpEF will have a normal chest x-ray.
HFpEF often shows normal chest x-ray

What can you learn from an electrocardiogram?
Every patient with suspected heart failure should have an electrocardiogram
(ECG) to check two details:
1. Rhythm
2. QRS duration
If the patient has a normal ECG, the diagnosis of heart failure is unlikely. But the
ECG may reveal abnormalities that increase the likelihood of heart failure such
as the following:
• Atrial fibrillation
• Q waves
• Left atrial enlargement
• Left ventricular hypertrophy
• Widened QRS complex
Normal Atrial fibrillation Q waves
Left atrial enlargement Left ventricular hypertrophy Widened QRS complex
HFpEF
In HFpEF patients, the ECG may show evidence of either of the following:
• Myocardial ischemia
• Prior infarction

Atrial fibrillation is most often associated with HFpEF, but it can occur with other
types of heart failure, as well.
Myocardial ischemia Prior infarction Atrial fibrillation
What can you learn from an echocardiogram?

An echocardiogram provides structural and functional information:
• Chamber size
• Eccentric or concentric left ventricular hypertrophy in cardiomyopathies
• Regional wall motion abnormalities, which can indicate coronary
artery disease
• Right ventricular function
• Pulmonary hypertension
• Valvular function
Pulmonary capillary wedge pressure

Doppler echocardiography can be used to estimate pulmonary capillary wedge
pressure (PCWP). PCWP is frequently used to assess left ventricular filling (i.e.,
left atrial pressure) and mitral valve function.
Normal PCWP is 4–12 mmHg. A PCWP of greater than 15 mmHg might indicate
severe left ventricle failure or severe mitral stenosis.
Ejection fraction
An echocardiogram is also essential for calculating the ejection fraction in heart
failure patients. You should reassess the ejection fraction if there’s a change in
clinical status or 3–6 months after the optimization of medical therapy (to allow
time for the medications to work).

HFpEF
In patients with suspected HFpEF, Doppler echocardiography can be used to
measure whether two measures have increased:
1. Left ventricular filling pressure
2. Stiffness of the left ventricle
For more details about how to make these assessments,

check out Medmastery’s Echocardiography
Essentials course or Point-of-Care Ultrasound
Masterclass course.
What can you learn from exercise testing?

Cardiopulmonary exercise testing (CPET) can be helpful in classifying how
symptomatic a heart failure patient is. But stress echocardiography is not helpful
in heart failure patients because there are significant regional wall
motion abnormalities.
CPET
What can you learn from CT coronary angiography?

Coronary artery disease is the number one cause of heart failure. So, if there’s
any suspicion of coronary artery disease, go straight to CT coronary angiography
to assess the severity of the disease.

Note, though, that this is an invasive procedure with a risk of serious
complications such as the following:
• Atheroemboli
• Myocardial infarction
• Ventricular tachyarrhythmias
• Stroke
• Death
Invasive coronary catheterization with angiography should be reserved for

patients with the following:
• Angina
• Positive exercise test
• Unexplained heart failure
To learn more about coronary angiography, check out

Medmastery’s Coronary Angiography Essentials course.
What can you learn from an invasive

hemodynamic assessment?
An invasive hemodynamic assessment is a test specifically for diagnosing
HFpEF. You’ll learn more about this in the next lesson.

Diagnosing HFpEF
As we’ve noted throughout this chapter, it can be challenging to diagnose heart
failure with preserved ejection fraction (HFpEF).
Why is it difficult to diagnose HFpEF?

Recall that in HFpEF, the following can be normal:
• Biomarkers, such as BNP
• Chest x-ray
• ECG
In HFpEF, biomarkers, chest x-ray, and ECG may be normal
HFpEF patients may even be asymptomatic. Or their symptoms may be absent

at rest and only become apparent with exercise.
As you are evaluating the possibility of HFpEF, remember there are many
etiologies of dyspnea with a normal ejection fraction, both cardiovascular and
non-cardiovascular:
• Cardiovascular etiologies of dyspnea
- HFpEF
- hypertrophic, infiltrative, or restrictive cardiomyopathy (cardiac amyloid)
- pulmonary arterial hypertension
- constrictive pericarditis
- high output heart failure
- valvular heart disease
- coronary artery disease

- pulmonary embolism
- right ventricular myopathies
• Non-cardiovascular etiologies of dyspnea
- pulmonary disease
- anemia
- obesity
- deconditioning
- renal artery stenosis
- thyroid disease
- neuromuscular and mitochondrial disease
How do you diagnose HFpEF?

If you aren’t sure if your patient has HFpEF, you can perform an invasive
hemodynamic assessment in the cardiac catheterization lab. This is the gold
standard for diagnosing HFpEF.
Calculate H2FPEF score

To decide who should go to the cardiac catheterization (cath) lab, use the H2FPEF
Score. This scoring system assigns points to several important criteria to help
us determine who should have an invasive hemodynamic assessment:
Variable Detail Points

Heavy Body mass index > 30 kg / m 2
2
H2
Hypertensive ≥ 2 anti-hypertensive medications 1
F Atrial fibrillation Paroxysmal or persistent 3
P Pulmonary hypertension Pulmonary artery systolic pressure 1
> 35 mmHg
E Elder, or older adult > 60 years 1
F Filling pressure High filling pressure, E / e’ > 9 1
H2FPEF score 0–9

Add these up to estimate the pre-test probability that your patient has HFpEF.
• High score 6–9
It’s very likely (over 90% probability) that your patient has HFpEF. You can be
confident in diagnosing HFpEF without the cath lab.
• Intermediate score 2–5

For intermediate probabilities, scores ranging from 2–5, you should obtain
a cardiology consult and invasive hemodynamic assessment to determine if
HFpEF is present.
• Low score 0–1

A low score of 0 or 1 is associated with a low probability of HFpEF, and the
patient’s symptoms are most likely due to a non-cardiac cause.
HFpEF is very likely
Need to perform invasive

hemodynamic assessment
Cardiac cause is unlikely
Interpreting H2FPEF score

Use invasive hemodynamic assessment to measure
pulmonary capillary wedge pressure
Using right heart catheterization, PCWP is measured. The PCWP approximates
the left ventricular filling pressure. High PCWP may indicate left ventricular
failure or mitral valve pathology .
PCWP is assessed first at rest and then during exercise. The following PCWPs
are diagnostic of HFpEF:
• ≥ 15 mmHg at rest
• ≥ 25 mmHg during exercise
Example
Let’s look at an example of a patient with possible HFpEF. A 65-year-old obese
female presents to your office complaining of dyspnea on exertion. She is
currently on three medications for hypertension. There is nothing notable in her
history or physical exam.
You order standard bloodwork, plus BNP and NT-proBNP biomarkers, a chest
x-ray, an ECG, and echocardiography. All bloodwork, including BNP, is normal.
The chest x-ray, ECG, and echocardiogram are also all normal.
Does this patient need an invasive hemodynamic assessment?
Let’s calculate her H2FPEF score to find out:
2 points for obesity + 1 point for hypertension + 1 point for age = 4

Her HFpEF score is 4 , giving her an intermediate probability of having HFpEF.
Recall that a score between 2 and 5 requires an invasive hemodynamic
assessment. So, you send her to the cardiac catheterization lab.
Right heart catheterization is performed and her PCWP is normal at rest, 9

mmHg. But this patient complained of dyspnea on exertion, which means she
will need to exercise to produce her symptoms. With exercise, the following
changes occur:
• PCWP goes up to 40 mmHg
• She becomes profoundly short of breath and tachypneic
• Cardiac output goes down
Always keep in mind that a little over half of HFpEF patients are going to
show hemodynamic derangements that are diagnostic of heart failure, but
only during exercise, and we can only make that assessment in the cardiac
catheterization lab.

Chapter 2
CAUSES OF
HEART FAILURE
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Identifying ischemic heart disease
Ischemic heart disease is also known as coronary artery disease and it is the
most common cause of heart failure.
Myocardial ischemia
In ischemic heart disease, there is a buildup of cholesterol
deposits forming plaques on the walls of the coronary arteries
that supply blood to the heart itself. Over time, atherosclerosis (a
narrowing of the arteries) develops, which results in decreased
blood flow to the myocardium, or heart muscle. This decreased
blood flow means the myocardium no longer receives enough
oxygen, resulting in areas of myocardial ischemia.
Myocardial ischemia can occur silently, or it may present with classic symptoms:
• Chest pain or pressure, typically on the left side
• Neck, jaw, shoulder, or arm pain
• Tachycardia
• Nausea and vomiting
• Sweating
• Fatigue
• Dyspnea on exertion
• Arrhythmias
If an atherosclerotic plaque ruptures, it can completely block a coronary artery

and result in myocardial infarction, or heart attack.
Heart failure in ischemic heart disease

Over time, ischemic heart disease and myocardial ischemia lead to a loss of
myocardial tissue and impaired myocardial contraction and relaxation. The left
ventricle becomes enlarged, dilated, and weak, resulting in heart failure.
Ischemic heart disease can result in any type of heart failure. But it is more
common in heart failure with reduced ejection fraction (HFrEF) and heart failure

with mid-range ejection fraction (HFmrEF) than in heart failure with preserved
ejection fraction (HFpEF).
The lower the ejection fraction, the more likely your patient with both heart
failure and ischemic heart disease will experience a new ischemic event like
myocardial infarction.
Did ischemic heart disease cause your patient’s heart failure?

