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
what would you use for enhancement of cardiac function?
positive ionotropes- Digoxin vasodilators- reduces preload and after load improve cardiac function
26
how much does ace inhibitors effect mortality?
35%
27
how much does beta blockers effect mortality?
38%
28
which drug removes salt and water?
loop diuretcs- furosemide
29
do loop diuretics work at low or high glomerular filtration rates
low
30
what are adverse drug reactions of loop diuretics?
``` dehydration hypotension hypokalaemia gout impaired glucose tolerance ```
31
what drug to drug reactions do you get when you combine frusemide and aminoglycosides?
aural and renal toxicity
32
what drug to drug reactions do you get when you combine frusemide and lithium?
renal toxicity
33
what drug to drug reactions do you get when you combine frusemide and NSAIDs?
renal toxicity
34
what drug to drug reactions do you get when you combine frusemide and antihypertensives?
profound hypertension
35
what drug to drug reactions do you get when you combine frusemide and vancomycin?
renal toxicity
36
what 4 things would you give/do to reduce mortality?
angiotensin blockade beta receptor blockade aldosterone blockade ANP/BNP enhancement
37
what are the ace inhibitors?
Rampipril, enalapril, lisinopril
38
what are adverse drug reactions with ACE inhibitors?
``` First dose hypotension Cough Angioedema Renal impairment Renal failure Hyperkalaemia ```
39
what are drug to drug reactions in combination with ACE inhibitors and NSAIDs?
acute renal failure
40
what are drug to drug reactions in combination with ACE inhibitors and potassium supplements
hyperkalaemia
41
what are the different roles of AT1 and AT2
``` AT1- Vasoconstriction Vascular proliferation Aldosterone secretion Cardiac myocyte proliferation Increased sympathetic tone ``` AT2- vasodilation antiproliferation apoptosis
42
what is valsartan-sacubitril (ARNI)?
combined valsartan and ARB and neprilysin
43
does ARB block AT1 or AT2 receptor?
AT1
44
what does neprilysin stop the break down of
ANP and BNP by neutral endopeptidases
45
alsosterone antagonist and ehat is proven to reduce mortality?
ACEi
46
is the use of beta blockers in the treatment of chronic heart failure hazardous?
potentially, patients must be selected carefully
47
what are the function of beta blockers?
block the action of the sympathetic system
48
what is ivabradine?
ivabradine is a specific inhibitor of the If current in the sinatrial node