Week 8: Chp 30: Heart Failure Flashcards
Heart failure is more common in?
- age >65
- African Americans
- overweight
- people who have had a heart attack
Risk Factors associated with development
-Coronary Artery Disease (CAD)
-Hypertension
-Diabetes Mellitus
-Metabolic Syndrome
-Obesity
-Smoking
-High Sodium Dietary Intake
>other conditions: valvular dysfunction; cardiomyopathies; infectious and inflammatory heart disorders such as pericarditis and endocarditis, dysrhythmias, and cardiotoxic substance exposure, such as alcohol, chemotherapy, and illicit drugs
Other conditions that can cause HF
- valvular dysfunction
- cardiomyopathies
- infectious and inflammatory heart disorders such as pericarditis and endocarditis
- dysrhythmias
- cardiotoxic substances such as alcohol, chemotherapy, and illicit drugs
What is Heart Failure?
progressive disease characterized by myocardial cell dysfunction, resulting in the inability of the heart to pump enough cardiac output to meet the demands of the body
Pathophysiology
- normal physiology of the heart is governed by the Frank-Starling Law, which states that the contractility of the myocardial muscle is influenced by the amount of blood within the ventricle prior to systole; in other words, high end diastolic volume stretches the myocardium, increasing the force of each contraction
- in people with risk factors for HF, such as hypertension, the constant demands on the myocardial muscles over time cause them to become weakened and unable to pump effectively
What is activated in response to decreased stroke volume and cardiac output?
compensatory mechanisms
-these responses are actions that enable the body to maintain function
Compensatory mechanisms
actions that enable the body to maintain function
- activated in response to decreased stroke volume and cardiac output
- SNS and neurohormonal compensatory Reponses
Compensatory Mechanism: Sympathetic Nervous System
the SNS releases epinephrine and norepinephrine, resulting in an increased heart rate, increased myocardial contractility, and increased vasoconstriction in an effort to increase cardiac output
- this additional workload stimulates ventricular remodeling, which results in hypertrophy or stiffening of the ventricular walls
- long-term effects of SNS responses are damaging; they produce an increase in cardiac workload and cardiac oxygen consumption, worsening the failure
Compensatory Mechanisms: Neurohormonal compensatory response: renin-angiotensin-aldosterone system (RAAS)
- this is done in reaction to decreased blood flow to the kidneys
- the kidneys interpret this as decreased volume and release an enzyme, renin
- renin converts angiotensin, an inactive peptide released by the liver, to angiotensin I
- Angiotensin I is enzymatically converted to angiotensin II by angiotensin-converting enzyme released by the lungs
- Angiotensin II produces peripheral vasoconstriction, which helps increase blood pressure and venous return to the heart
- Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, which results in sodium and water retention
- mechanism is effective in the short-term, but in the long term, they overtax an already weak heart with increased volume and workload
Angiotensin II produces?
peripheral vasoconstriction
-can increase BP and venous return to the heart
The release of aldosterone can result in?
sodium and water retention (where sodium goes, water goes)
Compensatory Mechanisms: Neurohormonal response: Natriuretic peptide
Brain natriuretic peptide, or B-type natriuretic peptide (BNP, is a hormone produced by the ventricular cardiac muscle
- it is released in reaction to “overstretching” of the ventricle in response to increased pressure and volume
- the result is a natural diuresis as well as arterial and venous dilation
- this action decreases both preload and afterload, which decreases the workload on the heart
What hormone is produced by the ventricular cardiac muscle and is released in reaction to “over stretching” of the ventricle in response to increased pressure and volume?
BNP (brain natriuretic peptide/ B-type natriuretic peptide
-results in natural diuresis as well as arterial and venous dilation; decreases both preload and afterload decreasing the workload of the heart
Heart Failure is Classified based on?
> ejection fraction
-percentage of blood that is ejected from the ventricle with each contraction
Ejection Fraction
percentage of blood that is ejected from the ventricle with each contraction
- normal: 55 to 70% of the total volume
- this is how heart failure is classified
Ejection Fraction ranges
- (HFrEF): patient with low EF have HF and reduced EF; systolic heart failure; have weakened contractions with an EF of 45% or less
- (HFpEF): patients with clinical manifestations of HF but an EF of greater than 45% are diagnosed with HF with preserved ejection fraction (EF); diastolic HF; inability of the ventricles to fill
HF is described according to?
