Module 2: Heart Failure

Question 1

Heart Failure - Definition

Answer 1

-Insufficient blood supply/oxygen to tissues and organs
-Decreased CO = less tissue perfusion, impaired gas exchange, fluid volume imbalance, decreased functional ability

**Inability to fill with enough blood = diastolic dysfunction
**Inability to pump enough blood out to body = systolic dysfunction
-Most common form of heart failure is a combination of the two

Question 2

Heart Failure Risk Factors

Answer 2

Hypertension
* Modifiable risk factor
* If aggressively treated and managed, incidence of HF can be reduced by 50%
 CAD (coronary artery disease)
 Co-morbidities contribute to development of HF
 Diabetes, metabolic syndrome, advanced age,
tobacco use, and vascular disease

Question 3

How does heart failure happen?

Answer 3

Any interference with mechanisms regulating
cardiac output (CO)
 Preload
 Afterload
 Myocardial contractility
 HR
 These factors affect stroke volume (SV), the amount of blood pumped per heartbeat

Primary causes
 Conditions that directly damage the heart
 Precipitating causes
 Conditions that increase workload of the heart

Genetic link
 Cardiomyopathies
* diseases that weaken the heart muscle and cause HF
* can be acquired or inherited
* inherited forms involve autosomal dominant traits with variable genetic expression
 Weakens ventricular structure and stability
 Post-viral myocarditis is thought to be caused by an interaction between a virus and genetic predisposition
 Specific genes and gene mutations are linked to the development of HTN and CAD

Question 4

Left Sided HF

Answer 4

Most common form of HF
 Results from inability of LV to
* Empty adequately during systole, or
* Fill adequately during diastole
 Further classified as
* HFrEF (systolic HF) - heart failure with reduced ejection fraction
-Decreased EF, which means the heart’s ability to contract and pump blood is impaired
-EF = amount of blood leaving heart each time it contracts
* HFpEF (diastolic HF)
-contraction is normal, but heart has become stiff, preventing it from filling properly during resting phase (diastole)
-stiffness means less blood enters the heart, leading to less blood pumped to body, even though pumping action (systole) might be normal
* Or combination of the two

Blood backs up into left atrium (LA)
 Increased pulmonary hydrostatic pressure causes
fluid leakage from the pulmonary capillary bed into
the interstitium and then the alveoli.
 This results in pulmonary congestion and edema

Question 5

Heart Failure with Reduced Ejection Fraction (HFrEF)

Answer 5

-systolic failure
Inability to pump blood effectively
-Caused by
 Impaired contractile function (heart doesn’t contract with enough force; It can be due to damage from a heart attack, chronic high blood pressure, or other heart diseases that weaken the heart muscle)
 Increased afterload (Afterload is the resistance the heart must overcome to eject blood. High afterload (like in hypertension) means the heart must work harder to pump blood, which can strain and weaken it over time)
 Mechanical abnormalities (These can include issues like problems with the heart valves. For example, a leaky or narrow valve can affect the heart’s ability to pump blood efficiently)
 Decreased LV ejection fraction (LVEF)- < 40%
In systolic heart failure, there is a decrease in the left ventricular ejection fraction (LVEF), which is the percentage of blood that is pumped out of the left ventricle with each heartbeat.
A normal LVEF ranges from 55% to 70%. In systolic failure, the LVEF is usually less than 40%, indicating that a significant portion of blood remains in the left ventricle after each heartbeat because the heart isn’t pumping effectively.

Question 6

Heart Failure with Preserved EF (HFpEF)

Answer 6

-diastolic HF
Inability of the ventricles to relax and fill during
diastole, resulting in decreased stroke volume
and CO
 Primary cause is HTN

Result of left ventricular hypertrophy from
hypertension, older age, female, diabetes, obesity
 Same end result as systolic failure
- Diagnosis based on
 Symptoms of HF
 Normal LVEF
 LV diastolic dysfunction

Question 7

Right Sided HF

Answer 7

RV does not pump effectively
 Fluid backs up into venous system
 Fluid moves into tissues and organs
 Left-sided HF is most common cause
 Other causes include RV infarction, PE, and cor
pulmonale (RV dilation and hypertrophy)

