Heart Failure Flashcards

1
Q

How is heart failure defined?

A

An abnormality of cardiac structure or function

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2
Q

In heart failure, what does the heart fail to do despite normal filling pressures?
Heart failure can be caused by myocardial failure or what other condition?

A

Deliver oxygen at a sufficient rate
Nearly-normal cardiac functions (High Output Failures)

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3
Q

While heart failure always leads to circulatory failure, what non-cardiac conditions can also lead to circulatory failures?

A

Hypovolaemic and septic shock

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4
Q

What compensatory mechanisms are activated in heart failure?

A
  • Increase in blood volume
  • Increased cardiac filling pressure
  • Increased heart rate
  • Increased cardiac muscle mass
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5
Q

What are the consequences of the compensatory mechanisms activated in heart failure?

A

Progressive declined contraction and relaxation

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6
Q

From a hemodynamic standpoint, heart failure can be secondary to what? In heart failure, is cardiac output usually above or below the normal range?

A

Systolic or diastolic dysfunction
Below normal range

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7
Q

What ejection fraction value is typical of acute failure resulting from myocardial infarction? How does diastolic dysfunction affect ejection fraction?

A

<45%
Ejection fraction may be normal

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8
Q

In “high-output” failure, why is increased cardiac output insufficient?

A

The demands of the body are too great

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9
Q

How is ejection fraction (EF) related to heart failure terminology?

A
  • Reduced ejection fraction: EF <40%
  • Mildly impaired EF: EF 40-49%
  • Preserved ejection fraction: EF ≥50%
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10
Q

What are some ways that heart failure is related to time-course?

A

New onset
Transient
Chronic

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11
Q

How can heart failure be related to progression?

A

Acute
Stable
Worsening

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12
Q

How is heart failure related to location?

A

Left heart
Right heart
Combined

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13
Q

How can heart failure be related to Cardiac Output?

A

High output failures
Low output failures

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14
Q

What are some more specific signs of heart failure?

A
  • Elevated jugular venous pressure
  • Hepatojugular reflux
  • Third heart sound (gallop rhythm)
  • Laterally displaced apical impulse
  • Cardiac murmur, Tachycardia
  • Ankle swelling, venous congestion (oedema)
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15
Q

What are some typical symptoms of heart failure?

A
  • Breathlessness
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Reduced exercise tolerance
  • Fatigue, tiredness, increased time to recover after exercise
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16
Q

In heart failure pathophysiology, what do the systemic responses in the renin–angiotensin–aldosterone and sympathetic nervous systems cause?

A

Further myocardial injury

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17
Q

What protective function does the natriuretic peptide system have in heart failure?

A

Counterbalance detrimental effects

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18
Q

What happens when compensatory mechanisms in heart failure become overwhelmed?

A

A failure ensues

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19
Q

What are the main adaptations that occur in heart failure?

A
  • Increase preload (Frank-Starling mechanism)
  • Alterations in myocyte regeneration and death
  • Myocardial hypertrophy (cardiac remodelling)
  • Activation of neurohumoral systems
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20
Q

What is the Frank-Starling mechanism?

A

Increase preload to sustain cardiac performance

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21
Q

In heart failure, what are the Favourable and Negative Impacts of ↑ Sympathetic Activity?

A
  1. Favourable Impact: ↑ HR, ↑ Contractility, ↑, →Vesocon. ↑Venous return, ↑Filling Pressure
  2. Negative Impact: Arteriolar Vasocon→ Afterload → ↑ Workload → ↑ Vasocon.
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22
Q

In heart failure, what are the Favourable and Negative Impacts of ↑ Renin-Angiotensin-Aldosterone System?

A
  1. Favourable Impact: Salt & Water retention ↑ Venous Return
  2. Negative Impact: ↑ Vasocon. ↑ Afterload
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23
Q

In heart failure, what are the Favourable and Negative Impacts of ↑ Vasopressin?

A
  1. Favourable Impact: Salt & Water retention ↑ Venous Return
  2. Negative Impact: ↑ Vasocon. ↑ Afterload
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24
Q

In heart failure, what are the Favourable and Negative Impacts of ↑ Interleukins & TNFα?

A
  1. Favourable Impact: Potential role in myocyte hypertrophy
  2. Negative Impact: Apoptosis
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25
Q

In heart failure, what are the Favourable and Negative Impacts of ↑ Endothelin?

A
  1. Favourable Impact: ↑ Vasocon. ↑ Venous return
  2. Negative Impact: ↑ Afterload, Myocardial hypertrophy.
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26
Q

What are some negative consequences of myocardial hypertrophy?

A

Ischemic changes, impairment of diastolic filling

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27
Q

What could increased contractility or inotropic (calcium overload) response cause in the heart?

A

Arrhythmia and sudden death

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28
Q

What term is applied to dilation and slow structural changes that occur in the stressed myocardium?

A

Remodelling (proliferation of connective tissue cells)

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29
Q

What happens to myocytes in the failing heart?

A

Die at an accelerated rate through apoptosis

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30
Q

What has long been exploited in treating heart failure patients to slow the process of remodelling?

A

Lowering wall stress

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31
Q

What are some cellular changes that occur in heart failure?

A
  • Changes in Ca+2 handling
  • Changes in adrenergic receptors
  • Changes in contractile proteins
  • Program cell death (Apoptosis)
  • Increase amount of fibrous tissue
32
Q

What do the changes in adrenergic receptors include in heart failure?

A

β1 receptors desensitization

33
Q

How many primary factors is cardiac performance a function of? What is the first primary factor of cardiac performance?

34
Q

What filling pressure represents the Frank-Starling relation on the ascending limb? What filling pressures result in pulmonary congestion?

A

< 15 mm Hg filling pressure
Greater than 20–25 mm Hg

35
Q

Why is preload usually increased in heart failure? How do venodilator drugs reduce preload?

A

Because of increased blood volume
Redistributing blood away from the chest

36
Q

What is the goal of salt restriction and diuretic therapy in heart failure?

A

Reduction of high filling pressure

37
Q

What is the second primary factor of cardiac performance? What represents this?

A

Afterload
Aortic impedance and systemic vascular resistance

38
Q

What happens to systemic vascular resistance as cardiac output falls in chronic failure? What systems cause this?

A

There is a reflex increase
Sympathetic outflow and circulating catecholamines

39
Q

What vasoconstrictor peptide may also be involved in reflex increase in systemic vascular resistance?

A

Endothelin

40
Q

What happens to the intrinsic function of the heart in failure?

A

The intrinsic function decreases

41
Q

What is the first compensatory mechanism that comes into play to maintain cardiac output?

A

Increase in heart rate

42
Q

What is the fourth primary factor of cardiac performance? What does heart muscle obtained by biopsy from patients with chronic low-output failure demonstrate?

A

Contractility
Reduction in intrinsic contractility

43
Q

What happens to the velocity of muscle shortening as contractility decreases? What happens to the rate of intraventricular pressure development as contractility decreases?

A

There is a reduction
Rate reduction

44
Q

What is the heart still capable of in response to inotropic drugs?

A

Some increase in all cardiac performance factors

45
Q

What are the three types of causes for HF?

A
  • Underlying causes
  • Fundamental causes
  • Precipitating causes
46
Q

What type of cardiomyopathies are known genetic causes of heart failure?

A

Dilated, arrhythmic right ventricular

47
Q

List the aetiologies of Heart Failure

A

Valvular Heart Disease
Myocardial Disease
Endocardial Disease
Pericardial Disease
High Output States
Arrhythmia
Conduction Disorders
Volume Overload
Congenital Heart Disease

48
Q

Contributory Causal Conditions of Heart Failure are split into what two categories?

A

CV (thyroid disease, severe anaemia, renal failure, cirrhosis)
Non-Cardiac (IHD-CAD-MI, hypertension, valve disease)

49
Q

What are the three classifications and staging systems for Heart Failure?

A
  • NHS Stages (Based on symptoms)
  • ACC/AHA stages of HF (based on structure and damage to heart)
  • NYHA functional classification (based on symptoms or physical activity)
50
Q

According to the NHS stages, what defines Class I heart failure? According to the NHS stages, what defines Class II heart failure? According to NHS stages, what defines Class III heart failure? According to NHS stages, what defines Class IV heart failure?

A

No symptoms during normal activities
Comfortable at rest, but normal activity triggers symptoms
Comfortable at rest, minor activity triggers symptoms
Unable to carry out any physical activity

51
Q

According to the ACC/AHA stages of HF, what defines Stage A heart failure? According to the ACC/AHA stages of HF, what defines Stage B heart failure? According to ACC/AHA, what defines Stage C heart failure? According to ACC/AHA, what defines Stage D heart failure?

A

At high risk, but without abnormality
Developed structural heart disease without symptoms
Symptomatic HF with structural heart disease
Advanced structural disease and marked symptoms

52
Q

According to the NYHA functional classification, what defines Class I heart failure? According to the NYHA functional classification, what defines Class II heart failure? According to NYHA, what is Class III heart failure? According to NYHA, what is Class IV heart failure?

A

No limitation of physical activity
Slight limitation of physical activity
Marked limitation of physical activity
Symptoms of HF present at rest

53
Q

What is a type of tachyarrhythmia? What is a type of bradyarrhythmia?

A

Atrial
Sinus node dysfunction

54
Q

What can cause volume overload?

A

Renal failure

55
Q

What is the mortality following hospitalization for heart failure at 30 days? What is the mortality following hospitalization for heart failure at 1 year? What is the mortality following hospitalization for heart failure at 5 years?

A

10.4%
22%
42.3%

56
Q

What is the mortality rate for patients with NYHA class IV heart failure? What is the in-patient mortality rate for HF with AMI?

A

> 50%
20-40%

57
Q

What is the mortality rate for HF with hypotensive shock? What is the mortality rate for HF with systolic dysfunction in 5 years?

A

Up to 80%
Up to 50%

58
Q

What does overall heart failure management include?

A

Nonpharmacological, pharmacological, and invasive strategies

59
Q

What is the purpose of diuretics in the pharmacotherapy of heart failure? What are the effects of ACEIs in the pharmacotherapy of heart failure? What are the effects of ARBs in the pharmacotherapy of heart failure?

A

To reduce oedema by reducing blood volume
Neurohormonal modification, vasodilatation, and survival benefit
Same as above

60
Q

What is the purpose of hydralazine and nitrates in the pharmacotherapy of heart failure? What is the purpose of beta blockers in the pharmacotherapy of heart failure?

A

Improve symptoms, ventricular function, and survival
Neurohormonal modification, symptom improvement, and survival benefit

61
Q

What is the purpose of aldosterone antagonists as an adjunct in heart failure treatment? What is the effect of digoxin on cardiac output and heart failure symptoms?

A

Additive diuresis, heart failure symptom control, improved heart rate variability
Small increase in cardiac output, improvement in symptoms

62
Q

What is the purpose of anticoagulants in the treatment of heart failure? What is the purpose of inotropic agents in the treatment of heart failure? What is the purpose of soluble guanylate cyclase (sGC) stimulators in heart failure treatment?

A

To decrease the risk of thromboembolism
To restore organ perfusion and reduce congestion
To augment smooth muscle relaxation and vasodilation

63
Q

What enzyme do ACE inhibitors block? For which patients is ACE Inhibitors indicated? In what ways do ACE inhibitors improve patient survival?

A

ACE which cleaves angiotensin I
Asymptomatic and symptomatic HFrEF
Improve clinical signs and symptoms of HF

64
Q

What receptors do ARBs block? How do ARBs affect bradykinin levels? What is a main advantage of ARBs over ACE inhibitors? Why are ARBs used in HF patients with cough or angioedema?

A

AT1 receptors
ARBs do not increase bradykinin levels
More complete blockade of angiotensin II
They do not increase bradykinin levels

65
Q

What do inotropic agents like milrinone, digoxin, dopamine, and dobutamine do? When are intravenous inotropic agents used?

A

Increase the force of cardiac contractions
Low cardiac output syndrome with organ hypoperfusion

66
Q

Which three β-blockers have shown benefit in HF? Why are β-blockers recommended for chronic, stable HF?

A

Bisoprolol, carvedilol and metoprolol succinate
They reduce morbidity and mortality

67
Q

What is a key difference between carvedilol and bisoprolol/metoprolol succinate?

A

Carvedilol blocks α-adrenoreceptors, others are β1-selective

68
Q

When are vasodilators like nitroprusside sodium used in heart failure? How do vasodilators like nitroprusside sodium affect preload and afterload? What are common adverse effects of vasodilators?

A

First-line therapy for acute heart failure without hypotension
They reduce preload and/or afterload
Headache, hypotension, and tachycardia

69
Q

What is the key focus when using diuretics for acute heart failure? What is the primary benefit of diuretics in heart failure? What is the effect of diuretics on preload, afterload, cardiac workload, and oxygen demand?

A

Impact on fluid and electrolytes
Reducing pulmonary congestion and peripheral oedema
Reduction of all

70
Q

When are diuretics like furosemide used in heart failure? Have diuretics been shown to improve survival in HF? Which type of diuretic is considered first-line? When are thiazide diuretics used?

A

Patients who require extensive diuresis
No
Loop diuretic
Patients with no response to loop diuretics

71
Q

What is an important consideration when using potassium-sparing diuretics with loop diuretics?

A

Careful renal function and potassium monitoring

72
Q

What is the result of spironolactone binding to intracellular cytoplasmic receptor sites? What are the effects of spironolactone on potassium and sodium levels? How does eplerenone compare to spironolactone?

A

Spironolactone–receptor complex inactive
Retention of K+ and excretion of Na
How does eplerenone compare to spironolactone?
Comparable actions, fewer endocrine effects

73
Q

For which patients are aldosterone antagonists recommended?

A

Moderately severe and severe heart failure

74
Q

How should Calcium Channel blockers be used in HF? When might CCBs be used in HF?

A

Generally contraindicated, use cautiously
Normal LVEF or to improve exercise tolerance