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Systems: Cardiovascualar AB > Heart Failure: Treatment > Flashcards

Heart Failure: Treatment Flashcards

1
Q

What is chronic heart failure characterised by?

A
  • Progressive cardiac dysfunction
  • Dyspnoea
  • Tiredness
  • Neurohormonal disturbances
  • Sudden death
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2
Q

Heart failure

A

Heart failure is the state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can do so only from high pressures

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3
Q

What are the types of heart failure?

A
  • Systolic heart failure (HFrEF)

- Diastolic (or relaxation) heart failure (HFpEF)

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4
Q

What does HFrEF involve?

A

Decreased pumping function of the heart which results in fluid back up in the lungs and heart failure

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5
Q

What does HFpEF involve?

A
  • Involves a thickened and stiff heart muscle
  • As a result heart does not fill with blood properly
  • This results in fluid backup in the lungs and heart failure
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6
Q

What is the prevalence of chronic heart failure?

A

2-10%

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7
Q

What does incidence of chronic heart failure increase with?

A

Age

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8
Q

What is the prognosis of chronic heart failure?

A

-Poor with 5 year mortality of 50% rising to 80% with 1 year

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9
Q

What are the risk factors for heart failure?

A
  • CAD
  • Hypertension
  • Valvular heart disease
  • Alcoholism
  • Viral infection
  • Diabetes
  • CHD
  • Obesity
  • Age
  • Smoking
  • High/low haematocrit
  • OSAS
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10
Q

What is the number 1 risk factor for HF?

A

Hypertension

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11
Q

What is Frank Starling Law?

A

If the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood

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12
Q

How is Frank Starling Law affected with systolic dysfunction?

A
  • In the failing or damages heart this relationship is lodt
  • As circulatory volume increases the heart dilates, the force of contraction weakens and CO drops further
  • Decreased CO activates the RAAS further
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13
Q

What does activation of the RAAS by decreased CO result in?

A

-A vicious cycle in which the RAAS is activated, circulatory volume increases and cardiac performance deteriorates further

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14
Q

What happens to the cardiac myocytes as the heart starts to dilate?

A

They undergo hypertrophy and then fibrosis and thus the heart is further weakened

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15
Q

When does HF usually occur?

A
  • Following sustained hypertension

- Following myocardial damage

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16
Q

Why does HF occur following systolic/diastolic dysfunction?

A
  • CO falls
  • Body registers this as a loss in circulatory volume
  • Vasoconstrictor system activation
  • Salt and water retaining system activation
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17
Q

What does RAAS cause the release of?

A
  • Angiotensin II

- Aldosterone

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18
Q

What is the result of the RAAS?

A
  • Salt and water retention
  • Vasoconstriction
  • Hypertrophy and fibrosis of cardiac myocytes
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19
Q

What does the release of noradrenaline and adrenaline by the SNS cause?

A
  • Vasoconstriction
  • Stimulates renin release
  • Myocyte hypertrophy
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20
Q

What is responsible for salt and water excretion and vasodilation?

A
  • Natriuretic peptide system ANP/BNP

- EDRF

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21
Q

What are ANP and BNP?

A

-Potent vasodilators and natriuretic peptides with short half lives

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22
Q

What is the final result of all these systems?

A
  • A failing heart that can not pump out sufficient blood to supply the needs of the body
  • Progressive retention of salt and water which results in oedema, pulmonary oedema
  • Progressive myocyte death and fibrosis
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23
Q

What are the 2 main aims of treatment?

A
  • Improve symptoms

- Improve survival

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24
Q

What drugs improve symptoms?

A
  • Diuretics

- Digoxin

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25
Q

What drugs improve survival?

A
  • B blockers

- Ivabradine

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26
Q

What drugs improve symptoms and survival?

A
  • ACE inhibitors/ARBs
  • Spironolactone
  • Valsartan-sacubitril
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27
Q

What is the outcome of symptomatic treatement?