- ejection fraction
- anatomical dysfunction
- disease progression
- and severity of symptoms
Biventricular failure
when both sides of the heart are affected
Left-sided HF
dysfunction of the left ventricle
Right-sided HF
inability of the right side of the heart to effectively pump blood to the pulmonary vasculature
Common signs of HF
-fatigue
-weight gain
-faster heart rates
-and hypo or hypertension
>heart murmur may be present if the cause of HF is valve dysfunction
>when auscultating heart tones, a third sound S3 may be a warning sign of worsening heart failure
-S4 is common in chronic HF
>the point of maximal intensity may be enlarged or displaced when ventricles enlarge
Left-Sided HF clinical manifestations
the weakened contraction results in poor peripheral perfusion and backflow of blood that causes fluid accumulation in the lungs
- SOB (dyspnea), orthopnea, fatigue, and crackles heard on auscultation
- pale color, weak pulses, cool temperature in extremities, delayed capillary refill
- fatigue, weakness
Right-Sided HF clinical manifestations
the weakened contraction of the right ventricle, results in backflow of blood into the right atrium and venous circulation
- jugular vein distention (JVD)
- generalized dependent edema
- hepatomegaly (enlarged liver)
- ascites (abdominal swelling)
Diagnosing of HF
dependent on history and physical assessment
-symptoms are nonspecific so diagnostic tests are done to rule out other disorders and determine the underlying cause
Diagnostic Tools
- chest x-ray, echocardiogram, and ECG to assess the presence of structural disease, ejection fraction, heart size, pulmonary congestion, or dysrhythmias
- multigated acquisition (MUGA) scans can also determine ejection fraction (EF)
- nuclear imaging studies, stress testing, and coronary angiography to evaluate blood flow to the heart are performed when coronary artery disease is suspected
Diagnostic Tests: Laboratory Tests
- cardiac biomarkers
- serum electrolytes
- CBC
- urinalysis
- glucose level
- fasting lipid profile
- liver function testing
- renal function test
Laboratory Tests: Serum electrolytes
electrolytes can be outside the normal range as a result of decreased kidney perfusion or medication
-Ex: potassium might be low because of diuretic therapy
Laboratory Tests: Renal Function
inadequate flow to the kidneys may impair renal function, resulting in elevated creatinine and blood urea nitrogen (BUN) levels
Laboratory Tests: CBC
decreased hemoglobin and hematocrit levels may indicate anemia, which may be a result of decreased blood flow to the kidneys that reduces the production of erythropoietin in the kidneys
Laboratory Tests: Cardiac Biomarkers
such as Troponin I or T, are used to rule out an acute ischemic event
-BNP and N-terminal pro-B-type natriuretic peptide (NT-proBNP), are increased because of the overstretching of the ventricles
>increased values in these tests can be used to diagnose HF
>BNP and NT-proBNP can also guide clinical decision making and track a patients response to therapy as well as indicate disease progression
Goal of HFrEF management
reduction of risk factors, manipulation of the critical components of cardiac output (preload, afterload, contractility), and control of the compensatory mechanisms
What does successful management do?
slows disease progression, prevents complications, reduces morbidity and mortality, and improves quality of life
Risk factor management may include
- blood pressure and glucose control
- weight loss
- optimizing serum lipids
- smoking cessation
Medications: Beta Blockers
beta blockers are used to control the sympathetic nervous system compensatory response in HF, such as tachycardia, in order to decrease cardiac workload
Medication: Ivabradine
a new medication that slows sinus-node firing, can be added for greater control of heart rate in patients taking maximal doses of beta blockers or who do not tolerate beta blockers
Preload
amount of stretch in the heart at the end of diastole (filling) and is affected by the amount and pressure of blood returning to the heart
-aldosterone antagonists diuretics such as spironolactone (Aldactone) and loop diuretics such as Furosemide (Lasix) are essential medications to decrease preload in patients with fluid retention
Medication: Aldosterone antagonists
spironolactone (Aldactone)
>as well as loop diuretics such as Furosemide (Lasix) are essential medications to decrease preload in patients with fluid retention
>spironolactone should be cautioned in patients with renal insufficiency because of the potential complication of hyperkalemia
>furosemide can cause hypokalemia and is often paired with a potassium replacement therapy
Why should the medication spironolactone be used cautiously in patients with renal insufficiency?
because of the potential complication of hyperkalemia (high potassium)
Why is furosemide paired with a potassium replacement therapy?
it is a loop diuretic that causes hypokalemia
Afterload
refers to the resistance within the vasculature
- increased afterload intensifies the workload on the heart, further impairing cardiac output
- afterload reduction is a main goal of medical management
- ACE inhibitors and ARBs
- ARNIs
- vasodilators
- Inotropes
Medications: Angiotensin-converting enzyme (ACE) inhibitors
usually the first line of medications used to control the RAAS compensatory response and reduce afterload
Medications: Angiotensin receptor blockers (ARBs)
control the RAAS compensatory response and reduce afterload
-can be used in patients who are intolerant of ACE inhibitors
Medications: Angiotensin receptor- neprilysin inhibitors (ARNIs)
new class of medication that combine an ARB with a neprilysin inhibitor (valsartan with sacubitril) and can be used in place of an ACE inhibitor or ARB -Neprilysin is an enzyme that breaks down natriuretic peptide (BNP), which produces natural diuresis and vasodilation; by blocking neprilysin, natriuretic peptide (BNP) remain active in increasing urine output and dilating blood vessels
Medications: Vasodilators
to reduce afterload (resistance in the vasculature)
-hydralazine and isosorbide
What Medications should be avoided in HF?
Calcium channel blockers, with the exception of amlodipine
-due to their myocardial depression effect and lack of demonstrated efficacy
Medication Safety Alert: ARNIs
Like ACE inhibitors, the neprilysin inhibitor in an ARNI prevents the breakdown of bradykinin as well as natriuretic peptides
- Bradykinin is a cause of angioedema (swelling of the tongue and oral pharynx)
- the combination of an ACE inhibitor and ARNI significantly increases the risk of angioedema
- An ANRI should not be given at the same time or within 36 hours of an ACE inhibitor
- an ARNI should not be given to patients who had angioedema in the past
Why cant you give an ACE inhibitor and an ARNI together?
increases the risk of angioedema (swelling)
Contractility
the force of the myocardial muscle contraction
Medication: inotropic medication
Digoxin (Lanoxin), or Dopamine
-increases cardiac contractility and reduce HR
Patients on digoxin are prone to what?
toxicities with symptoms such as nausea, vomiting, and visual disturbances (e.g. yellow halos around lights)
-monitor patients closely to avoid later signs of toxicity, such as bradycardia or dysrhythmias
IV medications
to treat acute exacerbations of HF
-effectively decrease preload and afterload and increase contractility
-Nitroglycerin and nitroprusside (Nitropress), potent vasodilators, are commonly used
-Intravenous inotropic agents (dopamine) can be used to increase contractility
-Inodilators, agents with both positive inotropic and vasodilator effects (dobutamine and milrinone), provide positive inotropic effects and reduce afterload
>all these medications require careful monitoring of BP, heart rate, and cardiac rhythm and frequent assessments to guide therapy and avoid adverse effects)
Device and Surgical Intervention
as HF progresses more invasive treatments are needed to support cardiac function and control the complications that result
- implantation of an automatic internal cardiac defibrillator (ICD) and pacemaker for dysrhythmia control and ventricular resynchronization; cardiac resynchronization therapy (CRT)
- continuous IV inotrope therapy, an intra-aortic balloon pump, and other mechanical circulatory support (MCS) devices such as a ventricular assess device (VAD) can be used to support the failing heart
- depending on cause of HF, valve replacement or heart transplantation may be considered
What is often indicated for patients with end-sage HF
palliative care
Self-management
critical component of HF treatment
-patients must assume responsibilities for symptom monitoring, medication adherence, and lifestyle changes
-daily weights taken about the same time each day and monitor fluid retention; weight gain indicates fluid retention (gain of 2lbs in a day or 5lbs in a week)
-sodium restricted diet (1500 mg/day in early stage, up to 4000 in later), maintaining optimal weight, and preventing cardiac cachexia (unintentional severe weight loss)
>a high BMI is associated with higher mortality
>although a low BMI is generally positive, weight loss in a patient with HF may reflect cardiac cachexia which may indicate higher mortality
Management by Interprofessional health team
teaching related to medications, sodium restriction, and weight management
-symptom monitoring, screening for depression and mental health comorbidities, evaluating social support structures, planning and encouraging participation in cardiac rehabilitation, and implementing behavior-change strategies such as motivational interviewing
>self-management is affected by the patient perceptions of interactions with the healthcare team members
Cardiac Rehabilitation for HF
persons with HF experience reduced capacity for physical activity, which can have detrimental effects on their quality of life and contribute to hospitalizations and mortality
- recommend cardiac rehabilitation in the management of heart failure
- patients who participated in exercise-based cardiac rehab programs had significantly fewer hospitalizations and improved quality of life
Heart Failure and Older Adults
HF is more common with aging
- older patients are more likely to have heart failure with preserved ejection fraction (HFpEF)
- older patients often have additional comorbidities which create complexities in care and a greater potential for medication interactions
- depression, anxiety, and cognitive impairment, which often undiagnosed, can reduce self management abilities and medication adherence, warranting careful screening for these conditions
- many HF medications have hypotensive effects or cause nocturia, which may increase fall risk; a careful risk-benefit analysis of interventions is required, particularly when medication changes occur
- due to declining renal function, potential poor nutritional status, and greater risk for dehydration, older patients need to be monitored more carefully for adverse effects
Complications of HF
- Pulmonary Edema
- Renal Failure
Complications of HF: Pulmonary Edema
acute complication of HF characterized by the accumulation of fluid in the interstitial and alveolar spaces of the lung, resulting from elevated filling pressures within the heart
-symptoms: SOB, low oxygen saturation, pink and frothy sputum, orthopnea, tachycardia, chest pain, and anxiety/fear
-treatments: supplementary oxygen administration and initiation of higher dose or IV diuretics
>depending on severity of edema, the patient may need more aggressive respiratory support with continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), or intubation with mechanical ventilation
-dysrythmias can also occur a the heart enlarges and catecholamine levels increase
Complications of HF: Pulmonary edema symptoms
-shortness of breath
-low oxygen saturation
-pink and frothy sputum
-orthopnea (difficulty breathing lying down)
-tachycardia
-chest pain
-anxiety/fear
>dysrhythmias can also occur as the heart enlarges and catecholamines levels increase
Complications of HF: Pulmonary Edema Treatments
-supplementary oxygen administration
-initiation of higher-dose or IV diuretics
>depending on the severity of the edema, the patient may need more aggressive respiratory support with continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), or intubation with mechanical ventilation
Complications: Renal Failure
due to the decrease in blood flow to the kidneys
Nursing Management: Assessment ad Analysis
the clinical manifestations of HF are due to the weakened myocardial contraction resulting in decreased cardiac output, a backup of blood, and poor peripheral perfusion
- poor mentation
- anorexia
- exercise intolerance
- JVD
- dependent peripheral edema
- weak peripheral pulses, cool extremities, delayed capillary refill
- cardiac cachexia (weight loss) or generalized body wasting
Nursing Diagnosis
- impaired oxygenation r/t accumulation of fluid in the lungs secondary to HF
- decreased cardiac output r/t altered preload, afterload, and contractility
- ineffective peripheral perfusion r/t decreased cardiac output secondary to HF
Nursing Interventions: Assessment
Assess:
- vital signs
- breath sounds
- monitoring for irregular heart rhythm or dysrhythmias
- skin color, temperature, peripheral pulses, and capillary refill time
- dry, persistent cough
- activity tolerance
- urine output
- daily weight
- laboratory data
- depression screening
- social support
Assessment: Vital Signs
- hypertension is present because of increased afterload
- hypotension may be caused by acute heart failure or be an adverse effect of medications
- tachycardia can be present as the heart attempts to compensate for decreased cardiac output
- tachypnea and decreased oxygen saturation may be present when fluid accumulates in the lungs because of left-sided HF
Assessment: Breath Sounds
crackles indicate pulmonary congestion
Assessment: monitoring for irregular heart rhythm or dysrhythmias
dysrhythmias are a common adverse affect of HF and medications used to treat HF
Assessment: Skin color, temperature, peripheral pulses, and capillary refill time
pale or cyanotic color, cool extremities, weak peripheral pulses, and sluggish refill time result from inadequate cardiac output
Assessment: Dry, persistent cough
common complication of ACE inhibitor
Assessment: Activity tolerance
dyspnea on exertion, weakness, and fatigue indicate decreased cardiac output and worsening heart failure
Assessment: Urine output
output may be reduced with decreased renal perfusion
- it can also be used to assess the effectiveness of diuretic therapy
- less than 30 mL/hr should be reported to the provider
Assessment: Daily Weight
to evaluate fluid retention and effectiveness of diuretics
Assessment: Laboratory Data
elevated BNP and NT-proBNP indicate overstretching of heart tissue
- elevated creatinine and BUN may be indicative of prerenal failure due to decreased cardiac output or over-diuresis
- elevated hepatic enzymes can be indicative of hepatomegaly
- hypokalemia is a common complication of diuretic administration
- anemia can be caused by reduced kidney perfusion resulting in decreased erythropoietin production and function
Assessment: Depression Screening
high rates of depression and anxiety are noted in the HF population
-these can impact self management
Assessment: Social Support
social isolation has been shown to be an independent predictor of mortality among HF patients
Nursing Interventions: Actions
- oxygen therapy
- elevate the head of the bed and provide a fan for dyspnea
- medication administration as ordered
- fluid and sodium restriction
Actions: administer oxygen therapy
to maintain adequate oxygenation
Actions: elevate the head of the bed and provide a fan for dyspnea
maximizes oxygenation and promotes comfort
Actions: Administer diuretics
diuretics decrease volume, thus preload
Actions: administer ACE inhibitors, ARBs, RNIs, and vasodilators
angiotensin-converting enzyme inhibitors, ARBs, ARNIs, and vasodilators decrease afterload, which helps to decrease the workload of the heart and decrease myocardial oxygen consumption
Actions: administer beta blockers
beta blockers decrease the sympathetic response (heart rate), thus reducing myocardial oxygen consumption
Actions: Administer inotropic agents
enhance contractility
Actions: Fluid and Sodium restriction
to prevent fluid overload
Teaching
- medication management
- maintain activity as tolerated. alternate rest and activity periods
- low-salt diet
- daily weight at home at same time each day, preferably in the morning after voiding
- cardiac rehabilitation
- signs and symptoms of worsening HF checklist
Teaching: Medication management
understanding and adhering to the medication treatment plan are essential for effective medication treatment
Teaching: Maintain activity as tolerated; alternate rest and activity periods
to reduce muscle wasting and functional losses; to decrease workload on the heart
Teaching: low-salt diet
to prevent fluid retention and exacerbation of HF
Teaching: Daily weight at home at the same time each day, preferably in the morning after voiding
evaluate fluid retention and need to call provider
Teaching: Cardiac rehabilitation
cardiac rehab reduces mortality, improves functional status, reduces hospitalizations, and improves quality of life
Teaching: Signs and symptoms of worsening HF checklist
(edema, SOB, fatigue, and orthopnea)
-knowing the symptoms can expedite treatment and reduce hospitalizations)
Heart Failure patients are at risk for what?
frequent exacerbations due to even small changes in fluid status, salt intake, or being exposed to common ailments such as a cold
-reducing stressors that lead to exacerbations is key
Successful management requires?
- collaboration with the patient, family, and interprofessional team to develop and implement a treatment plan
- that plan should include frequent assessment, comprehensive patient education, and self-management
What does a well managed patient look like?
reduced dyspnea and fatigue, is able to actively participate in activities of daily living, and has reduced hospitalizations
