Heart Failure Flashcards

1
Q

What are the characteristics of Systolic Heart Failure (HF-REF)?

A
  • weakened heart muscle
  • left ventricle loses ability to generate enough pressure to eject blood forward through aorta
  • reduced ejection fraction <40% (N = >55%)
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2
Q

What are the characteristics of Diastolic Heart Failure (HF-PEF)?

A
  • inability of ventricles to relax and fill during diastole (can’t fill enough)
  • decreased filling results in decreased stroke vol & CO
  • results in venous engorgement in both pulmonary and vascular systems
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3
Q

What is the most common form of HF?

A

Systolic (HF-REF)

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4
Q

What are the four compensatory mechanisms in HF?

A

(1) SNS: increases catecholamines
(2) Neurohormonal responses
- RAAS: increases renin
- Posterior Pituitary gland: secretes ADH
(3) Ventricular dilation
(4) Ventricular hypertrophy

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5
Q

Explain the SNS compensatory mechanism

A

increases epinephrine & norepinephrine to improve CO by increasing
- HR
- myocardial contractility
- and peripheral vasoconstriction

leads to increased cardiac workload and need for oxygen (vasoconstriction causes an increase in preload)

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6
Q

Explain the RAAS (neuro-hormonal) compensatory mechanism

A

kidneys respond to decreased blood flow by producing more renin

renin converts angiotensin I -> II by ACE and in response, the adrenal cortex releases aldosterone resulting in
- Na and H20 retention
- peripheral vasoconstriction
- increased BP

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7
Q

Explain the Posterior Pituitary Gland (neuro-hormonal) compensatory mechanism

A

responds to decreased cerebral perfusion pressure and secretes ADH (causes sodium and water retention) creating increased blood volume in an already overloaded state

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8
Q

Explain the Ventricular dilation compensatory mechanism

A

Heart chambers enlarge due to chronically elevated pressure

Initially adaptive to cope with increasing blood volume but eventually muscle fibers become overstretched and lose the ability to contract effectively = decreased CO

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9
Q

Explain the Ventricular hypertrophy compensatory mechanism

A

Increase in muscle mass and cardiac wall thickness in response to overwork and strain

Initially adaptive but over time hypertrophic heart muscle has poor contractility requiring more oxygen to perform

Coronary artery circulation becomes poor, and the heart is prone to dysrhythmias

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10
Q

Explain the counter-regulatory mechanisms (hormones)

A

Natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide [BNP]) are hormones produced by heart muscle in response to increased blood vol

These hormones regulate renal, cardiovascular, and hormonal compensation

Cardiac decompensation occurs when these mechanisms can no longer maintain CO and tissue perfusion becomes insufficient

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11
Q

Explain left-sided HF

A
  • LV cannot pump blood effectively to the systemic circulation
  • Causes blood to back up to the left atrium and pulmonary veins
  • Pulmonary congestion and edema
    -> dyspnea, cough, crackles, and impaired O2 exchange
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12
Q

Explain right-sided HF

A
  • RV cannot eject sufficient amounts of blood
  • Causes blood to back up in the right atrium and venous system
    -> peripheral edema, hepatomegaly, ascites, JVD, anorexia, GI distress, weight gain
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13
Q

Clinical manifestations of Acute Decompensated HF

A
  • Pulmonary edema: decreases lung compliance and increases resistance in small airways = mild increase in RR and decrease in PaO2
  • As pulmonary venous pressure increases, more fluid leaks into interstitial space = tachypnea & SOB
  • If pulmonary pressure continues to increase, fluid moves into alveoli and disrupts gas exchange = respiratory acidosis
  • Affected patients are anxious, pale, cyanotic, clammy, cold, severe dyspnea and orthopnea, wheezing, coughing, blood-tinged sputum
  • Auscultation will reveal crackles, wheezes, and ronchi throughout the lungs
  • HR is rapid and BP may be elevated or decreased
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14
Q