Ischemic heart disease is the leading cause of death worldwide and it affects
both men and women. Patients commonly have the following characteristics:
• Older age
• Many cardiovascular risk factors and comorbidities
• Higher levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP)
Patients with ischemic heart disease and HFpEF are more likely to experience
angina on exertion, so always ask about this symptom.
Keep in mind that ischemic heart disease is common so

it can also be present in patients with heart failure from
other causes.
Identifying and treating ischemic heart disease

If you have any suspicion of coronary
artery disease, you should use
computed tomography (CT) coronary
angiography to assess the severity of
the disease. The extent of coronary
artery disease seen on angiography
is directly related to the patient’s
prognosis, with more extensive disease
indicating a higher mortality risk.

Ischemic heart disease can be treated with medications for relieving angina,
antiplatelet medications to prevent blood clots, and lipid-lowering medications
to slow further damage.
If significant coronary artery disease is found on angiography, myocardial

viability can be assessed by further testing:
• Thallium perfusion imaging
• Positron emission tomography (PET) scanning
• Dobutamine echocardiography
Hibernating myocardium
Hibernating myocardium is an area of muscle tissue that is in a state of dormancy
due to inadequate blood supply. If hibernating myocardium is identified and the
patient’s ejection fraction is less than or equal to 35%, then revascularization will
likely reverse some of the ischemic dysfunction in the heart.
Revascularization can be accomplished with either a percutaneous coronary

intervention (PCI), where angioplasty and stenting are performed or coronary
artery bypass graft (CABG) surgery.

Recognizing common underlying causes
Now that we’ve talked about ischemic heart disease, let’s explain seven other
common underlying causes of heart failure:
1. Hypertension
2. Atrial fibrillation
3. Valvular disease
4. Viral infection
5. Diabetes
6. Thyroid disease
7. Alcohol misuse
8. Cocaine misuse
Hypertension
Hypertension can damage the body for years before obvious
symptoms develop.
The pressure of blood flowing in the arteries increases over

time. The artery walls will eventually become less elastic and
limit the blood flow throughout the body. High blood pressure
forces the heart to work harder to pump blood to the body. This eventually causes
the muscle of the left ventricle to thicken and weaken and heart failure develops.
High blood pressure will also damage the inner lining of the arteries, including
the coronary arteries. So, hypertension can cause coronary artery disease, which
can also result in heart failure.
Is hypertension the cause of your patient’s heart failure?

Hypertension will be readily apparent when taking your patient’s blood
pressure. Patients at risk of developing hypertension are those with some
common characteristics:
• Physical inactivity
• Obesity
• Unhealthy diet
• Smoking habit

• High levels of alcohol consumption
• Certain health conditions like diabetes
Hypertension can be treated with lifestyle modifications and medications.
To learn more about treating hypertension, check out my Hypertension Mini

course in the Medmastery Library.
Valvular disease
Another common cause of heart failure is valvular disease. When there are one
or more damaged heart valves, the heart must work harder to pump blood to
the body.
This is the case whether the valve is regurgitant, with

blood leaking back into the chamber, or if the valve is
stenotic with a narrowed opening.
Is valvular disease the cause of your patient’s

heart failure?
Valvular disease can often be identified if you hear a heart murmur during a
physical exam. Valve function can be examined using echocardiography.
Valve disease can also develop secondary to heart failure. Once the left ventricle
becomes dilated, some degree of mitral and tricuspid regurgitation may occur.
Surgical valve replacement can improve cardiac function and heart

failure symptoms.
Viral infections
Viral infections can cause myocarditis, an inflammation of
the heart muscle, which can lead to left ventricular dilation
and heart failure.

Common causes of viral myocarditis include adenovirus (common cold virus),
hepatitis B and C, herpes simplex virus, severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2), and parvovirus (also known as fifth disease).
Other viruses known to infect the myocardium include coxsackievirus, influenza
virus, echovirus, cytomegalovirus, and human immunodeficiency virus (HIV).
Is viral myocarditis the cause of your patient’s heart failure?

If your patient was recently ill with a viral illness and flu-like symptoms, ask
about the symptoms of myocarditis which include chest pain, shortness of
breath, and palpitations.
Patients with mild symptoms often make a full recovery over time. Others will
need continued treatment for chronic heart failure.
Diabetes
Diabetes can also cause heart failure. In patients with
diabetes, high blood glucose can damage the heart muscle
cells, blood vessels, and nerves that control the heart. Over
time, this can lead to heart failure. Diabetes is associated
with both HFrEF and HFpEF.
Patients with type 2 diabetes are more likely to be obese

and have high blood pressure and coronary artery disease. All of these are risk
factors for developing heart failure.
In diabetic patients, blood sugar should be monitored and controlled with

medications to help prevent heart failure.
Thyroid disease
Hypothyroidism and hyperthyroidism can both cause heart failure. Thyroid
hormones affect heart contractility, heart rate, blood pressure, and
cholesterol levels.

In hypothyroidism, the heart rate is slowed, blood pressure
increases, the arteries become less elastic, and cholesterol
is elevated.
Hyperthyroidism causes the heart to beat faster and

harder, which results in high blood pressure and can
trigger arrhythmias.
All these issues contribute to the development of ischemic heart disease and
heart failure, so properly treating thyroid conditions can improve the patient’s
cardiovascular health.
Alcohol misuse
In patients who misuse alcohol, the toxicity of the alcohol
damages and weakens the heart muscle. This can result in
left ventricular dilation with reduced ejection fraction. More
advanced cases often develop biventricular failure. With early
diagnosis, abstinence can lead to a dramatic improvement in
cardiac function.
Cocaine misuse
Lastly, cocaine misuse can cause unexplained heart failure
in a young person. Cocaine causes inflammation in the
heart muscle which leads to stiffening of the muscle and
eventually heart failure. Abstinence usually leads to a
complete reversal of myocardial dysfunction.

Introducing cardiomyopathies
Cardiomyopathies are diseases of the myocardium, the muscle of the heart.
Depending on the type of cardiomyopathy, the heart muscle can become
stiffened, thickened, or enlarged.
All cardiomyopathies can cause symptoms

of heart failure, exercise limitation, and
arrhythmia. Cardiomyopathies are caused
by a wide variety of disorders, some of
which are genetically inherited.
In the past, it was common to refer to other

heart diseases as cardiomyopathies. So, we used to talk about ischemic, valvular,
or hypertensive cardiomyopathy. But the terminology has changed. Since
these are not diseases of the myocardium, they should no longer be referred to
as cardiomyopathies.
There are five classes of cardiomyopathies:

1. Dilated
2. Hypertrophic
3. Restrictive
4. Arrhythmogenic
5. Unclassified
Let’s discuss each of these in more detail.
Dilated cardiomyopathy
Dilated cardiomyopathy (DCM) causes dilation and impaired contraction
of one or both ventricles. Some patients may even have dilation of all four
chambers. Affected patients develop impaired systolic function and symptoms
of heart failure.

Up to 50% of patients have a genetic mutation, which is often inherited in an
autosomal dominant pattern. The other half has an unknown etiology and are
considered to have idiopathic dilated cardiomyopathy.
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) involves unexplained left ventricular
hypertrophy (or thickening). The left ventricular volume is normal or reduced and
diastolic dysfunction is present.
There are four main causes of hypertrophic cardiomyopathy:

1. Amyloidosis (protein buildup in the organs)
2. Friedreich’s ataxia (a genetic disease that leads to progressive nervous
system damage)
3. Fabry disease (which causes fat deposits in tissues)
4. Glycogen storage disease (where glycogen collects in the tissues)
Patients with hypertrophic cardiomyopathy have diastolic stiffness of the left

ventricle, but up to 75% of patients also have dynamic left ventricular outflow
tract obstruction, either at rest or with mild exertion. The obstruction is dynamic,
so the symptoms come and go.
There is a classic triad of symptoms:

1. Exertional dyspnea
2. Exertional angina
3. Exertional presyncope
Many genetic mutations are known to cause hypertrophic cardiomyopathy, so

familial genetic screening is recommended. If the patient doesn’t have a known
mutation, family members should be screened with imaging.

Restrictive cardiomyopathy
Restrictive cardiomyopathy (RCM) is characterized by stiff ventricles with
impaired ventricular filling and will eventually lead to heart failure. It is caused by
a variety of diseases:
• Amyloidosis
• Hemochromatosis (which causes iron buildup in the heart and other organs)
• Sarcoidosis (which involves inflammation and scarring of the heart muscle
and other organs)
• Scleroderma (hardening of the tissues)
On echocardiography, restrictive cardiomyopathy will appear as a normal-

looking left ventricle with a normal ejection fraction but huge atria. The atria are
so big because it takes so much pressure to fill the stiff ventricles.
Arrhythmogenic cardiomyopathy
In arrhythmogenic cardiomyopathy (ACM) there are structural abnormalities of
the myocardium accompanied by an unexplained arrhythmia.
Arrhythmogenic right ventricular cardiomyopathy is one example. In this

condition, the ventricular muscle that is not in contact with the interventricular
septum or apex (the free wall) is replaced by fatty tissue, leading to ventricular
tachycardia. This decrease in heart muscle causes irregular heart rhythms.
Unclassified cardiomyopathy
Unclassified cardiomyopathies are disorders that don’t fit into the other categories.
One example is left ventricular non-compaction cardiomyopathy (LVNC).
During normal embryonic development, the heart muscle compacts from a loose,
sponge-like mass into a smooth and solid muscle. In LVNC, compaction does
not occur and pieces known as trabeculations extend into the left ventricle.
LVNC can cause heart failure, thromboembolism, and ventricular arrhythmias.

Chapter 3
MANAGING CHRONIC
STABLE HEART FAILURE
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Identifying stages of heart failure
The American College of Cardiology (ACC) and the American Heart Association
(AHA) classify heart failure into four stages, A through D, based on structural
changes within the heart.
ACC / AHA stages of heart failure

Heart failure progresses in one direction through the stages, but many patients
don’t seek medical attention until a later stage.
Once structural changes occur in the heart, they are irreversible. The ACC / AHA
stages are used to determine how advanced the disease is, and which treatments
are most appropriate.
ACC / AHA stages of heart failure
Disease severity
Stage A
Stage A patients don’t have any structural abnormalities or symptoms of
heart failure yet, but they have risk factors for developing heart failure, such as
hypertension or diabetes.
A less common example of a Stage A patient would be someone who has

received anthracycline chemotherapy.

Stage B
Patients with Stage B heart failure have structural abnormalities of the heart
but haven’t developed symptoms of heart failure yet. For example, a patient
incidentally found to have a low ejection fraction on echocardiography would be
classified as Stage B.
Stage C
Stage C patients have structural abnormalities of the heart and symptoms of
heart failure. These are the patients that will present to you with symptoms of
congestion. Remember that, while symptoms can be managed, the structural
changes are irreversible.
Stage D
Stage D patients are advanced heart failure patients whose symptoms are
refractory to management with medication. Patients at Stage D often have
repeated hospitalizations and require specialized interventions such as
mechanical circulatory support, continuous inotropic infusions, cardiac
transplantation, or palliative care.
ACC / AHA stage Descriptors

Stage A Risk factors for developing heart failure only
Stage B Structural abnormalities of the heart without symptoms
of heart failure
Stage C Irreversible structural abnormalities of the heart and
symptoms of heart failure (e.g., congestion)
Stage D Advanced heart failure with symptoms that are
refractory to management with medication
Heart failure with preserved ejection fraction (HFpEF)

is limited to patients with symptoms of heart failure
(i.e., ACC / AHA Stages C and D). It doesn’t occur in
Stage A and B patients.

New York Heart Association classification
The New York Heart Association (NYHA) classification is a functional
classification system to assess symptom severity and the degree of limitation
during physical activity. The NYHA classification is a subjective assessment
done by a clinician and can change over short periods of time.
The NYHA classes are used to determine whether your patient’s symptoms are
improving or getting worse.
NYHA classification assesses symptom severity
A Class I heart failure patient has no physical activity limitation.
Class II patients have mild physical activity limitation, such as heart failure
symptoms during ordinary physical activity, but no heart failure symptoms
at rest.
Class III patients have a marked limitation of physical activity. For example,
patients have heart failure symptoms while walking a short distance but have no
heart failure symptoms at rest.
A Class IV heart failure patient has difficulty performing basic daily activities,
and has heart failure symptoms, even at rest.
NYHA classification Descriptions

Class I No limitation on physical activity
Class II Mild physical activity limitation
Class III Marked limitation of physical activity
Class IV Difficulty performing basic daily activities

Using both ACC / AHA and NYHA classifications
Patients can also be classified according to both systems. A Stage A patient
doesn’t have heart failure yet, so they don’t have an associated NYHA class.
A Stage B patient has structural changes in the heart but no symptoms, so they
are NYHA Class I with no limitation to physical activity.
Stage C patients may be Class II, III, or IV depending on how limited their physical
activities are (slight, marked, or severe) and whether or not they are comfortable
at rest or.
Stage D patients are Class IV because they are always uncomfortable with
activity and symptoms persist at rest.
ACC / AHA stage A B C D
NYHA class None I II, III, IV IV

Treating Stages A and B HFrEF
In this lesson , I’ll cover the medical management of Stage A and Stage B heart
failure with reduced ejection fraction (HFrEF).
Managing Stage A
Remember that Stage A patients don’t have heart failure yet. While there aren’t
any structural changes in their heart, they do have risk factors for developing
heart failure in the future. So, Sstage A treatment is focused on managing those
risk factors by treating any or all of the following:
• Hypertension
• Ischemic heart disease
• Hyperlipidemia
• Diabetes
• Performing valve replacement if indicated
Managing Stage B heart failure with reduced

ejection fraction
Recall that Stage B HFrEF patients have structural abnormalities of the heart but
no symptoms of heart failure yet. The goal of medical therapy in this group of
patients is to increase cardiac output.
Despite the absence of symptoms, Stage B patients have a poor prognosis, but
treatment can improve morbidity and mortality.
All Stage B patients should be on an

angiotensin-converting enzyme (ACE)
inhibitor or an angiotensin II receptor
blocker (ARB) plus a beta-blocker. ACE
inhibitors and ARBs work by causing
vasodilation which decreases blood
pressure. Both types of drugs act on
the renin-angiotensin-aldosterone
system (RAAS) which is a complex

system that regulates blood pressure. This reduces the afterload, so that cardiac
output is improved.
ACE inhibitors and ARBs

ACE inhibitors improve morbidity and mortality in HFrEF. But 20% of patients
will develop a non-productive cough on an ACE inhibitor and some will
develop angioedema.
ARBs have a lower risk of cough and angioedema, so switch from an ACE
inhibitor to an ARB if ACE inhibitors are contraindicated.
Note that these medications may cause a transient, asymptomatic rise in

creatinine, but their use should be continued unless creatinine is more than 30%
above the patient’s baseline. As the blood pressure decreases, creatinine will
usually return to baseline.
When treating patients with ACE inhibitors or ARBs, dosing varies depending on
the medication. See Appendix 1 for dosing information.
Beta-blockers
Beta-blockers improve mortality in HFrEF. Beta-blockers block the release of
adrenaline and noradrenaline to slow the heart rate and reduce the contractile
force of the heart. Beta-blockers also act on the renin-angiotensin-aldosterone
system to promote vasodilation and lower blood pressure.
For HFrEF, there are three preferred agents:

1. Carvedilol
2. Metoprolol succinate (not metoprolol tartrate)
3. Bisoprolol
If the patient’s blood pressure is normal, use carvedilol. However, carvedilol tends
to decrease blood pressure and cause bronchospasm more than metoprolol
succinate or bisoprolol. So, if the patient has significant asthma or hypotension,
then use metoprolol succinate or bisoprolol.

Here are a few other things to consider:
• Use metoprolol succinate or bisoprolol in anyone who is borderline
hypotensive.
• Keep in mind that beta-blockers do not need to be avoided in patients who
have asymptomatic hypotension.
• Using bisoprolol at night can help minimize its effects on blood pressure
during the day.
• Beta-blockers do not have as much of an effect on blood pressure in patients
over the age of 65 years.
See Appendix 1 for dosing information.

Treating Stage C HFrEF
Remember that Stage C patients are symptomatic and have structural
abnormalities of the heart. The treatment goals for these patients are to reduce
symptoms, decrease hospitalizations, and reduce mortality.
Like Stage B HFrEF, management of Stage C HFrEF includes an ACE inhibitor

or ARB and a heart failure-specific beta-blocker such as carvedilol, metoprolol
succinate, or bisoprolol.
Stage C HFrEF will also frequently require diuretics and aldosterone antagonists .
Diuretics for Stage C HFrEF

Diuretics are used to relieve symptoms of volume overload. There are two types
of diuretics:
1. Loop diuretics
2. Thiazide diuretics
Loop diuretics
Loop diuretics should be started first. They cause the kidneys to excrete more
sodium and water into the urine. Then, fluid that has accumulated in the tissues
is drawn back into the bloodstream. Congestive symptoms such as edema and
dyspnea will improve.
Loop diuretics include furosemide, torsemide, bumetanide, and ethacrynic acid.