Question 8

Biventricular Failure

Answer 8

Both right and left ventricular dysfunction
 Inability of both ventricles to pump effectively
 Fluid build-up and venous engorgement
 Decreased perfusion to vital organs

Question 9

Compensatory Mechanism: Renin-Angiotensin-Aldosterone-System (RAAS) - Compensatory Mechanism of HF

Answer 9

Homeostatic regulatory system
* Goal is increased preload (blood in ventricles at the end of diastole) and ventricular contractility (strength which ventricles contract) to maintain CO; increasing preload = increasing blood filling = increasing CO
* Promotes sodium and water retention

The RAAS plays a crucial role in regulating blood pressure and fluid balance in the body
-When blood volume or blood pressure is low, the kidneys release an enzyme called renin. Renin triggers a series of reactions that lead to the production of angiotensin II, a potent vasoconstrictor that narrows blood vessels, increasing blood pressure.
-Angiotensin II also stimulates the release of aldosterone from the adrenal glands. Aldosterone promotes sodium and water retention by the kidneys, which increases blood volume and, consequently, preload.

By retaining sodium and water, the RAAS effectively increases the volume of fluid in the bloodstream. This increased blood volume helps to raise or maintain preload, thereby supporting cardiac output

Question 10

Neurohormonal response—RAAS

Answer 10

As CO falls, renal perfusion decreases and renin
is released
1. Angiotensin I is converted to Angiotensin II, a potent vasoconstrictor
2. Release of aldosterone from adrenal cortex results in sodium and water retention, potassium excretion
3. Peripheral vasoconstriction and increased BP
4. Pituitary gland releases ADH which results in water reabsorption

Question 11

Sympathetic Nervous System Role in Reducing HF

Answer 11

Baroreceptors sense low arterial pressure
 Catecholamines are released
 Stimulation of β-adrenergic receptors increases HR (chronotropy) and ventricular contractility (inotropy)

Question 12

Factors Contributing to HF Development (Endothelin; Proinflammatory cytokines)

Answer 12

Endothelin is a vasoconstrictor peptide
* Acts as a negative inotrope in the heart, decreasing ventricular contractility in the failing heart
 Proinflammatory cytokines are released
* Further depress heart function by causing hypertrophy and cell death

Question 13

Dilation to prevent HF

Answer 13

Enlargement of the heart chambers that occurs when pressure in left ventricle is elevated over time
 Initially effective (Frank-Starling Law)
 Eventually this mechanism becomes inadequate and CO decreases

Question 14

Hypertrophy to prevent HF

Answer 14

Hypertrophy
 Adaptive increase in muscle mass and heart wall
thickness
 Initially effective
 Over time leads to poor contractility, increased O2
needs, poor coronary artery circulation, and risk for
dysrhythmias

Question 15

Remodeling to prevent HF

Answer 15

Change in the structure of the heart
 Caused by continuous activation of neuro-hormonal responses (RAAS and SNS)
 Hypertrophy of ventricular myocytes
 Ventricles become larger but less effective pumps
 Can cause life-threatening dysrhythmias and sudden cardiac death (SCD)

Question 16

Natriuretic Peptides

Answer 16

-group of hormones that play crucial balance in regulating fluid balance, BP, and cardiovascular function
-Diff types:

**Atrial Natriuretic Peptide (ANP):
ANP is produced and released by the atrial cells of the heart. It is released in response to increased blood volume and stretching of the atrial walls, typically occurring when the heart is working harder than usual, such as in conditions of high blood pressure or heart failure.

**Brain (B-Type) Natriuretic Peptide (BNP):
Despite its name, BNP is predominantly released from the ventricles of the heart, not the brain.
Like ANP, BNP is released in response to stretching of the ventricular walls due to increased blood volume or pressure.

Response to Increased Blood Volume and Cardiac Wall Stretching:
Both ANP and BNP are released when the heart muscle cells are stretched beyond a certain point, which typically happens in conditions where the heart is strained.

**Effects of Natriuretic Peptides:
-Diuresis: They increase urine production by the kidneys, which helps to reduce blood volume.

-Vasodilation: They cause blood vessels to widen (dilate), which can reduce blood pressure.