A
  • Inhibition of detrimental neurohormonal adaptations
  • Enhancement od beneficial neurohormonal adaptations
  • Enhancement of cardiac function
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28
Q

What is the mainstay of symptomatic treatment?

A

Loop diuretics

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29
Q

Give 2 examples of loop diuretics.

A
  • Furosemide

- Bumetanide

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30
Q

Give examples of B blockers used

A
  • Carvedilol
  • Bisoprolol
  • Metoprolol
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31
Q

What are the groups of drug available to block the effects of angiotensin II?

A
  • ACE inhibitors (Ramipril)

- Angiotensin antagonists (Valsartan, Losartan)

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32
Q

What blocks the effects of aldosterone?

A

Spironolactone

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33
Q

How are beneficial hormonal changes enhanced?

A

Natriuretic peptide systems

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34
Q

What metabolises ANP/BNP/

A

Neutral endopeptidase

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35
Q

What prevents metabolism and enhances ANP/BNP actions?

A

Neprolysin

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36
Q

What enhances cardiac function?

A
  • Positive inotropes

- Vasodilators

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37
Q

What is the only positive inotrope in use?

A

-Digoxin

38
Q

What do positive inotropes do?

A

Improve the ability of the heart to pump and so improve cardiac status

39
Q

How do nitrovasodilators improve cardiac function?

A

Reduce preload and afterload

40
Q

What is hydralazine?

A

Arterial dilator whown to improve cardiac function

41
Q

What does furosemide do?

A

-Removes excess salt and water

42
Q

What do loop diuretics do?

A
  • Induce profound diuresis
  • Inhibit the Na-K-Cl transporter in the loop of Henle
  • Work at very low glomerular filtration rates
  • Prevent the reabsorption of 20% of filtered sodium and water
43
Q

What can be used in diuretic resistant patients?

A

Loop diuretics in combination with thiazide diuretics

44
Q

What can a combination of loop diuretics and thiazide diuretics induce?

A

Diuresis of 5-10 litres per day

45
Q

What are the adverse drug reactions of loop and thiazide diuretics combination?

A
  • Dehydration
  • Hypokalaemia
  • Hyponatraemia
  • Gout
  • Impaired glucose tolerance, diabetes
46
Q

What drugs does furosemide interact with?

A
  • Aminoglycosides
  • Lithium
  • NSAIDs
  • Antihypertensives
  • Vancomycin
47
Q

Furosemide and aminoglycosides

A

Aural and renal toxicity

48
Q

Furosemide and lithium

A

Renal toxicity

49
Q

Furosemide and NSAIDs

A

Renal toxicity

50
Q

Furosemide and antihypertensives

A

Profound hypotension

51
Q

Furosemide and vancomycin

A

Renal toxicity

52
Q

How is mortality reduced/

A
  • Angiotensin blockade
  • B receptor blockade
  • Aldosterone blockade
  • ANP/BNP enhancement
53
Q

What do ACEI not block?

A

The conversion of angiotensin I to angiotensin II by alternative enzymes such as chymase

54
Q

What organs can angiotensin II damage?

A
  • Brain
  • Blood vessels
  • Heart
  • Kidneys
55
Q

What effect can Ang II have on the kidney?

A
  • Decrease GFR
  • Increased proteinuria
  • Increased aldosterone release
  • Glomerular sclerosis
  • Renal failure
56
Q

What effect can Ang II have on the heart?

A
  • LV hypertrophy
  • Fibrosis
  • Remodelling
  • Apoptosis
  • Heart failure
  • MI
57
Q

What effect can Ang II have on the blood vessels?

A
  • Atherosclerosis
  • Vasoconstriction
  • Vascular hypertrophy
  • Endothelial dysfunction
  • Hypertension
58
Q

What effect can Ang II have on the brain?

A

Stroke

59
Q

Give 3 examples of ACE inhibitors.