Oral furosemide is usually the first choice.
Oral torsemide or bumetanide often works for patients who don’t respond well
to furosemide. Ethacrynic acid is expensive, so it is reserved for patients with a
sulfa allergy.
Loop diuretic dosing

When initiating diuretic therapy for your patients, consider the dosing required
for each medication. Use the table in Appendix 1 to help guide your clinical
decision-making when prescribing diuretics.

The following steps may assist you in intensifying diuretic therapy for
your patients:
1. Ensure proper use.

After initiating oral furosemide, if the patient is still volume overloaded, make
sure the patient is taking the medication as prescribed.
2. Optimize diet.
Assess for any dietary factors that worsen volume overloading such as
eating too much salt or drinking too much water. Ask the patient what they
ate for dinner last night as it can be very revealing.
3. Progressively increase the dose.

Next, you should increase the dose until there is an increase in urine output
and a 0.5–1 kg decrease in daily weight. You can double the dose, then triple
it, then move to twice daily dosing if needed.
4. Consider alternative medication.

If the patient is still volume overloaded, think about transitioning to an
alternative loop diuretic and adding in as-needed doses of a thiazide diuretic.
5. Try intravenous (IV) diuresis.

Some patients will remain volume overloaded despite maximal loop diuretic
therapy. In these cases, try outpatient IV diuresis with 120 mg or 200 mg of
IV furosemide. This can often prevent a heart failure hospitalization.
Thiazide diuretics
Thiazide diuretics, such as hydrochlorothiazide, act similarly to loop diuretics
but on a different part of the kidney tubules. Thiazide diuretics also cause
vasodilation which lowers blood pressure.
Thiazide diuretics are not as effective in patients with heart failure, so they
should be used in conjunction with loop diuretics.

Only use thiazide diuretics after loop diuretic therapy has
been maximized.
Use thiazide diuretics only as needed, because thiazide diuretics can cause
severe electrolyte disturbances such as hypokalemia, hypomagnesemia,
hyponatremia, and azotemia.
Side effects of diuretics

There are two things you need to know about the side effects of diuretics:
1. Diuretics can cause hypotension.
Patients can tolerate some asymptomatic hypotension so you should
keep increasing the diuretic dose if they have asymptomatic hypotension.
Once the patient is clinically euvolemic (i.e., normal blood volume), the
diuretic dose should be adjusted to the minimum dose required to
maintain euvolemia.
2. Diuretics may cause a transient, asymptomatic rise in creatinine.

Keep treating the volume overload, rather than treating the creatinine level.
Aldosterone antagonists
Aldosterone antagonists, such as spironolactone and eplerenone, are approved
for any symptomatic HFrEF patients with three main signs:
1. Ejection fraction of 35% or less
2. Glomerular filtration rate of at least 30 mL / min / 1.73 m2
3. Potassium level of 5.0 mmol / L or lower
Aldosterone antagonists block the hormone aldosterone, resulting in

increased sodium and water excretion by the kidneys and a lessening of
congestive symptoms.

The main concern with these medications is hyperkalemia. You need to monitor
potassium levels and renal function at four time points:
1. 3 days after starting the medication
2. 7 days after starting the medication
3. Monthly for 3 months
4. Every 3 months after monthly monitoring is finished
Always start with spironolactone because it is the less expensive option. Only
switch to eplerenone if spironolactone causes gynecomastia.
For dosing information, refer to Appendix 1.

Considering additional medications in HFrEF
We’ve already discussed the first-line
medications for treating HFrEF. But what
if you still need a little extra help?
In this lesson, we’ll look at some

additional medications you can use to
treat your heart failure patient with a
reduced ejection fraction.
Hydralazine-nitrates
Let’s start with hydralazine-nitrates. These provide a mortality benefit for Black
patients who are taking optimal doses of an ACE inhibitor and beta-blocker but
are still symptomatic. It’s also reasonable to use hydralazine nitrates in any
patients who cannot tolerate an ACE inhibitor or ARB due to renal dysfunction
or hyperkalemia.
Hydralazine-nitrates relax the blood vessels to reduce the heart’s workload and
increase the supply of blood and oxygen to the heart muscle.
Digoxin
Digoxin is associated with reduced heart failure hospitalizations but has no
mortality benefit.
Consider digoxin in patients who have atrial fibrillation with suboptimal heart
rate control despite a beta-blocker.
Digoxin is also used in patients who are hypotensive and need better heart
rate control but who can’t use higher doses of beta-blockers or are beta-
blocker intolerant.
Digoxin slows down the heart rate and improves the filling of the ventricles.

ARNi
An angiotensin II receptor blocker (ARB) combined with a neprilysin inhibitor is
known as an ARNi.
One example is sacubitril-valsartan. Sacubitril is a neprilysin inhibitor. Neprilysin

is the enzyme that inactivates natriuretic peptides. Valsartan is an ARB. We
discussed ARBs like valsartan in a previous lesson.
You learned earlier that proBNP (pro-B-type natriuretic peptide) is produced in

the cardiomyocytes and then cleaved into two peptides—biologically inactive
NT-proBNP (N-terminal pro-B-type natriuretic peptide), and biologically
active BNP.
The enzyme neprilysin breaks BNP into inactive metabolites. So, medications
like sacubitril inhibit neprilysin, and result in higher circulating levels of BNP,
which helps alleviate some of the symptoms of heart failure.
Recall that BNP inhibits the renin-angiotensin-aldosterone system, acts as

a vasodilator, and lowers blood volume by increasing sodium and water loss
through the kidneys.
Since ARNi medications artificially increase BNP levels,

BNP can no longer be used as a biomarker for heart failure
in patients who are taking these drugs. However, the
level of NT-proBNP is not affected by ARNi medications
so it can still be used as a biomarker for heart failure in
these patients.
When compared to ACE inhibitors, ARNi use in HFrEF reduces hospitalizations

and cardiovascular deaths, suggesting ARNi medications are more effective.
There may be certain HFrEF cases where an ARNi can be started as the initial
treatment. Often, if HFrEF patients remain symptomatic while on an ACE / ARB,

they can switch to an ARNi. However, keep in mind that ARNi medications are
more expensive!
Precautions when using ARNi medications

Sacubitril increases the circulating levels of BNP. It tends to be more of a
vasodilator than an ACE inhibitor or ARB therapy alone so watch for hypotension.
Patients need a systolic blood pressure greater than 100 mmHg before starting
these drugs.
Also, note that any ACE inhibitor must be stopped 48 hours prior to starting an
ARNi to decrease the risk of angioedema.
Ivabradine
Ivabradine is a drug that inhibits the pacemaker function of the sinoatrial node,
reducing the heart rate so the heart can pump more blood through the body each
time it beats (i.e., increase stroke volume).
Ivabradine is only used for patients in sinus rhythm with a heart rate greater
than 70 beats per minute (bpm).
All patients should be on optimal doses of an ACE inhibitor or ARB and a

beta-blocker as first-line therapy for a minimum of 3 months. In most cases,
these drugs will bring the heart rate below 70 bpm. This means that ivabradine
is rarely used in clinical practice.
For those rare patients with a heart rate above 70 bpm and an ejection
fraction less than 35%, ivabradine reduces hospital admissions, but it does not
affect mortality.
Sodium-glucose cotransporter 2 inhibitors

Lastly, consider sodium-glucose cotransporter 2 (SGLT2) inhibitors which are
a class of medications originally developed to treat diabetes. SGLT2 inhibitors
lower blood sugar, but they also improve heart failure symptoms by reducing
body weight and lowering blood pressure.

SGLT2 inhibitors decrease heart failure-related hospitalizations and deaths in
diabetic and non-diabetic patients.
Additional medications to treat HFrEF**
Agent Target patient populations Action Outcome
Hydralazine- • Symptomatic Black • Decrease workload of • Mortality

nitrate patients currently the heart by relaxing benefit
taking ACE inhibitors blood vessels
and beta-blockers • Increase oxygen
• Renal dysfunction supply to the heart
• Hyperkalemia
Digoxin • Atrial fibrillation with • Slows heart rate • Reduced

poor heart rate control • Improves filling of hospitalizations
• Hypotension and ventricles
intolerance to high
doses of beta-blockers
ARNi • Symptomatic HFrEF • Increases circulating • Reduced

while treated by ACE BNP hospitalizations
inhibitor or ARB • Vasodilates • Mortality
• Increase blood volume benefit
Ivabradine • Sinus rhythm with • Inhibits sinoatrial • Reduced

heart rate greater than node hospitalizations
70 bpm • Decreases heart rate
• Increases stroke
volume
SGLT2 • Diabetic and non- • Reduces blood sugar • Reduced

inhibitors diabetic patients • Reduces body weight hospitalizations
• Lowers blood • Mortality

pressure benefit
For dosing information, see Appendix 1

**

Addressing comorbidities with HFrEF
Management of HFrEF also requires managing associated conditions such as
hypertension, diabetes, arrhythmias, sleep-disordered breathing, and pregnancy.
Hypertension
You learned earlier in this course that chronic hypertension can cause heart
failure. However, hypertension can also be a comorbid condition in patients with
heart failure due to other causes.
So, how do we treat hypertensive patients who have Stage B or C HFrEF?
For these patients, standard heart failure

treatment is an ACE inhibitor (or ARB), a beta-
blocker, and a loop diuretic.
If a patient remains hypertensive while on

optimal doses of these drugs, a thiazide
diuretic should be added since it has an
antihypertensive effect. Secondary agents such as an aldosterone antagonist
and hydralazine-nitrate should also be added when indicated.
Calcium channel blockers are a mainstay of hypertension treatment, but

diltiazem and verapamil can worsen heart failure symptoms so they should
be avoided.
Amlodipine is a vasoselective calcium channel blocker so it can be used in the

treatment of hypertension with HFrEF.
Diabetes
Recall that patients with diabetes need to appropriately manage their blood
sugar to prevent the development of heart failure.
But what about diabetic patients who have already developed HFrEF?

