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05. Year 1: Cardiovascular System COPY > Heart Failure - Treatment > Flashcards

Heart Failure - Treatment Flashcards

1
Q

What is chronic heart failure characterised by?

A

Progressive cardiac dysfunction

Breathlessness

Tiredness

Neurohormonal disturbances

Sudden death

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2
Q

What is heart failure?

A

State at 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 is the state at 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 pressure?

A

Heart failure

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4
Q

What are the different kinds of heart failure?

A

Systolic heart failure

Diastolic (or relaxation) heart failure

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5
Q

What is systolic heart failure?

A

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

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6
Q

Where does fluid backup to in systolic heart failure?

A

Lungs

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7
Q

What is diastolic heart failure?

A

Thickened and stiff heart muscle causes it to not fill with blood properly, fluid will backup into venous system

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8
Q

Where does fluid backup to in diastolic heart failure?

A

Venous system

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9
Q

What is the prevalence of chronic heart failure?

A

2-10%

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10
Q

How does the incidence of chronic heart failure change with age?

A

Increases with age

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11
Q

What is the prognosis of heart failure like?

A

Poor

5 year mortality of 50% rising to 80% in a year for some patients

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12
Q

What are some risk factors for heart failure?

A

Coronary artery disease

Hypertension

Valvular heart disease

Alcoholism

Infection (viral)

Diabetes

Congenital heart defects

Other (obesity, age, smoking)

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13
Q

What is the process of the pathological progression of cardiovascular disease?

A

1) Myocardial injury
2) Pathologic remodelling
3) Low ejection fraction
4) Death

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14
Q

What is the process of systolic dysfunction?

A

1) In a failing or damaging heart the Frank-Sarling relationship is lost
2) Circulatory volume increase and the heart dilates, the force of contraction weakens and cardiac output drops further
3) Cardiac output then activates renin-angiotensin-aldosterone system (RAAS) further
4) Results in cycle in which RAAS is activated, circulatory volume increases and cardiac performance deteriorates further
5) As the heart starts to dilate the cardiac myocytes undergo hypertrophy and then fibrosis and the heart is further weakened

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15
Q

What is the Frank-Sarling law?

A

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

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16
Q

What does RAAS stand for?

A

Renin-angiotensin-aldosterone system

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17
Q

What does heart failure usually occur following?

A

Sustained hypertension

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18
Q

What does RAAS cause the release of?

A

Angiotensin and aldosterone

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19
Q

What does angiotensin and aldosterone (RAAS) cause?

A

Salt and water retention

Vasoconstriction

Hypertrophy

Fibrosis of cardiac myocytes

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20
Q

What does activation of the sympathetic system cause the release of?

A

Noradrenaline and adrenaline

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21
Q

What does noradrenaline and adrenaline (sympathetic system) cause?

A

Vasocontriction

Stimulate renin release

Myocyte hypertrophy

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22
Q

What is salt and water excretion caused by?

A

Natriuretic peptide system

EDRF

Atrial and brain natriuretic peptides

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23
Q

What is the final result of the processes occuring in a failing heart?

A

Failing heart that cannot pump out sufficient blood

Progressive retention of salt and water resulting in oedema and pulmonary oedema

Progressive myocyte death and fibrosis

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24
Q

What are the aims of treatment for heart failure?

A

Improve symptoms

Improve symptoms and survival

Improve survival

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25
Q

What drugs are used to improve the symptoms of heart failure?

A

Diuretics

Digoxin

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26
Q

What drugs are used to improve symptoms and survival of heart failure?

A

ACE inhibitors/ARBs

Spirolactone

Vaslartan-sububitril

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27
Q

What drugs are used to improve survival of heart failure?

A

Beta blockers

Ivabradine

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28
Q

What are some different treatment regimens for heart failure?

A

Inhibition of detrimental neurohormonal adaptations

Enhancement of beneficial neurohormonal adaptations

Enhancement of cardiac function

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29
Q
A
30
Q

How is inhibition of detrimental neurohormonal adaptations achieved?

A

Beta blockers (such as carvedilol, bisoprolol and metoprolol)

Stopping RAAS activation:
ACE inhibitors (such as ramipril or angiotensin antagonists such as valsartan or losartan to stop angiotensin II)
Aldosterone blocked by spironolactone

Loop diuretics

31
Q

How is enhancement of beneficial neurohormonal adaptations achieved?

A

Natriuretic peptid system

ANP/BNP (which are potent natriuretic agents and vasodilators)

Neprolysin (prevents metabolism and enhances ANP/BNP actions

32
Q

What does ANP stand for?

A

Atrial natriuretic peptides

33
Q

What does BNP stand for?

A

Brain natriuretic peptides

34
Q

How is enhancement of cardiac function achieved?