Clinical Manifestations of Chronic HF

A
  • Fatigue: poor CO, anemia
  • Dyspnea at rest or mild exertion
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Cough: dry, nonproductive
  • Tachycardia
  • Edema
  • Nocturia: impaired renal perfusion during the day, when lying flat blood moves back into CVS
  • Skin Changes: dusk, lower extremities are shiny, swollen, and diminished hair growth
  • Behavioural changes: restlessness, confusion, impaired memory d/t decreased cerebral perfusion
  • Chest pain: decreased coronary artery perfusion
  • Weight changes: progressive gain
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15
Q

Complications of HF

A

(1) Pleural Effusion
(2) Dysrhythmias - enlargement of heart changes normal electrical pathways
(3) Left Ventricular Thrombus - increased LV and decreased CO increase risk of formation and stroke
(4) Hepatomegaly - venous system backing up into liver leading to impaired liver function and possibly cirrhosis
(5) Renal failure - decreased CO leads to hypoperfusion of kidneys = renal insufficiency or failure

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16
Q

Explain the role of Echocardiography in the Diagnosis of HF

A

distinguish HF-REF from HF-PEF

17
Q

Explain the role of BNP in the Diagnosis of HF

A

distinguish dyspnea caused by HF from other causes

18
Q

Explain the role of a Chest X-ray in the Diagnosis of HF

A

can help distinguish pleural effusions from other causes of dyspnea (i.e., pneumonia), can also visualize cardiomegaly

19
Q

What is the first-line medication therapy in HF?

A

ACE inhibitors
(i.e., ramipril, perindopril)

20
Q

What is the action of ACE inhibitors? (i.e., ramipril, perindopril)

A

Block the conversion of angiotensin I -> II, reducing aldosterone and thereby reducing retention of Na and H2O

  • Promotes vasodilation
  • Maintains tissue perfusion
  • Reduces ventricular filling pressure
  • Risk for hypotension, chronic cough, and renal insufficiency
  • Risk for life-threatening angioedema (rare)
21
Q

What is the action of Beta Blockers? (i.e., metoprolol)

A

block negative effects of SNS on the failing heart including increased HR

  • Risk for reduced myocardial contractility
  • Can also cause bradycardia, fatigue, asthma exacerbations, edema
22
Q

What is the action of Potassium-sparing diuretics? (Mineral Corticoid Receptor Antagonists, i.e., spironolactone)

A

Block sodium and water excretion as well as potassium excretion by blocking aldosterone

  • Risk for additive effects with ACE inhibitors: monitor renal function and potassium
23
Q

What are the primary risk factors of HF?

A

coronary artery disease and hypertension

24
Q

What are some secondary risk factors of HF?

A

Diabetes, smoking, obesity, and high serum cholesterol

25
Q

What often causes Diastolic HF (HF-PEF)?

A

left ventricular hypertrophy (due to hypertension), myocardial ischemia, valve disease, and cardiomyopathy

26
Q

Explain Nursing Management of Acute Decompensated HF (6 points)

A
  • Decrease intravascular volume: loop diuretics
  • Decrease Venous return: Elevating the head of the bed with feet dangling
  • Decrease Afterload: Monitor vital signs - decreased BP reduces afterload; however, it must be adequate to maintain renal and cerebral perfusion
  • Improving Gas Exchange: Morphine can reduce preload and afterload and decrease myocardial oxygen demand; Administer oxygen if sats <90%
  • Improving Cardiac Function: inotropic therapies and hemodynamic monitoring
    Reduce Anxiety: Calm approach, morphine
27
Q

Explain Collaborative Care of Chronic HF

A
  • Referral to multidisciplinary clinic or specialist care for heart failure
  • Non-pharmacologic therapies: Oxygen, Self-management teaching
  • Devices: pacemakers, implantable cardioverter-defibrillator, mechanical circulatory support (short-term), Cardiac Transplantation
28
Q

List Signs and Symptoms of Hypokalemia

A
29
Q

List Signs and Symptoms of Hyperkalemia

A
30
Q
A
31
Q

Explain Nutritional Therapy for pts with HF

A
  • <2g of sodium
  • DASH diet
  • Stop using saltshaker
  • Daily weight to monitor fluid retention (same time, before breakfast, wearing same type of clothing)
  • Contact PCP if the patient experiences weight gain of 2 kg over a 2-day period or 2.5 kg over 5-day period