Blood sugar still needs to be controlled in
these patients following diabetes guidelines.
One class of medications, SGLT2 inhibitors,
lower blood sugar while also improving heart
failure symptoms by reducing body weight and
lowering blood pressure.
SGL2T inhibitors decrease heart failure-related hospitalizations and deaths in

diabetic and non-diabetic patients.
Arrythmias
Patients with HFrEF are at risk for supraventricular tachycardias, particularly
atrial fibrillation.
Check out the Atrial Fibrillation Management

Essentials Course in the Medmastery Library, for
information on treating this condition.
Ventricular arrhythmias, identified by a prolonged

QRS duration, are also common in HFrEF, and
they are a risk factor for sudden cardiac death. These patients often require a
biventricular pacemaker combined with an implantable cardioverter-defibrillator.
HFrEF patients with bradycardia may require a pacemaker.
Sleep-disordered breathing
Sleep-disordered breathing is underdiagnosed in heart failure patients, but it is
important to recognize and treat because it contributes to the progression of
heart failure. Every time there is an apneic episode, the oxygen level drops, the
body tells the heart to beat faster, and the blood pressure rises.
Overnight polysomnography should be used to assess any patients with heart

failure who mention sleep-related symptoms.

The most common forms of sleep-disordered breathing are obstructive sleep
apnea and central sleep apnea.
Obstructive sleep apnea

In obstructive sleep apnea, upper airway obstruction reduces or momentarily
stops airflow during sleep, despite ongoing respiratory effort.
Patients (or their bed partner) notice a number

of signs or symptoms:
• Poor sleep quality
• Snoring
• Sleep disruption
• Easy fatigability
• Awakening with a sensation of gasping
or choking
• Morning headaches
• Poor concentration or memory impairment
Continuous positive airway pressure (CPAP) is the treatment for obstructive

sleep apnea. It can improve cardiac function, blood pressure, exercise capacity,
and quality of life for heart failure patients.
Central sleep apnea

Central sleep apnea is characterized by cycles of increased and decreased
respiratory effort with periods of not breathing.
Patients may complain of the following symptoms:

• Paroxysmal nocturnal dyspnea
• Insomnia
• Excessive daytime sleepiness
• Difficulty concentrating
For heart failure patients with central sleep apnea, adaptive servo-ventilation
significantly improves ejection fraction and exercise capacity.

Pregnancy
Lastly, heart failure in pregnancy requires special
consideration of the effects of any medications on the fetus
and the mother. This will require referral to a maternal-fetal
medicine specialist for management.

Treating HFpEF
As you’ve learned, ACE inhibitors, ARBs, and beta-blockers are all useful in
treating HFrEF. However, these medications have failed at treating heart failure
with preserved ejection fraction (HFpEF).
What are the options for treating HFpEF patients?

Aldosterone antagonists such as spironolactone are recommended for certain
HFpEF patients with an ejection fraction of 45% or more. These patients must
also meet additional criteria:
• Good renal function (glomerular filtration rate (GFR) > 30 mL / min / 1.73 m2
and creatinine < 120 µmol / L )
• Potassium < 5 mmol / L
• Either a high BNP or hospital admission within the past year
Creatinine values can be affected by body mass, age, race, sex, and hydration
status. Reference ranges for these values can also vary from lab to lab.
Diuretics should also be used to relieve symptoms of volume overload.
Remember that treating heart failure

patients also requires identifying and
treating any associated comorbidities.
There are a number of comorbidities
commonly associated with HFpEF:
• Hypertension
• Ischemic heart disease
• Diabetes and metabolic syndrome
• Obesity
• Arrhythmias
• Sleep-disordered breathing
• Chronic obstructive lung disease
• Kidney disease

SGLT2 inhibitors target all these major comorbidities. So, they are being used
more often in the treatment of HFpEF.
Hypertension is seen in 80–90% of patients with HFpEF. Use a beta-blocker

plus an ACE inhibitor or ARB to get systolic blood pressure below 130 mmHg.
Spironolactone can also be added as needed.
Treat hypertension carefully because HFpEF patients are

often older and don’t tolerate hypotension well.
Renovascular hypertension may be present in patients with HFpEF due to

ischemic heart disease. Recurrent unexplained heart failure decompensation
and / or sudden-onset pulmonary edema occur in some patients with renovascular
hypertension and HFpEF. Treatment options include antihypertensive drugs
and revascularization.
Two-thirds of HFpEF patients have coronary artery disease. It’s reasonable

to pursue coronary revascularization in HFpEF patients with angina or other
symptoms of ischemia.
Weight loss and a healthy diet can be very beneficial in HFpEF patients with
obesity or diabetes and metabolic syndrome. Exercise training increases
exercise capacity and can improve the quality of life.
Lastly, atrial fibrillation is common in patients with HFpEF and should be

managed according to the current guidelines.

Handling follow-up appointments
Patients with heart failure require ongoing follow up with their family physician.
Since heart failure patients can be complex with multiple comorbidities, it’s often
desirable to co-manage these patients in a multi-disciplinary team that includes
a cardiologist and other healthcare professionals.
Lifestyle modifications
Food and drink intake
Some critically important lifestyle modifications have
proven to be beneficial in heart failure patients:
• Restrict salt intake to less than 2 g per day
• Restrict fluid intake to less than 2 L per day
• Abstain from alcohol or consume no more than
two drinks per week
Monitoring weight
Patients should also be encouraged to monitor and
record their daily weight. They can be instructed that if their weight goes up,
they should double their furosemide dose until their weight goes back to normal.
This way hospital emergency department visits are avoided as the patient is
self-monitoring and knows when to take action.
A general guideline by the American Heart Association is to watch for a sudden

weight gain of 2–3 pounds (0.9–1.4 kg) or more in 24 hours, or more than
5 pounds (2.3 kg) in a week.
Exercise
For patients with stable New York Heart Association (NYHA) Class II or Class III
heart failure, referral to a cardiac rehabilitation program is recommended. These
programs assist patients in maintaining a healthy lifestyle by offering education,
counseling, and exercise plans.

It’s recommended that heart failure patients exercise for 30 minutes, five times
per week. Exercise can improve mortality and symptoms in patients who have
reduced ejection fraction.
Assessing compliance with lifestyle modifications

At each visit, you should assess the patient’s ability to perform activities of daily
living, review their diet and sodium intake, assess their volume status and weight,
and ask about the use of alcohol, tobacco, illicit drugs, alternative therapies, and
chemotherapy drugs.
Always ask about angina on exertion which patients with ischemic heart disease
and HFpEF are more likely to experience.
Medication management
For HFrEF, The CHAMP heart failure trial identified that
only 1% of patients included in the trial were on guideline-
recommended doses of all three main drug classes:
1. ACE inhibitor (or ARB)
2. Beta-blocker
3. Aldosterone antagonist
It can take months to increase medications to guideline-recommended doses,

but ensuring your patient is taking optimal drug doses is important for improving
morbidity and mortality. Make small dose increases every one to two weeks.
It’s important to stress to patients that taking optimal medication doses can
improve life expectancy.
You should keep the cost of medications in mind. It is

often an important factor for patients. ACE inhibitors,
beta-blockers, and aldosterone antagonists are all
relatively inexpensive. But hydralazine nitrates can cost
a few hundred dollars a year and an ARNi (angiotensin
receptor blocker (ARB) + neprilysin inhibitor) costs
thousands of dollars per year.