-Decreased Blood Pressure: Through diuresis and vasodilation, these peptides collectively contribute to a decrease in blood pressure.

-Counteracts SNS and RAAS: The Sympathetic Nervous System (SNS) and the Renin-Angiotensin-Aldosterone System (RAAS) both work to increase blood pressure and volume. Natriuretic peptides counteract these systems, providing a regulatory balance to maintain optimal blood pressure and volume levels.

Clinical Significance:
BNP and its inactive fragment, NT-proBNP, are commonly measured in clinical settings as markers for heart failure. Elevated levels of these peptides are often used to diagnose or assess the severity of heart failure.

Question 17

Nitric Oxide and Prostaglandin

Answer 17

-important substances released by the vascular endothelium (the inner lining of blood vessels). They play a critical role in the body’s response to various physiological conditions, including those involving compensatory mechanisms.

Release from Vascular Endothelium:
-Both NO and Prostaglandin are produced and released by the endothelial cells lining the blood vessels.
-This release can be triggered by various stimuli, often as part of the body’s compensatory response to maintain blood flow and pressure.

-Response to Compensatory Mechanisms:
Compensatory mechanisms are responses that the body activates to counteract changes, such as alterations in blood pressure or blood volume.
In response to these changes, the endothelium releases NO and Prostaglandin as part of the process to maintain or restore vascular homeostasis.

Function of Nitric Oxide (NO) and Prostaglandin:
-Vasodilation: Both NO and Prostaglandin are vasodilators, meaning they cause the smooth muscle cells in the arterial walls to relax. This relaxation leads to the widening of blood vessels (vasodilation).
-Decreased Afterload: Vasodilation reduces the resistance against which the heart must pump blood, a parameter known as afterload. By decreasing afterload, the heart can pump blood more easily, reducing the work required by the heart muscle.

Effect on Blood Pressure and Heart Function:
The vasodilation effect of NO and Prostaglandin helps in regulating blood pressure. It can also improve blood flow to various tissues and organs.
By reducing afterload, these substances can help improve heart function, especially in conditions where the heart is under stress, such as in heart failure.

Question 18

Acute Decompensated HF (ADHF) Clinical Manifestations

Answer 18

Increase (usually sudden) in symptoms of HF with
decrease in functional status
 Requires rapid escalation of therapy and
hospitalization
 Pulmonary congestion and volume overload due to sodium and fluid accumulation

Early: increased pulmonary venous pressure
 Mild increase in the respiratory rate
 Decrease in PaO2

Later: interstitial edema
 Tachypnea, shortness of breath

Further progression: alveolar edema
 Respiratory acidosis

Can manifest as pulmonary edema
 Life-threatening situation—alveoli fill with fluid
 Most commonly associated with left-sided H

Question 19

Pulmonary Edema Clinical Manifestations

Answer 19

Anxious, pale, cyanotic
 Dyspnea
 Orthopnea
 Tachypnea
 Paroxysmal nocturnal
dyspnea
 Use of accessory
muscles
 Cough with frothy, blood-
tinged sputum
 Crackles and wheezes
 Tachycardia
 Hypotension or
hypertension
 Abnormal S3 or S4

Question 20

ADHF Clinical Manifestations

Answer 20

-Based on hemodynamic and clinical status, patients
can be categorized into one of four groups
-These categories help in understanding the patient’s volume status (dry or wet) and perfusion status (warm or cold), which are crucial for guiding treatment

1. Dry-warm
   Dry indicates that the patient does not have fluid overload.
   Warm suggests good perfusion, meaning the body (including extremities) is receiving an adequate blood supply.
   Patients in this category are generally stable and may be experiencing mild symptoms of heart failure or are in a compensated state.
2. Dry-cold
   Dry indicates a lack of fluid overload, but there may be issues like dehydration.
   Cold refers to poor perfusion, where the extremities might be cool to the touch, indicating reduced blood flow.
   This category can signify more advanced heart failure where the heart’s pumping ability is significantly impaired, leading to insufficient blood flow to the body despite the absence of fluid overload.
3. Wet-warm (most common)
   Wet suggests fluid overload or congestion, which is a common issue in heart failure.
   Warm indicates that perfusion is still adequate. Despite fluid accumulation, the body is receiving enough blood supply.
   This is the most common presentation of ADHF, where patients exhibit symptoms like edema and shortness of breath due to fluid accumulation, but the perfusion to vital organs is maintained.
4. Wet-cold
   Wet indicates fluid overload, leading to symptoms such as swelling and shortness of breath.
   Cold signifies poor perfusion, meaning vital organs and extremities are not receiving enough blood.
   This is a more severe and critical state of heart failure, characterized by signs of congestion along with inadequate blood flow to the body’s organs. Patients in this category often require urgent and aggressive medical treatment.