A

Positive inotropes (such as digoxin, improved hearts ability to pump)

Vasodilators:
Nitrovasodilators reduce preload and after load improve cardiac function
Hydralazine is an arterial dilator

35
Q

How is mortality of heart failure with treatment?

A

Still high

36
Q

What is an example of a loop diuretic?

A

Furosemide

37
Q

What does a loop diuretic do?

A

Removes excess salt and water by inducing profound diuresis by inhibiting Na-K-Cl transporter in the loop of Henle

38
Q

What can loop diuretics be used in combination with?

A

Thiazide diuretics

39
Q

What are potential adverse reactions from loop diuretics?

A

Dehydration

Hypotension

Hypokaemia

Hyponatraemia

Gout

Impaired glucose tolerance

40
Q

What are potential drug-drug interactions of loop diuretics (furosemide)?

A

Aminoglycosides (renal toxicity)

Lithium (renal toxicity)

NSAIDs (renal toxicity)

Antihypertensives (profound hypotension)

Vancomycin (renal toxicity)

41
Q

How is mortality of heart failure reduced?

A

Angiotensin blockage

Beta receptor blockage

Aldosterone blockage

ANP/BNP enhancement

42
Q

What does ACEI stand for?

A

Angiotensin converting enzyme inhibitors

43
Q

What are examples of angiotensin converting enzyme inhibitors?

A

Ramipril

Enalapril

Lisonopril

44
Q

How do angiotensin converting enzyme inhibitors work?

A

Competitively block angiotensin converting enzyme, preventing the conversion of angiotensin I into angiotenin II

Reduces preload and afterload on the heart

45
Q

What are potential adverse drug reactions of angiotensin converting enzyme inhibitors?

A

First dose hypotension

Cough

Angioedema

Renal impairment

Renal failure

Hyperkalaemia

46
Q

What are potential drug-drug interactions of angiotensin converting enzyme inhibitors?

A

NSAIDS (acute renal failure)

Potassium supplements (hyperkalaemia)

Potassium sparing diuretics (hyperkalaemia)

47
Q

What does ARBs stand for?

A

Angiotensin receptor blockers

48
Q

How do angiotensin receptor blockers work?

A

Selectively block angiotensin II AT1 receptor

49
Q

What is more effective for heart block out of ACEI and ARBs?

A

ARBs

50
Q

When is ARBs recommended to be used in heart failure?

A

In ACEI intolerance

51
Q

What does ARNI stand for?

A

Valsartan-sucubiril

52
Q

How does valsartan-sacubitril (ARNI) work?

A

ARB blocks AT1 receptor and Neprilysin stops breakdown of ANP and BNP by neural endopeptidases

53
Q

What is valsartan-sacubitril (ARNI) a combination of?

A

Valsartan and ARB and Neprilysin

54
Q

What receptor do ARBs block?

A

AT1 receptor

55
Q

What is an example of an aldosterone antagonist?

A

Spironolactone

56
Q

What is spironolactone and where does it act?

A

Potassium sparring diuretic that acts in the distal tubule

57
Q

When are aldosterone antagonists proven to reduce mortality?

A

When used in combination with ACEIs

58
Q

What are examples of beta blockers?

A

Carvedilol

Bisoprolol

Metoprolol

59
Q

Why must patients treated with beta blockers be selected carefully?

A

Beta blockers are potentially hazardous in chronic heart failure

60
Q

How do beta blockers work?

A

Block the actions of the sympathetic system

61
Q

When should beta blockers only be used?

A

When patient has been stabilised and not during an acute presentation

62
Q

How does ivabradine work?

A

Inhibitor of the If current in the sinoatrial node

Does not modify myocardial contractility and intracardiac conduction even in patients with impaired systolic function

63
Q

What is an example of a positive inotrope?

A

Digoxin

64
Q

How do positive inotropes (digoxin) work?

A

Increases availability of calcium in the myocyte

65
Q

What is a complication with digoxin?

A

Narrow therapeutic index

66
Q

What are potential side effects of digoxin?

A

Arrhythmias

Nausea

Confustion

67
Q

What is an example of an anticoagulant?

A

Warfarin

68
Q

Why is warfarin sometimes used in heart failure?

A

Dilated ventricle gives rise to thrombus formation and thrombo-embolic events, which warfarin prevents

69
Q

What are different therapeutic regimes for heart failure?

A
70
Q

How is the benefit of treatment monitored?

A

Symptomatic relief (shortness of breath, tiredness, lethargy)

Clinical relief (peripheral oedema, ascites, weight)

Monitor weight regularly (increase medication according to symptoms or weight)

Patient education

05. Year 1: Cardiovascular System COPY (41 decks)

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