All drugs and supplements that patients are taking should be reviewed.
Some drugs should be avoided in heart failure patients since they worsen heart
failure symptoms:
• The calcium channel blockers diltiazem and verapamil are important to avoid.
• Amlodipine seems to be associated with a worsening of right and left-sided
heart failure, so only use it as a last resort for blood pressure control if all
else has failed.
• Most antiarrhythmics (except amiodarone) are contraindicated in heart
failure with reduced ejection fraction .
• The diabetic medication thiazolidinedione is contraindicated in heart failure.
• Erythropoietin-stimulating agents for treating anemia should be avoided in
patients who have reduced ejection fraction.
And nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided as they

can exacerbate any inflammatory conditions and interfere with the response
to diuretics.
Abbreviations: HFpEF, heart failure with preserved ejection fraction;

HFrEF, heart failure with reduced ejection fraction
Drugs that are useful with HFrEF and HFpEF

Diagnostic imaging
Lastly, a repeat echocardiogram is recommended for patients who have had
a change in clinical status or those that have received a new treatment. The
echocardiogram will reassess cardiac structure and function, including chamber
size, ejection fraction, and valvular function.

Chapter 4
MANAGING ADVANCED
HEART FAILURE
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Identifying Stage D HFrEF
In this chapter, you will learn about treating advanced heart failure patients
(i.e., Stage D). These patients have marked heart failure symptoms that aren’t
responding to treatment. They often require repeated hospitalizations during
acute decompensated heart failure episodes.
How do you identify a patient with Stage D

heart failure?
Guidelines from the American College
of Cardiology (ACC) and American Heart
Association (AHA) recommend using the
mnemonic “I NEED HELP” to identify patients
with advanced heart failure.
• I is for intravenous (IV) inotropes.
Stage D patients often require positive
inotropes to increase contractility and venodilation.
• N is for New York Heart Association (NYHA) Class III or IV.

These are the patients whose physical activity is limited by their heart failure
symptoms, which often continue at rest.
• E is for end-organ dysfunction.

Stage D patients will often present with liver or kidney dysfunction since
these organs are the first to be affected by decreased perfusion.
• E is for an ejection fraction of 35% or less.

• D is for defibrillator shocks.
Stage D patients with an implantable cardioverter-defibrillator will receive a
shock whenever their heart enters an arrhythmia.
• H is for hospitalizations.
Stage D patients often have repeated hospitalizations for acute
decompensated heart failure episodes.

• E is for escalating diuretics.
These patients often need repeated diuretic dose increases to control
their edema.
• L is for low systolic blood pressure.

A systolic blood pressure of 90 mmHg or less often means that there is
decreased perfusion of the vital organs.
• P is for progressive medication intolerance.

Stage D patients have poorly functioning livers and kidneys which can no
longer clear drug metabolites at the same rate. These patients experience
undesirable side effects due to the build-up of drug metabolites.
Characteristics of advanced heart failure

I IV inotropes
N NYHA Class III or IV

E End-organ dysfunction
E Ejection fraction ≤ 35%
D Defibrillator shocks
H Hospitalizations
E Escalating diuretics
L Low systolic blood pressure
P Progressive medication intolerance
What are the first steps in managing advanced

heart failure?
There are four initial steps to take when managing advanced heart failure:
1. Confirm that all pharmacologic therapy is at optimal doses.
2. Assess whether cardiac resynchronization therapy or an implantable
cardioverter-defibrillator would be of benefit if they have not already
been employed.
3. Ensure that all comorbidities have been recognized and treated.
4. Refer the patient to a specialist with expertise in the management of
refractory heart failure.

Further evaluations
Patients should be evaluated with right heart
catheterization in certain situations:
• Patient is not responsive to diuretics
• Patient has respiratory distress
• Patient has impaired systemic perfusion
• Patient has worsening renal function
A right heart catheter can measure various pressures such as central venous
pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure,
as well as the mixed venous oxygen saturation and cardiac output. All these
measurements may be helpful in management.
Goals of management
In advanced heart failure patients, our aim is to control symptoms, improve
quality of life, reduce hospital readmissions, and establish end-of-life goals.
These goals can be accomplished using several treatment options:

• IV medications for acute decompensated heart failure
• Mechanical circulatory support devices to restore stroke volume
and perfusion
• Heart transplantation
• Palliative care
We’ll look at each of these in more detail throughout this chapter.

Recognizing acute decompensated
heart failure
Recall that when heart failure occurs, the heart and body initially try to
compensate for the reduced volume of pumped blood by making changes
like enlarging the ventricles, increasing the heart rate, and increasing the
blood pressure.
When these compensatory mechanisms are working, chronic heart failure

patients have what is known as compensated heart failure. This means that
most chronic heart failure patients are treated with oral medications, and they
are stable enough to not need urgent medical interventions.
But what happens when these compensatory mechanisms fail?
When this happens, the symptoms of congestion become so severe that patients
require hospitalization. This is known as acute decompensated heart failure.
In the past, most episodes of acute decompensated heart

failure occurred in patients with HFrEF but as HFpEf has
become more common, it now causes up to half of all
acute decompensated heart failure episodes.
Acute decompensated heart failure can also occur in patients without a history
of heart failure. This is often due to a new acute event such as a myocardial
infarction, hypertensive crisis, or ruptured mitral chordae tendineae.
What causes acute decompensated heart failure?

Acute decompensated heart failure most commonly occurs when heart failure
patients don’t take their medications properly or when they fail to restrict their
salt and water intake.

There are several other common causes:
• Less than optimal medication doses
• New ischemic event
• New arrhythmia such as atrial fibrillation
• Uncontrolled hypertension
• Thyroid abnormalities
• Infection
• Anemia
• Cardiotoxins
Keep in mind that calcium channel blockers and beta-blockers are negative
inotropes that weaken the heart’s contractions and slow the heart rate. Starting
one of these medications or suddenly increasing the dose can cause acute
decompensated heart failure in some patients.
How do you identify a patient with acute

decompensated heart failure?
When examining a patient, there are some key signs that will help to identify
acute decompensated heart failure:
1. Worsening dyspnea and fatigue with daily activities
2. Orthopnea
3. Paroxysmal nocturnal dyspnea
4. Elevated jugular venous pressure (JVP)
5. Sudden weight gain of more than 1.5 kg in 2 days
6. Third heart sound (S3)
7. Hepatomegaly
8. Pulmonary rales on auscultation
9. Pulmonary edema on chest x-ray
Keep in mind that peripheral edema is not always obvious as fluid can hide
throughout the body. In addition, B-type natriuretic peptide (BNP) levels are
not always elevated, so a normal BNP level doesn’t rule out decompensated
heart failure.

What are the indications for hospitalization?
Acute decompensated heart failure patients require hospitalization when they
become unstable. Unstable patients could present with any or all of the following:
• Tachycardia (heart rate > 120 beats per minute (bpm))
• Hypotension (systolic blood pressure < 80 mmHg)
• Tachypnea (> 20 breaths / minute)
• Hypoxia (pulse oximetry ≤ 92%)
There are two life-threatening emergencies to watch

out for when treating acute decompensated heart
failure patients:
1. Acute respiratory distress syndrome (ARDS)

These patients often have low blood oxygen, rapid
breathing, and characteristic clicking or bubbling
sounds on lung auscultation.
2. Cardiogenic shock
These patients often present with altered mental status because there isn’t
enough blood flow to the brain to think properly.
Patients who present in either of these ways need immediate, aggressive treatment.

Evaluating acute decompensated
heart failure
There are two key questions to ask yourself when evaluating your patient with
acute decompensated heart failure:
1. Is the patient perfusing well?
2. Is the patient congested?
How do you evaluate perfusion and congestion?

To evaluate perfusion, calculate the pulse pressure, assess if the extremities are
warm or cool, and examine the patient’s mental status.
Patients with good perfusion are classified as warm while those with inadequate
perfusion are classified as cold.
When considering if the patient is congested, recall that the indicators of

congestion are orthopnea, pulmonary rales, elevated JVP, ascites, edema, or
weight gain.
Patients with congestion are classified as wet whereas patients without

congestion are classified as dry.
Classifying acute decompensated heart failure

Using these two questions, acute decompensated heart failure patients can be
divided into four groups for treatment:
1. Warm and wet
2. Warm and dry
3. Cold and wet
4. Cold and dry

Congested?
Yes
(Warm)
Perfusing? Yes No
(Wet) (Dry)
No
(Cold)
Four types of acute decompensated heart failure
Before we look at these four types of patients, let’s review two important
concepts from earlier in this course—preload and afterload. Recall that preload
is the initial stretching of the heart’s muscle cells due to the ventricle filling with
blood before a contraction occurs. Afterload is the force that the heart pumps
against when it contracts.
Warm and wet heart failure

In heart failure, the left ventricle has decreased contractility so the amount of
blood it can pump with each heartbeat is decreased. To compensate, the left
ventricle is overfilled to increase the preload which increases the stroke volume.
When these compensatory mechanisms

fail, we commonly get an acute
decompensated heart failure patient who
is warm and wet. They are perfusing, but
also congested.
This patient urgently needs IV vasodilators

to reduce their afterload which will
increase the stroke volume so that more

blood and oxygen reach the vital organs. IV diuretics are also used to rapidly
remove the excess fluid.
Warm and dry heart failure

A chronic heart failure patient who is perfusing well and not congested (warm
and dry) usually has adequately compensated heart failure and not acute
decompensated heart failure.
However, if they have come to the emergency room with worsening symptoms,
then you need to look for a non-cardiac cause of their symptoms such as septic
shock or pneumonia.
Cold and wet heart failure

Patients who are cold and wet are not perfusing, but they are congested. They
need IV vasodilators to decrease the afterload and improve the stroke volume,
as well as IV diuretics to remove the excess fluid.
However, the lack of perfusion means the organs aren’t getting enough oxygen.
This can be improved by giving positive inotropes intravenously to increase
ventricular contractility.
Cold and dry heart failure

Lastly, a cold and dry patient is not perfusing well and is not
congested. This is the least common presentation of acute
decompensated heart failure.
This is an end-stage patient, and the treatment focus is

no longer vasodilatation or diuresis. Treatment is positive
inotropes by IV to increase organ perfusion and you must
consider more aggressive interventions.
A cardiologist specializing in heart failure should be

consulted to see if a mechanical circulatory support device is needed to restore
stroke volume and perfusion.

