Module 2: Heart Failure Flashcards
Heart Failure - Definition
-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
Heart Failure Risk Factors
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
How does heart failure happen?
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
Left Sided HF
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
Heart Failure with Reduced Ejection Fraction (HFrEF)
-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.
Heart Failure with Preserved EF (HFpEF)
-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
Right Sided HF
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)
Biventricular Failure
Both right and left ventricular dysfunction
Inability of both ventricles to pump effectively
Fluid build-up and venous engorgement
Decreased perfusion to vital organs
Compensatory Mechanism: Renin-Angiotensin-Aldosterone-System (RAAS) - Compensatory Mechanism of HF
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
Neurohormonal response—RAAS
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
Sympathetic Nervous System Role in Reducing HF
Baroreceptors sense low arterial pressure
Catecholamines are released
Stimulation of β-adrenergic receptors increases HR (chronotropy) and ventricular contractility (inotropy)
Factors Contributing to HF Development (Endothelin; Proinflammatory cytokines)
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
Dilation to prevent HF
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
Hypertrophy to prevent HF
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
Remodeling to prevent HF
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)
Natriuretic Peptides
-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.
Nitric Oxide and Prostaglandin
-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.
Acute Decompensated HF (ADHF) Clinical Manifestations
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
Pulmonary Edema Clinical Manifestations
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
ADHF Clinical Manifestations
-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
- 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. - 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. - 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. - 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.
Chronic Heart Failure Symptoms
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
Heart Failure Complications
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
Heart Failure Diagnostic Studies
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.
ADHF Care
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)
ADHF Drug Therapy
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
Chronic HF Care
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
Chronic HF Drug Therapy
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)
Chronic HF Care
Implantable cardioverter-defibrillator (ICD)
Biventricular pacing/cardiac resynchronization
therapy (CRT)
Remote monitoring
Chronic HF Nutrition
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
HF Support Devices
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)
Intraaortic Balloon Pump (IABP)
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
Ventricular Assist Devices (VADs)
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
Heart Transplant
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:
