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Nursing 172 > Week 8: Chp 30: Heart Failure > Flashcards

Week 8: Chp 30: Heart Failure Flashcards

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1
Q

Heart failure is more common in?

A
  • age >65
  • African Americans
  • overweight
  • people who have had a heart attack
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2
Q

Risk Factors associated with development

A

-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

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3
Q

Other conditions that can cause HF

A
  • valvular dysfunction
  • cardiomyopathies
  • infectious and inflammatory heart disorders such as pericarditis and endocarditis
  • dysrhythmias
  • cardiotoxic substances such as alcohol, chemotherapy, and illicit drugs
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4
Q

What is Heart Failure?

A

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

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5
Q

Pathophysiology

A
  • 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
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6
Q

What is activated in response to decreased stroke volume and cardiac output?

A

compensatory mechanisms

-these responses are actions that enable the body to maintain function

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7
Q

Compensatory mechanisms

A

actions that enable the body to maintain function

  • activated in response to decreased stroke volume and cardiac output
  • SNS and neurohormonal compensatory Reponses
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8
Q

Compensatory Mechanism: Sympathetic Nervous System

A

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
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9
Q

Compensatory Mechanisms: Neurohormonal compensatory response: renin-angiotensin-aldosterone system (RAAS)

A
  • 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
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10
Q

Angiotensin II produces?

A

peripheral vasoconstriction

-can increase BP and venous return to the heart

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11
Q

The release of aldosterone can result in?

A

sodium and water retention (where sodium goes, water goes)

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12
Q

Compensatory Mechanisms: Neurohormonal response: Natriuretic peptide

A

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
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13
Q

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?

A

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

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14
Q

Heart Failure is Classified based on?

A

> ejection fraction

-percentage of blood that is ejected from the ventricle with each contraction

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15
Q

Ejection Fraction

A

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
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16
Q

Ejection Fraction ranges

A
  • (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
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17
Q

HF is described according to?

A
  • ejection fraction
  • anatomical dysfunction
  • disease progression
  • and severity of symptoms
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18
Q

Biventricular failure

A

when both sides of the heart are affected

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19
Q

Left-sided HF

A

dysfunction of the left ventricle

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20
Q

Right-sided HF

A

inability of the right side of the heart to effectively pump blood to the pulmonary vasculature

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21
Q

Common signs of HF

A

-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

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22
Q

Left-Sided HF clinical manifestations

A

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
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23
Q

Right-Sided HF clinical manifestations

A

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)
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24
Q

Diagnosing of HF

A

dependent on history and physical assessment

-symptoms are nonspecific so diagnostic tests are done to rule out other disorders and determine the underlying cause

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25
Q

Diagnostic Tools

A
  • 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
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26
Q

Diagnostic Tests: Laboratory Tests

A
  • cardiac biomarkers
  • serum electrolytes
  • CBC
  • urinalysis
  • glucose level
  • fasting lipid profile
  • liver function testing
  • renal function test
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27
Q

Laboratory Tests: Serum electrolytes

A

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

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28
Q

Laboratory Tests: Renal Function

A

inadequate flow to the kidneys may impair renal function, resulting in elevated creatinine and blood urea nitrogen (BUN) levels

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29
Q

Laboratory Tests: CBC

A

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

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30
Q

Laboratory Tests: Cardiac Biomarkers

A

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

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31
Q

Goal of HFrEF management

A

reduction of risk factors, manipulation of the critical components of cardiac output (preload, afterload, contractility), and control of the compensatory mechanisms

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32
Q

What does successful management do?

A

slows disease progression, prevents complications, reduces morbidity and mortality, and improves quality of life

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33
Q

Risk factor management may include

A
  • blood pressure and glucose control
  • weight loss
  • optimizing serum lipids
  • smoking cessation
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34
Q

Medications: Beta Blockers

A

beta blockers are used to control the sympathetic nervous system compensatory response in HF, such as tachycardia, in order to decrease cardiac workload

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35
Q

Medication: Ivabradine

A

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

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36
Q

Preload

A

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

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37
Q

Medication: Aldosterone antagonists

A

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

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38
Q

Why should the medication spironolactone be used cautiously in patients with renal insufficiency?

A

because of the potential complication of hyperkalemia (high potassium)

39
Q

Why is furosemide paired with a potassium replacement therapy?

A

it is a loop diuretic that causes hypokalemia

40
Q

Afterload

A

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
41
Q

Medications: Angiotensin-converting enzyme (ACE) inhibitors

A

usually the first line of medications used to control the RAAS compensatory response and reduce afterload

42
Q

Medications: Angiotensin receptor blockers (ARBs)

A

control the RAAS compensatory response and reduce afterload

-can be used in patients who are intolerant of ACE inhibitors

43
Q

Medications: Angiotensin receptor- neprilysin inhibitors (ARNIs)

A 
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
44
Q

Medications: Vasodilators

A

to reduce afterload (resistance in the vasculature)

-hydralazine and isosorbide

45
Q

What Medications should be avoided in HF?

A

Calcium channel blockers, with the exception of amlodipine

-due to their myocardial depression effect and lack of demonstrated efficacy

46
Q

Medication Safety Alert: ARNIs

A

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
47
Q

Why cant you give an ACE inhibitor and an ARNI together?

A

increases the risk of angioedema (swelling)

48
Q

Contractility

A

the force of the myocardial muscle contraction

49
Q

Medication: inotropic medication

A

Digoxin (Lanoxin), or Dopamine

-increases cardiac contractility and reduce HR

50
Q

Patients on digoxin are prone to what?

A

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

51
Q

IV medications

A

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)

52
Q

Device and Surgical Intervention

A

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
53
Q

What is often indicated for patients with end-sage HF

A

palliative care

54
Q

Self-management

A

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

55
Q

Management by Interprofessional health team

A

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

56
Q

Cardiac Rehabilitation for HF

A

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
57
Q

Heart Failure and Older Adults

A

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
58
Q

Complications of HF

A
  • Pulmonary Edema

- Renal Failure

59
Q

Complications of HF: Pulmonary Edema

A

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

60
Q

Complications of HF: Pulmonary edema symptoms

A

-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

61
Q

Complications of HF: Pulmonary Edema Treatments

A

-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

62
Q

Complications: Renal Failure

A

due to the decrease in blood flow to the kidneys

63
Q

Nursing Management: Assessment ad Analysis

A

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
64
Q

Nursing Diagnosis

A
  • 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
65
Q

Nursing Interventions: Assessment

A

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
66
Q

Assessment: Vital Signs

A
  • 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
67
Q

Assessment: Breath Sounds

A

crackles indicate pulmonary congestion

68
Q

Assessment: monitoring for irregular heart rhythm or dysrhythmias

A

dysrhythmias are a common adverse affect of HF and medications used to treat HF

69
Q

Assessment: Skin color, temperature, peripheral pulses, and capillary refill time

A

pale or cyanotic color, cool extremities, weak peripheral pulses, and sluggish refill time result from inadequate cardiac output

70
Q

Assessment: Dry, persistent cough

A

common complication of ACE inhibitor

71
Q

Assessment: Activity tolerance

A

dyspnea on exertion, weakness, and fatigue indicate decreased cardiac output and worsening heart failure

72
Q

Assessment: Urine output

A

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
73
Q

Assessment: Daily Weight

A

to evaluate fluid retention and effectiveness of diuretics

74
Q

Assessment: Laboratory Data

A

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
75
Q

Assessment: Depression Screening

A

high rates of depression and anxiety are noted in the HF population
-these can impact self management

76
Q

Assessment: Social Support

A

social isolation has been shown to be an independent predictor of mortality among HF patients

77
Q

Nursing Interventions: Actions

A
  • oxygen therapy
  • elevate the head of the bed and provide a fan for dyspnea
  • medication administration as ordered
  • fluid and sodium restriction
78
Q

Actions: administer oxygen therapy

A

to maintain adequate oxygenation

79
Q

Actions: elevate the head of the bed and provide a fan for dyspnea

A

maximizes oxygenation and promotes comfort

80
Q

Actions: Administer diuretics

A

diuretics decrease volume, thus preload

81
Q

Actions: administer ACE inhibitors, ARBs, RNIs, and vasodilators

A

angiotensin-converting enzyme inhibitors, ARBs, ARNIs, and vasodilators decrease afterload, which helps to decrease the workload of the heart and decrease myocardial oxygen consumption

82
Q

Actions: administer beta blockers

A

beta blockers decrease the sympathetic response (heart rate), thus reducing myocardial oxygen consumption

83
Q

Actions: Administer inotropic agents

A

enhance contractility

84
Q

Actions: Fluid and Sodium restriction

A

to prevent fluid overload

85
Q

Teaching

A
  • 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
86
Q

Teaching: Medication management

A

understanding and adhering to the medication treatment plan are essential for effective medication treatment

87
Q

Teaching: Maintain activity as tolerated; alternate rest and activity periods

A

to reduce muscle wasting and functional losses; to decrease workload on the heart

88
Q

Teaching: low-salt diet

A

to prevent fluid retention and exacerbation of HF

89
Q

Teaching: Daily weight at home at the same time each day, preferably in the morning after voiding

A

evaluate fluid retention and need to call provider

90
Q

Teaching: Cardiac rehabilitation

A

cardiac rehab reduces mortality, improves functional status, reduces hospitalizations, and improves quality of life

91
Q

Teaching: Signs and symptoms of worsening HF checklist

A

(edema, SOB, fatigue, and orthopnea)

-knowing the symptoms can expedite treatment and reduce hospitalizations)

92
Q

Heart Failure patients are at risk for what?

A

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

93
Q

Successful management requires?

A
  • 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
94
Q

What does a well managed patient look like?

A

reduced dyspnea and fatigue, is able to actively participate in activities of daily living, and has reduced hospitalizations

Nursing 172 (120 decks)

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