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1st year systems > 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 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 different types of heart failure?

A

Systolic heart failure (HFrEF)

diastolic heart failure

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4
Q

what is systolic heart failure

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 is diastolic heart failure

A

involves a thickened and stiff heart muscle
as a result, the heart does not fill with blood properly
this results in fluid back up in the lungs and heart failure

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6
Q

how many people does chronic heart failure effect?

A

2-10%

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7
Q

what are risk factors for heart failure?

A 
coronary artery disease
hypertension
diabetes
congenital heart defects
valvular heart disease
alcoholism
other-
obesity
age
smoking
obstructive sleep apnea
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8
Q

whats the number 1 risk for heart failure?

A

hypertension

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9
Q

what is the 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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10
Q

what happens in systolic dysfunction?

A

in the failing or damaged heart this relationship is lost

as circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further

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11
Q

when is RAAS activated in systolic dysfunction

A

when cardiac output is decreased

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12
Q

what happens to cardiac performance and circulatory volume when RAAS is activated?

A

circulatory volume increases and cardiac performance deteriorates further

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13
Q

how does fibrosis occur when heart starts to dilate from RAAS?

A

cardiac myocytes undergo hypertrophy and then fibrosis and thus the heart is further weakened

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14
Q

why does heart failure usually occur?

A

following sustained hypertesion

following myocardial damage

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15
Q

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

A

vasoconstriction
stimulate renin release
myocyte hypertrophy

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16
Q

what kind of system is salt and water excretion and vasodilation?

A

natriuretic peptide system ANP/BNP

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17
Q

what does the progressive retention of salt and water results in?

A

oedema and pulmonary oedema

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18
Q

what are the aims of treatment for people with heart failure?

A

improve symptoms

improve survival

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19
Q

what treatment would you use to improve the symptoms?

A

diuretics

digoxin

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20
Q

what treatment would you use to improve symptoms and survival?

A

ACE inhibitors
spironolactone
valsartan-sacubitril

21
Q

what treatment would you use to improve survival?

A

beta blockers and ivabradine

22
Q

what are the aims of symptomatic treatment?

A

inhibition of detrimental neurohormonal adaptations

enhanceent of beneficial neurohoronal adaptations

enhancement of cardiac function

23
Q

what is the systematic treatment?

A

loop diuretics

furosemide or bumetanide

24
Q

what system enhances beneficial hormonal changes?

A

natriuretic peptide system

ANP/BNP

25
Q

what would you use for enhancement of cardiac function?

A

positive ionotropes- Digoxin

vasodilators- reduces preload and after load improve cardiac function

26
Q

how much does ace inhibitors effect mortality?

A

35%

27
Q

how much does beta blockers effect mortality?

A

38%

28
Q

which drug removes salt and water?

A

loop diuretcs- furosemide

29
Q

do loop diuretics work at low or high glomerular filtration rates

A

low

30
Q

what are adverse drug reactions of loop diuretics?

A 
dehydration
hypotension
hypokalaemia
gout
impaired glucose tolerance
31
Q

what drug to drug reactions do you get when you combine frusemide and aminoglycosides?

A

aural and renal toxicity

32
Q

what drug to drug reactions do you get when you combine frusemide and lithium?

A

renal toxicity

33
Q

what drug to drug reactions do you get when you combine frusemide and NSAIDs?

A

renal toxicity

34
Q

what drug to drug reactions do you get when you combine frusemide and antihypertensives?

A

profound hypertension

35
Q

what drug to drug reactions do you get when you combine frusemide and vancomycin?

A

renal toxicity

36
Q

what 4 things would you give/do to reduce mortality?

A

angiotensin blockade
beta receptor blockade
aldosterone blockade
ANP/BNP enhancement

37
Q

what are the ace inhibitors?

A

Rampipril, enalapril, lisinopril

38
Q

what are adverse drug reactions with ACE inhibitors?

A 
First dose hypotension
Cough
Angioedema
Renal impairment
Renal failure
Hyperkalaemia
39
Q

what are drug to drug reactions in combination with ACE inhibitors and NSAIDs?

A

acute renal failure

40
Q

what are drug to drug reactions in combination with ACE inhibitors and potassium supplements

A

hyperkalaemia

41
Q

what are the different roles of AT1 and AT2

A 
AT1- 
Vasoconstriction
Vascular proliferation 
Aldosterone secretion
Cardiac myocyte proliferation
Increased sympathetic tone

AT2-
vasodilation
antiproliferation
apoptosis

42
Q

what is valsartan-sacubitril (ARNI)?

A

combined valsartan and ARB and neprilysin

43
Q

does ARB block AT1 or AT2 receptor?

A

AT1

44
Q

what does neprilysin stop the break down of

A

ANP and BNP by neutral endopeptidases

45
Q

alsosterone antagonist and ehat is proven to reduce mortality?

A

ACEi

46
Q

is the use of beta blockers in the treatment of chronic heart failure hazardous?

A

potentially, patients must be selected carefully

47
Q

what are the function of beta blockers?

A

block the action of the sympathetic system

48
Q

what is ivabradine?

A

ivabradine is a specific inhibitor of the If current in the sinatrial node

1st year systems (74 decks)

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