We often use temporary, percutaneous measures like balloon pumps,
percutaneous circulatory assist devices (e.g., Tandem Heart and Impella), and
extracorporeal membrane oxygenation (ECMO) devices in these individuals as a
bridge to more permanent treatment like a left ventricular assist device (LVAD)
or heart transplant.

Using intravenous medications
In this lesson, we’ll take a closer look at the three classes of intravenous
medications used to treat acute decompensated heart failure patients:
1. Diuretics
2. Vasodilators
3. Inotropes
Diuretics
Loop diuretics are the main treatment for
patients with fluid overload (warm and
wet or cold and wet).
It’s important to start IV diuretics

right away when patients arrive in the
emergency room with acute decompensated heart failure. You can give either a
continuous infusion or a bolus every 12 hours as they are equivalent.
The goal for urine output is 3–5 L / day, even if the patient remains symptomatic.
However, be sure to watch for electrolyte disturbances.
Ensure the patient is compliant with salt and water restriction or the diuretics
aren’t going to work.
If the patient is resistant to diuretics, you can double the dose every two hours
and add thiazide diuretics if necessary.
For congested patients who are unresponsive to aggressive diuresis, we

sometimes consider ultrafiltration or hemodialysis which will remove fluid but
does not preserve renal function the way diuresis does. This is an expensive
treatment and should only be considered in diuretic-resistant patients who are
hemodynamically stable.

Vasodilators
Recall that IV vasodilators are used temporarily to decrease the afterload and
increase the stroke volume to help get warm and wet or cold and wet patients
out of the acute episode.
Patients will feel better and might be able to leave the hospital sooner, but these
medications have no impact on outcomes.
Nitroprusside is the most common IV vasodilator, and it provides balanced

arterial and venous dilation. However, it requires continuous blood pressure
monitoring with an arterial line to make sure the dose is titrated appropriately.
Additionally, abruptly stopping this medication will send patients right back into
acute decompensated heart failure.
Nitroglycerin is another option. It reduces left ventricular filling pressure

primarily by venodilation and, at higher doses, lowers afterload. But it also
requires invasive monitoring with an arterial line.
Nesiritide doesn’t require such careful dose titration, but it is more expensive.
Clevidipine is a short-acting calcium channel blocker that works like nitroprusside

but is less expensive. It also requires continuous invasive monitoring because
calcium channel blockers can exacerbate heart failure if they cause too much
negative inotropic effect.
Inotropes
It’s important to start positive inotropes by IV as
soon as possible for acute decompensated heart
failure patients who aren’t perfusing well (cold and
wet or cold and dry). These medications increase
contractility and vasodilation.
In patients classified as cold, organ perfusion is

rapidly declining. Kidney function is going to drop

off and it might not be regained. Kidney dysfunction is an especially big risk
factor for mortality, so we want to preserve perfusion to the kidney for as long
as possible.
Positive inotropes are also used for patients in cardiogenic shock or as a

temporary bridge for patients waiting for a heart transplant or LVAD.
Lastly, positive inotropes can be used long-term for palliative care, to enhance a
patient’s quality of life.
However, positive inotropes are contraindicated in HFpEF and any patients with
adequate perfusion (warm and wet or warm and dry).
Examples of positive inotropes include dobutamine, milrinone, and dopamine. If

you try one inotrope and you’re not able to achieve optimized blood pressure and
cardiac output, you can switch to a different one or add a second one.
When managing acute decompensated heart failure

patients, always remember to titrate diuretics, vasodilators,
and positive inotropes up to guideline-directed doses in
order to maximize their effectiveness.

Preparing patients for discharge
Acute decompensated heart failure patients are complex and there are a lot
of factors to take into consideration when preparing them for discharge from
the hospital. On average, patients with acute decompensated heart failure are
hospitalized for about 5 days.
What should you do before discharge?

There are five steps to take prior to discharging a patient with acute
decompensated heart failure:
1. Perform right heart catheterization
Right heart catheterization should be considered in patients with an
inadequate response to therapy, significant hypotension, or declining renal
function. This can be used to determine how well the heart is functioning
by measuring volume status, filling pressure, and cardiac output. These
measurements will be helpful when deciding on more aggressive treatments
such as an LVAD or heart transplant.
2. Resolve fluid overload

A patient being considered for discharge should be euvolemic, meaning
there is a normal volume of fluid in their body. This can be assessed by
weighing the patient to see if they are back at their previous weight (i.e., the
weight they were before they decompensated and became fluid-overloaded).
3. Check electrolyte levels

Check that the patient’s electrolyte levels are good. If the patient’s volume
or electrolyte levels are not normal, they will need further treatment
before discharge.
4. Transition from IV to oral medications

All IV medications should be stopped, and the patient should be on optimal
doses of oral medications. They should be stable on these oral medications
for 48 hours before being discharged.

5. Provide education
Make sure to educate the patient and family about salt and water restriction
and medications before they go home.
What should you do after discharge?

After discharge, there should be a phone call or visit from a nurse within 3 days.
Follow-up with the physician should happen within 7–10 days of discharge.
Frequent check ins are important because 30-day mortality is 8–14% and
1-year mortality is 26–37% for acute decompensated heart failure patients.
Patients who are discharged have a significant risk of readmission. Around 25%
of them will need to be readmitted within 30 days and 50% will be readmitted
within 6 months. These patients place a large financial burden on the
healthcare system.
We often attempt to predict which patients are at the highest risk of readmission
so we can allocate maximal resources toward keeping them well at home and
out of the hospital. Patients at the highest risk of readmission demonstrate
some identifiable risk factors:
• Non-compliance with medications or salt and fluid restriction
• Low systolic blood pressure
• Persistent NYHA Class III or IV symptoms
• Multiple comorbidities especially chronic kidney disease, diabetes, chronic
obstructive pulmonary disease (COPD), or metastatic cancer.
For these patients at a high risk of readmission, you

should refer them to a cardiologist who specializes
in treating advanced heart failure. The cardiologist
can also determine if heart transplant or a ventricular
assist device are necessary.

Exploring other treatments
In this lesson, we’ll briefly review mechanical circulatory support, heart
transplant, and palliative care options for advanced heart failure patients.
Mechanical circulatory support

Mechanical circulatory support devices are used in
HFrEF patients to restore perfusion.
Short-term mechanical circulatory support devices

include intra-aortic balloon pumps, percutaneous
circulatory assist devices (e.g., Tandem Heart and
Impella), and ECMO.
Long-term mechanical circulatory support devices

include LVADs or biventricular support (a total artificial heart). Long-term
devices are used as a bridge to a heart transplant, or as permanent therapy in
patients who are not transplant candidates.
Heart transplant
The main indication for a heart transplant is to improve long-
term survival. So, the patient’s prognosis is the most important
factor for deciding whether to pursue a heart transplant or not.
There are six types of patients who should be considered for heart transplants:
1. Patients with cardiogenic shock who are not maintaining adequate perfusion
2. Patients with persistent NYHA Class IV symptoms
3. Patients with severe angina
4. Patients with life-threatening arrhythmias
5. Patients with cardiomyopathies and NYHA Class III to IV symptoms
6. Patients with congenital heart disease who have NYHA Class IV symptoms

Heart transplant is contraindicated in any patient with a life expectancy of
less than 2 years. It’s also contraindicated when multiple organ dysfunction
is present.
Patients who continue to misuse substances are also not considered for
heart transplants.
Palliative care
Patients should be referred to palliative care when oral therapies are failing
and symptoms continue to worsen. Palliative care may also be appropriate
for patients who are not eligible for mechanical circulatory support or a heart
transplant, or for patients who are not interested in undergoing these procedures.
Palliative care will prioritize the relief of pain and other distressing symptoms.
Keep in mind that the goal of palliative care is to improve

symptoms, not to improve survival.

