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PHRM3011 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is the difference in QoL between chronic heart failure and terminal malignancy?

A

in chronic HF, QoL declines progressively whereas in terminal malignancy, QoL declines RAPIDLY

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2
Q

What are the two causes of HF?

A

cardiac abnormality

insult to the heart (genetics.hypoxia/MI)

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3
Q

What are the two types of HF?

A

HF with preserved ejection fraction - DIASTOLIC

HF with reduced ejection fraction - SYSTOLIC

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4
Q

What HF can diabetes cause?

A

Diastolic HF

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5
Q

What is impaired in each type of HF?

A

Diastolic - impaired relaxation so not good filling

systolic - impaired contraction so heart changes shape

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6
Q

In which HF does the heart change its shape?

A

systolic HF

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7
Q

In which HF is LVEF (left ventricular ejection fraction) lower?

A

systolic HF (

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8
Q

What HF can obesity and alcohol cause?

A

Systolic HF

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9
Q

What are the common causes of HF of both types?

A

IHD, Hypertension, cardiomyopathy

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10
Q

Which HF has lots of evidence of Tx?

A

Systolic HF

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11
Q

What is released by the heart by itself in response to stress?

A

Natriuretic peptides (eg. BNP)

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12
Q

What does the NP cause?

A

vasodilation which decreases BP, vasopressin, aldosterone, hypertrophy, and increase sodium loss/diuresis

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13
Q

Activation of SNS by the ventricular dysfunction raises what?

A

HR, contractility, RAAS activity, vasopressin

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14
Q

Activation of AT1R raises what level?

A

BP, sympathetic tone, aldosterone, hypertrophy, fibrosis which leads to LT harm (WORSEN HF)

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15
Q

What is special and RARE about one of the Sx of HF?

A

Paroxysmal nocturnal dyspnoea (PND) –> cannot breathe well unless upright position

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16
Q

What are the Sx of HF?

A

dry cough, reduced exercise, fatigue, ankle oedema, breathlessness, low BP, tachycardia, increased JVP, increased Cr (because less Cr is filtered due to less CO), increased urea, low sodium (to retain water to maintain BP)

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17
Q

Describe each class of HF

A
  1. Asymptomatic ventricular dysfunction has no limitation to physical activity
  2. mild HF has slight limitation
  3. moderate HF has marked limitation
  4. severe HF has symptoms even at rest
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18
Q

How do we diagnose HF?

A 
by echo (ultrasound of heart), measure LVEF
and BNP level (if higher than 100 --> HF)
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19
Q

What should we do in acute HF in hospital?

A

Give IV diuretics to increase contraction and an inotrope (dobutamine) to push blood to kidney for better drug delivery
Reduce BB temporarily because of negative inotrope effects
Restrict fluid intake

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20
Q

What is the difference between using diuretic in acute and chronic HF?

A

Acute: higher dose via IV continously
Chronic: lowest dose possible via ORAL, titration plan is individualised

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21
Q

What do we measure to see the effect of diuretics in HF?

A

Urine output, patient weight

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22
Q

What are the ADE of diuretics?

A

low Na+, K+, Mg+, high Cr

to manage low Na+, reduce diuretic a bit

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23
Q

Do diuretics impact neurohormonal systems?

A

No

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24
Q

What two drugs are used in ALL systolic HF patients?

A

ACEI/ BB

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25
Q

What are the evidences of effect of diuretics in HF?

A

LIMITED in reducing mortality BUT

BETTER in reducing hospital admission

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26
Q

Why is ACEI used in HF?

A

To delay progression of disease and improve Sx in LT

27
Q

What should you avoid with ACEI?

A

NSAIDS/Diuretics, K-sparing diuretics (increased potassium), sacubitril (increased angioedema)

28
Q

What should you monitor when using ACEI in HF?

A

BP, renal function, potassium levels

29
Q

What are the evidences of effect of ACEI in HF?

A

GOOD in reducing mortality AND hospital admission

30
Q

Why is BB used in HF?