Question 21

Chronic Heart Failure Symptoms

Answer 21

 Fatigue
 Dyspnea (SOB)
 Orthopnea (SOB when lying down)
 Paroxysmal nocturnal dyspnea (sudden severe SOB at night during sleep)
 Cough
 Tachycardia
 Palpitations
 Edema
-Dependent, liver, abdominal cavity, lungs
-Edema may be pitting
 Changes in urine output
-Nocturia
Skin changes
 Neurological manifestations
 Mental status and behavioral changes
 Sleep problems
 Chest pain
 Weight changes

Question 22

Heart Failure Complications

Answer 22

 Pleural effusion (excess fluid accumulates in pleural space, gap between lungs and chest wall)
 Dysrhythmias and dyssynchronous contraction (diff parts of the heart contract at irregular, uncoordinated times)
-Atrial and ventricular
 Atrial or left ventricular thrombus
 Hepatomegaly (abnormal Engagement of liver)
 Cardiorenal syndrome (heart and kidneys dysfunction together; acute or chronic dysfunction in one organ leads to acute and chronic dysfunction of another)
 Anemia

Question 23

Heart Failure Diagnostic Studies

Answer 23

Determine and treat underlying cause
 Echocardiogram
 Provides information on LVEF, heart valves, presence of effusion or thrombus,
 ECG, ambulatory heart monitors, chest x-ray, 6-
minute walk test, MUGA scan, Cardiac MRI,
cardiopulmonary exercise stress test, cardiac
catheterization/angiogram, EMB
 BNP and NT-proBNP levels
-BNP (B-type Natriuretic Peptide) and NT-proBNP (N-terminal pro b-type Natriuretic Peptide) are important biomarkers used in the diagnosis and management of heart failure. They are peptides released by the heart in response to increased pressure and stretch of the heart muscle, particularly the ventricles.

Question 24

ADHF Care

Answer 24

Goals of therapy:
 Relieving symptoms
 Optimizing volume status
 Supporting oxygenation, ventilation, CO, and end
organ perfusion
 Identifying and addressing causes
 Avoiding complications
 Teaching related to HF exacerbations
 Planning discharge

Ongoing monitoring and assessment
 VS, O2 saturation, weight, mentation, ECGs,
indicators of volume overload
 High Fowler’s position
 Hemodynamic monitoring if unstable
 Supplemental oxygen, BiPaP
 Mechanical ventilation if unstable

Ultrafiltration (aquapheresis) for patients with
volume overload and resistance to diuretics
 Mechanical cardiac assist devices for patients with
deteriorating HF
 Intraaortic balloon pump (IABP)
 Ventricular assist devices (VADs)
 Extracorporeal membrane oxygenation (ECMO)

Question 25

ADHF Drug Therapy

Answer 25

Diuretics
 Decrease volume overload (preload)
* Loop diuretics—Furosemide
 Vasodilators
 Reduce circulating blood volume and improve
coronary artery circulation
* IV nitroglycerin
* IV sodium nitroprusside
* IV nesiritide
Morphine
 Reduces preload and afterload
 Relieves dyspnea and anxiety
-Positive inotropes
 β-agonists (dopamine, dobutamine, norepinephrine [Levophed]), phosphodiesterase inhibitors (milrinone)
 Digitalis

Question 26

Chronic HF Care

Answer 26

Main treatment goals
 Treat the underlying cause and contributing factors
 Maximize CO
 Improve ventricular function
 Improve quality of life
 Preserve target organ function