A
  • Ramipril
  • Enalapril
  • Lisinopril
60
Q

What do ACEI do?

A
  • Competitively block angiotensin converting enzyme
  • Prevent the conversion of angiotensin I to angiotensin II
  • Reduce preload and afterload on the heart
61
Q

What do ACEI reduce in CHF patients?

A
  • Morbidity

- Mortality

62
Q

What do ACEI reduce in post MI patients?

A
  • Morbidity
  • Mortality
  • Onset of HF
63
Q

What are the adverse drug reactions of ACEI?

A
  • First dose hypotension
  • Cough
  • Angioedema
  • Renal impairment
  • Renal failure
  • Hyperkalaemia
64
Q

What drugs do ACEI interact with?

A
  • NSAIDs
  • Potassium supplements
  • Potassium sparing diuretics
65
Q

ACEI and NSAIDs

A

Acute renal failure

66
Q

ACEI and potassium supplements

A

Hyperkalaemia

67
Q

ACEI and potassium sparing diuretics

A

Hyperkalaemia

68
Q

What do ARBs do?

A
  • Selectively block the angiotensin II, AT1 receptor

- Effective but not as effective as ACEI

69
Q

What are patients given if they are intolerant of ACEI?

A

ARBs

70
Q

What effect does Ang II have on AT1?

A
  • Vasoconstriction
  • Vascular proliferation
  • Aldosterone secretion
  • Cardiac myocyte proliferation
  • Increased sympathetic tone
71
Q

What effect does angiontensin II have on AT2?

A
  • Vasodilation
  • Antiproliferation
  • Apoptosis
72
Q

What is valsartan-sacubitril (ARNI)

A

Combined valsartan and ARB and neprilysin

73
Q

How does valsartan-sacubitril work?

A
  • ARB blcoks AT1 receptor

- Neprilysin stops bread down of ANP and BNP by neutral endopeptidases

74
Q

Give an example of an aldosterone antagonist

A

Spironolactone

75
Q

What does spironolactone do?

A
  • Potassium sparing diuretic
  • Inhibits the actions of aldosterone
  • Acts in the distal tubule
76
Q

What is spironolactone used in combination with?

A

Loop diuretics

77
Q

What is spironolactone particularly useful in?

A

Resistant oedema

78
Q

When has spironolactone be proven to reduce mortality?

A

In combination with ACEI

79
Q

What do B blockers do?

A

-Block the actions of the sympathetic system

80
Q

What may B blockers precipitate?

A

Severe deterioration in CHF

81
Q

When should B blockers be used in the treatment of HF?

A

Only when the patient has been stabilised and not during acute presentation

82
Q

What is ivabradine?

A

Specific inhibitor of the If current in the SA node

83
Q

What does ivabradine not do?

A
  • No action on other channels in the heart or vascular system
  • Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function
84
Q

What is the recommendation for the use of ivabradine?

A

Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving standard therapy, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest.

85
Q

What does digoxin do?

A

Increases the availability of calcium in the myocyte

86
Q

What are the side effects of digoxin?

A
  • Narrow therapeutic index
  • Arrhythmias
  • Nausea
  • Confusion
87
Q

What is warfarin?

A

Anticoagulant

88
Q

Why is warfarin used in HF?

A

Dilated ventricle gives rise to thrombus formation and thrombo-embolic events

89
Q

What is the therapeutic regime for HF?

A
  • Furosemide +/- thiazide
  • Furosemide + pulsed metolazone
  • ACEI
  • ARB
  • B blocker +/- ivabradine
  • MRA-spironolactone (25mg)
  • Digoxin
  • Warfarin
90
Q

How is the benefit of drug therapies monitored?

A
  • Symptomatic relief (SOB, tiredness, lethargy)
  • Clinical relief (peripheral oedema, ascites, weight)
  • Monitor weight regularly
  • Patient education

Systems: Cardiovascualar AB (42 decks)

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