A

when pt is not fluid overloaded and because BB reduce the force of contraction and improve Sx in LT

31
Q

Are the benefits of BB immediate in HF?

A

No

32
Q

What should we increased the dose of first when taking ACEI and BB together?

A

Increase ACEI first (maximise)

BB need gradual increase to avoid Sx worsening

33
Q

What are the ADE of BB?

A

Lethargy, dreams, bradycardia, mask hypoglycaemia Sx, bronchoconstriction

34
Q

What should we avoid with BB?

A

digoxin, amiodarine which decreases the pulse

35
Q

What are the evidences of effect of BB in HF?

A

GOOD in reducing mortality AND hospital admission

36
Q

What are the two aldosterone antagonists used in HF?

A

Spironolactone and eplerenone

37
Q

What are the ADE of spironolactone?

A

gynaecomastia (breast tissue), hyperkalaemia

38
Q

When should we use eplerenone?

A

post MI with LV dysfunction,

in mild HF with ACEI+ BB

39
Q

What are the evidences of effect of aldosterone antagonists in HF?

A

GOOD in reducing mortality AND hospital admission

40
Q

When should we stop aldosterone antagonist herapy in HF?

A

When potassium level is higher than 6mmol/L

41
Q

When is digoxin good to use?

A

in patient WITH BOTH HF AND AF

if Sx is not controlled with ACEI + BB

42
Q

What are the evidence of effect of digoxin in HF?

A

If there is no AF, there is no effect on mortality BUT it DOES reduce hospitalisation!

43
Q

What should we avoid with digoxin?

A

Verapamil, amiodarone (IF used together, halve digoxin dose)

44
Q

What are the sx of digoxin toxicity?

A

nausea, vomiting, bradycardia

45
Q

What do nitrates do?

A

Mimic vasodilation of ACEI –> decrease symptom and mortality

46
Q

What is the problem with nitrate use?

A

the dose is too high to be used in practice

47
Q

What vasodilators are useful in African Americans?

A

isosorbide dinitate and hydralazine

48
Q

What are the evidence of the effect of vasodilators in HF?

A

Decreased mortality and hospital admission

49
Q

What are the three other drugs for HF and hen are the used?

A

Ivrabradine when HR is high
Ferrous sulphate when iron deficient anaemia exists
Fish Oil on optimised therapy

50
Q

What does ARNI do and what does it include?

A

It prevents the breakdown of NP and also acts like sartan

it contains sacubitril and valsartan

51
Q

What are the ADE of ARNI?

A

Hypotension, angioedema, valsartan SE

52
Q

What can exacerbate HF? (6)

A

NSAIDS
Negative inotropes (verapamil/diltiazem) only slow down rate
antiarrhythmic drugs (increase mortality)
CAMS (licorice, ginger, ginseng..)
Effervescent/ soluble tablets like verocca
Lactulose (need lots of water)

53
Q

What could be the reasons of worsening of HF sx?

A

arrhythmia, increased thyroid, anaemia, infection

54
Q

What can condition in thyroid do to HF?

A

Tyroid can fasten HR and worsen proression of HF

55
Q

How can thyroid be toxicated?

A

by amiodarone (commonly used by lots of people)

56
Q

What is our primary goal in managing Sx of HF?

A

monitoring sx and potential ADE NOT optimising meds

57
Q

Why should we avoid fibres in constipation?

A

because it needs lots of water

so we suggest coloxy/senna or movicol mixed with water

58
Q

What are the sx of symptomatic HF?

A

Feeling cold, dizzy, postural hypotention –> cut dose

59
Q

In chronic SHF, what are the list of drugs we should use?

A
  1. ACEI
  2. BB
  3. Aldosterone antagonist
  4. Digoxin
60
Q

In fluid overload, we use what?

A

diuretics (+thiazides)

61
Q

In acute oedema, we use what?

A

nitrates + diuretics

62
Q

In acute SHF, we use what?

A

vasodilators, inotropes

63
Q

What should we absolute avoid in HF only?

A

Verapamil and diltiazem

PHRM3011 (12 decks)

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