APPENDIX
www.medmastery.com
Appendix 1: Drugs commonly used to
treat HFrEF
ACE inhibitors and ARBs
Agent Initial dose Goal dose Comments
Captopril 6.25 mg t.i.d. 50 mg t.i.d.

ACE
Enalapril 2.5 mg b.i.d. 10–20 mg b.i.d.
inhibitor
Lisinopril 2.5–5 mg q.d. 20–40 mg q.d.
Ramipril 1.25–2.5 mg q.d. 10 mg q.d.
Candesartan 4–8 mg q.d. 32 mg q.d. Lower risk of

ARB Valsartan 20–40 mg b.i.d. 160 mg b.i.d. cough and
Losartan 25–50 mg q.d. 50–150 mg q.d. angioedema
Beta-blockers**
Carvedilol 3.125 mg b.i.d. 25 mg b.i.d. for Preferred agent when BP is

patients < 85 kg normal
50 mg b.i.d. for Causes greater reduction in
patients > 85 kg BP and more bronchospasm
than the other two options
Metoprolol 12.5–25 mg 200 mg daily Preferred agent when

succinate q.d. patient has hypotension or
significant asthma
Bisoprolol 1.25 mg q.d. 10 mg q.d. Preferred agent when

patient has hypotension or
significant asthma
Dosing at night minimizes
effects on BP
Note that beta-blockers do not have as much of an effect on blood pressure in patients over 65.
**
Beta-blockers do not need to be avoided in patients who have asymptomatic hypotension.

Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker;
b.i.d., twice a day; BP, blood pressure; q.d., once a day; t.i.d., three times a day
Heidenreich, et al. Circulation. 2022

Diuretics to treat Stage C HFrEF**
Furosemide 20–40 mg q.d. or b.i.d. 600 mg Bioavailability ranges

from 10–100%
Bumetanide 0.5–1.0 mg q.d. or b.i.d. 10 mg Bumetanide and

torsemide are
preferred agents due
Torsemide 10–20 mg q.d. 200 mg
to more consistent
bioavailability
Ethacrynic acid 20–50 mg q.d. or b.i.d. 200 mg Very expensive

For use with patients
with sulfa allergy
**
Note that some patients will remain volume overloaded despite maximal loop diuretic therapy.
In these cases, try outpatient IV diuresis with 120 mg or 200 mg of IV furosemide.
Abbreviations: b.i.d., twice a day; q.d., once a day; t.i.d., three times a day
Casu, et al. Eur Cardiol. 2015
Aldosterone antagonists to treat HFrEF
Spironolactone 12.5–25 mg q.d. 20–50 mg q.d. Preferred agent (less

expensive)
Eplerenone 25 mg q.d. 50 mg q.d. Only use if spironolactone

causes gynecomastia
Abbreviations: b.i.d., twice a day; q.d., once a day


Additional medications to treat HFrEF
Agent Initial dose Goal dose Target population(s)
Hydralazine- 37.5 mg 75 mg hydralazine, Symptomatic Black

nitrate hydralazine, 40 mg isosorbide patients taking ACE
(fixed-dose 20 mg isosorbide dinitrate t.i.d. inhibitors and beta-
combination) dinitrate t.i.d. blockers
Renal dysfunction
Hyperkalemia
Digoxin 0.125–0.25 mg Individualized dose AF with suboptimal

q.d. **
required to achieve heart rate control
serum digoxin Hypotension and
concentration of intolerance to higher
0.5–< 0.9 ng / mL beta-blocker doses
ARNi (sacubitril- 49 mg sacubitril, 97 mg sacubitril, Still symptomatic

valsartan) 51 mg valsartan 103 mg valsartan patients on ACE
b.i.d. b.i.d. inhibitors / ARBs
Ivabradine 5 mg b.i.d. 7.5 mg b.i.d. Sinus rhythm and

heart rate > 70 bpm
SGLT2 inhibitors 10 mg q.d. 10 mg q.d. When added

(dapagliflozin and benefits of lowering
empagliflozin) blood sugar and
reducing body
weight are desirable
**
Lower doses may be necessary in patients of advanced age or with reduced kidney function.
Abbreviations: ACE, angiotensin-converting enzyme; AF, atrial fibrillation; ARB, angiotensin II
receptor blocker; b.i.d., twice a day; bpm, beats per minute; q.d., once a day; SGLT2, sodium-glucose
cotransporter 2; t.i.d., three times a day

Reference list
American Heart Association. 2022. Self-Check Plan for HF Management. Heart.org.
https://www.heart.org. Accessed December 7, 2022.
American Heart Association. Types of Heart Failure. American Heart Association.

https://www.heart.org. Modified May 31, 2017. Accessed November 1, 2022.
Armstrong, C. 2014. ACCF and AHA release guidelines on the management of heart
failure. Am Fam Physician. 90: 186–189. PMID: 25077725
Borlaug, BA, Nishimura, RA, Sorajja, P, et al. 2010. Exercise hemodynamics enhance
diagnosis of early heart failure with preserved ejection fraction. Circ Heart Fail.
3: 588–595. PMID: 20543134
Casu, G and Merella, P. 2015. Diuretic therapy in heart failure—current approaches.

Eur Cardiol. 10: 42–47. PMID: 30310422
Harjola, VP, Miró, O, Vranckx, P, et al. Chapter 4: Acute heart failure. European Society
of Cardiology. https://escardio.org. Accessed November 1, 2022.
Heidenreich, PA, Bozkurt, B, Aguilar, D, et al. 2022. 2022 AHA/ACC/AFSA Guideline for
the Management of Heart Failure: A Report of the American College of Cardiology/
American Heart Association Joint Committee on Clinical Practice Guidelines.
Circulation. 145: e895–e1032. PMID: 35363499
Javaloyes, P, Miró, Ò, Gil, V, et al. 2019. Clinical phenotypes of acute heart failure based
on signs and symptoms of perfusion and congestion at emergency department
presentation and their relationship with patient management and outcomes. Eur J
Heart Fail. 21: 1353–1365. PMID: 31127677
Mangini, S, Pires, PV, Braga, FGM, et al. 2013. Decompensated heart failure. Einstein
(Sao Paulo). 11: 383–391. PMID: 24136770
Njoroge, JN and Teerlink, JR. 2021. Pathophysiology and therapeutic approaches to

acute decompensated heart failure. Cir Res. 128: 1468–1486. PMID: 33983837
Severino, P, D’Amato, A, Pucci, M, et al. 2020. Ischemic heart disease and heart failure:
Role of coronary ion channels. Int J Mol Sci. 21: 3167. PMID: 32365863

Vedin, O, Lam, CSP, Koh, AS, et al. 2017. Significance of ischemic heart disease in
patients with heart failure and preserved, midrange, and reduced ejection fraction:
A nationwide cohort study. Circ Heart Fail. 10: e003875. PMID: 28615366
Yancy, CW, Jessup, M, Bozkurt, B, et al. 2013. 2013 ACCF / AHA guideline for the
management of heart failure: A report of the American College of Cardiology
Foundation / American Heart Association task force on practice guidelines. Circulation.
128: 240–327. PMID: 23741058

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Medmastery Medical Treatment of Heart Failure

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Medmastery Medical Treatment of Heart Failure

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MEDICAL TREATMENT OF

Franz Wiesbauer, MD MPH

Introduction to heart failure

Causes of heart failure

Managing chronic stable heart failure

Managing advanced heart failure

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What happens during heart failure?

2. Increase muscle mass

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These temporary measures mask heart failure but it continues to worsen

How does heart failure develop?

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• Genetic or hereditary causes:

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How do we describe heart function?

Stroke volume = end-diastolic volume – end-systolic volume

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What causes left-sided heart failure?

How do we classify left-sided heart failure?

EF (%) = (stroke volume / end-diastolic volume) x 100

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≤ 40% ≥ 50% 41–49%

Heart failure with reduced ejection fraction

We’ll talk about these in more detail in a later lesson.

Systolic heart failure

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Dyspnea often occurs when the patient is exerting

If not treated promptly, pulmonary edema can lead to respiratory distress.

Heart failure with preserved ejection fraction

Diastolic heart failure

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HFpEF is more difficult to diagnose than HFrEF. HFpEF is most common

Heart failure with mid-range ejection fraction

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How does right-sided heart failure develop?

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Not everyone with heart failure will have visible congestion.

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Which symptoms are relevant to heart failure?

It’s important to have heart failure in your differential

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Which clues can help identify the underlying cause of

• Alcohol or recreational drug use

• History of radiation or chemotherapy

• Family history of heart failure

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Arrhythmia • Tachycardia (i.e., pulse > 100 bpm at rest)

Coronary artery disease • Angina or exertional dyspnea

Alcoholic cardiomyopathy • Alcohol consumption

Drug-related heart disease • Recreational drug use

Cardiotoxicity • History of radiation or chemotherapy

Genetic • Family history of heart failure, sudden

Abbreviations: bpm, beats per minute

How do you identify heart failure with preserved

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