-Oxygen therapy
 Relieves dyspnea and fatigue
-Physical and emotional rest
 Conserve energy and decrease oxygen needs
 Dependent on severity of HF
-Structured exercise program
 CR associated with better outcomes

Question 27

Chronic HF Drug Therapy

Answer 27

RAAS inhibitors
 ACE inhibitors
 Angiotensin II receptor blockers
 Neprilysin-angiotensin receptor inhibitors
 Aldosterone antagonists
* Monitor potassium levels (hyperkalemia)

-β-adrenergic blockers
-Vasodilators
 Nitrates
-Combination therapy
 BiDil
-Positive inotropic agents
 Digitalis

Inhibitor of cardiac sinus node
 Ivabradine (Corlanor)
 Must be in sinus rhythm with resting HR of greater than 70 beats/min and taking optimal doses of other medications
* Inhibits sinus node
* Reduces HR
* Decreases hospitalization for patients with HFrEF

Dapagliflozin (Farxiga)
 Sodium-glucose cotransporter-2 (SGLT-2) inhibitor
 Reduces the risk of CV death and hospitalization for patients with HFrEF
 Unique osmotic diuretic properties

Diuretics
 Reduce edema, pulmonary venous pressure, and
preload
 Promote sodium and water excretion
* Loop diuretics
* Thiazide diuretics
* Monitor potassium levels (hypokalemia)

Question 28

Chronic HF Care

Answer 28

Implantable cardioverter-defibrillator (ICD)
 Biventricular pacing/cardiac resynchronization
therapy (CRT)
 Remote monitoring

Question 29

Chronic HF Nutrition

Answer 29

Low sodium diet
 Individualize recommendations and consider cultural background
 AHA web site has dietary guidelines
 Sodium is usually restricted to 2 g/day

Fluid restriction for stage D HF patients
 Daily weights important
 Same time, same clothing each day
 Weight gain of 3 pounds (1.4 kg) over 2 days or a 3
to 5 pounds (2.3 kg) gain over a week should be
reported to HCP

Question 30

HF Support Devices

Answer 30

Used to decrease cardiac work and improve organ
perfusion
**Short-term management
 IABPs, extracorporeal membrane oxygenation
(ECMO), and continual flow pumps
**Long-term
 Ventricular assist devices (VADs) include
percutaneous devices (PVAD) and transplanted
devices (LVADs, BiVADs)

Question 31

Intraaortic Balloon Pump (IABP)

Answer 31

Provides temporary circulatory assistance by
reducing afterload
 Benefits
 Decreased ventricular workload
 Increased myocardial perfusion
 Augment circulation
 Temporary use only

Consists of:
 Sausage-shaped balloon
 Pump that inflates and deflates balloon
 Control panel for synchronizing balloon inflation to cardiac cycle
 Fail-safe features

Balloon inserted into femoral artery and placed
in descending thoracic aorta
 Confirm placement with x-ray
 Pump inflates balloon with helium in conjunction
with ECG

 IABP therapy is known as counterpulsation
because the timing of balloon inflation is
opposite to ventricular contraction.
 The IABP assist ratio is 1:1 in the acute phase of
treatment. This means that there is one IABP
cycle of inflation and deflation for every
heartbeat.

Complications:
 Thrombus and embolus formation
 Thrombocytopenia
 Ischemia to periphery, kidneys, bowel
 Infection

Mechanical Complications:
 Improper timing of balloon inflation
 Balloon leak
 Malfunction of balloon or console

Question 32

Ventricular Assist Devices (VADs)

Answer 32

Short- and long-term support for failing heart
 Allows more mobility than IABP
 Shunts blood from left atrium or ventricle to
device, then to the aorta
 Internal or external
 Left, right, or biventricular

Question 33

Heart Transplant

Answer 33

Gold standard therapy suitable for some patients in
end-stage HF
 3000 on list; average 2000 available
 Survival rate of 85% to 90% at 1 year; 75% at 3
 Selection process identifies patients who would
most benefit from a donor heart
 Candidates must undergo a comprehensive
physical, diagnostic, and psychologic evaluation

-Wait time is long, many patients die while waiting

Post Transplant Monitoring: