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2. Cardiovascular System > 38. `Heart Failure Treatment (Pharmacology) > Flashcards

38. `Heart Failure Treatment (Pharmacology) Flashcards

1
Q

What is heart failure characterised by? (5)

A
  1. progressive cardiac dysfunction
  2. dyspnoea
  3. tiredness
  4. neurohormonal disturbances
  5. sudden death
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2
Q

Define heart failure.

A

Heart failure is a state in which the heart is unable to pump blood at the rate commensurate with the requirements of the tissues or can do so only from high pressures. It’s a SYNDROME not a disease.

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3
Q

What are 2 types of heart failure?

A
  1. systolic heart failure

1. diastolic (or relaxation) 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 (or relaxation) heart failure?

A
  • Involves a thickened and stiff heart muscle and as a result the heart doesn’t 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 and what is the prognosis like?

A
  • prevalence is 2-10% of population

- poor prognosis, with 5 year mortality of 50% and rising to 80% in a year for some patients

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7
Q

What does chronic heart failure incidence increase with?

A

Increases with age (and if you’re male)

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8
Q

What are the main risk factors for heart failure? (11)

A
  1. coronary artery disease
  2. hypertension
  3. valvular heart disease
  4. alcoholism
  5. infection (viral)
  6. diabetes
  7. congenital heart defects
  8. Other: obesity, age, smoking, high or low haematocrit level (RBC), obstructive sleep apnoea
  9. dyslipidaemia (abnormal lipid amount)
  10. history of MI or angina
  11. l.ventricular hypertrophy
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9
Q

What do all the cardiac risk factors lead to eventually? What is the pathological progression for chronic heart failure?

A
  • All risk factors lead to myocardial injury which leads to neurohormonal stimulation and myocardial toxicity
  • Pathologic remodelling and low ejection fraction leads to symptoms (e.g. fatigue, dyspnoea, oedema)
  • Pump failure due to symptoms leads to chronic heart failure and sometimes sudden death
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10
Q

State Frank-Starling Law.

A

If the muscle of a healthy heart is stretched, it will contract at a greater force and pump out more blood. (i.e. bigger preload means stronger contraction which means more stroke volume)

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11
Q

What happens to Frank-Starling Law in systolic dysfunction?

A
  • this relationship is lost in failing or damaged heart
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12
Q

Describe what happens to the heart in systolic dysfunction in terms of:

  • circulatory volume
  • force of contraction
  • cardiac output
  • RAAS system
A
  • as circulatory volume increases, the heart dilates but force of contraction weakens and cardiac output drops
  • decrease in cardiac output activates RAAS system (renin angiotensin aldosterone system)
  • ongoing cycle of RAAS is activated, circulatory volume increases and cardiac performance (pump) deteriorates
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13
Q

What occurs to the heart over time, as RAAS continues to be dilated when pumping ability decreases?

A
  • the heart starts to dilate as volume of blood increases but pumping weakens
  • cardiac myocytes undergo hypertrophy and fibrosis
  • heart is further weakened
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14
Q

What causes diastolic dysfunction heart failure or preserved ejection fraction heart failure?

A

Sustained hypertension

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15
Q

What causes systolic dysfunction heart failure?

A

myocardial damage i.e. MI

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16
Q

What happens to the body when it detect a fall in cardiac output?

A
  • body registers it as loss in circulatory volume
  • vasoconstrictor system activation (sympathetic system)
  • slat and water retaining system activation (RAAS)
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17
Q

What is the main mechanism which tries to compensate during heart failure?

A

Renin angiotensin aldosterone system (RAAS)

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18
Q

What does ACE do?

A

Converts angiotensin 1 into angiotensin 2 which induces aldosterone secretion

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19
Q

What does aldosterone secretion do in terms of:

  • salt and water retention
  • plasma volume
  • preload
  • cardiac workload
A
  • increases salt and water retention
  • increases plasma volume
  • increases preload
    -increases cardiac workload
    which all lead to heart failure
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20
Q

What does peripheral venoconstriction as a result of angiotensin 2 do to:

  • afterload
  • cardiac output
A
  • increases afterload
  • decreases cardiac output
    which all lead to heart failure
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21
Q

What does the RAAS system cause the release of?

A
  • angiotensin 2

- aldosterone

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22
Q

What is the end results of RAAS? (3)

A
  • salt and water retention
  • vasoconstriction
  • hypertrophy of fibrosis of cardiac myocytes
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23
Q

Activation of sympathetic system causes the release of noradrenaline and adrenaline, which cause what? (3)

A
  • vasoconstriction
  • stimulate renin release
  • myocyte hypertrophy
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24
Q

What two chemicals cause salt and water excretion and vasodilation?

A
  1. natriuretic peptide system (ANP and BNP) atrial and brain
  2. EDRF: endothelium derived relaxing factor
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25
Q

What is the final result of chronic heart failure? (3)

A
  • failing heart that can’t pump out sufficient blood to supply needs of the body
  • progressive retention of salt and water which results in oedema and pulmonary oedema
  • progressive myocyte death and fibrosis
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26
Q

What does heart failure treatment aim to do? (3)

A
  1. improve symptoms
  2. improve survival
  3. improve symptoms AND survival
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27
Q

What medication aims to improve heart failure symptoms? (2)

A
  1. diuretics

2. digoxin

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28
Q

What medication aims to improve heart failure survival? (2)

A
  1. beta blockers

2. Ivabradine

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29
Q

What medication aims to improve heart failure symptoms and survival? (3)

A
  1. ACEIs and ARBs
  2. spironolactone
  3. Valsartan-sacubitril
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30
Q

What does symptomatic treatment aim to do? (3)

A
  1. inhibit detrimental neurohormonal adaptations.
  2. enhance beneficial neurohormonal adaptations
  3. enhance cardiac function
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31
Q

What are the most common diuretics used for treatment of chronic heart failure symptoms? (2)

A
  1. furosemide
  2. bumetanide
    (symptomatic treatment)
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32
Q

What beta blockers are commonly used to block sympathetic system activation/detrimental hormonal changes in chronic heart failure? (3)

A
  1. carvedilol
  2. bisoprolol
  3. metoprolol
    (blocking detrimental hormonal changes)
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33
Q

What 2 groups of drugs are available to block the effects of angiotensin II?

A
  1. ACEIs: ramipril

2. Angiotensin antagonists: Valsartan and Losartan (ARBs)

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34
Q

What does spironolactone do which aims to improve symptoms and survival?

A
  • blocks effects of aldosterone
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35
Q

What converts angiotensinogen to angiotensin 1?

A

renin

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36
Q

What converts angiotensin 1 into angiotensin 2?

A

ACE

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37
Q

When angiotensin 2 is converted by non-ACE pathways into aldosterone, what effects does this cause? (4)

A
  1. sympathetic activation
  2. vasoconstriction
  3. cell growth
  4. Na/H2O retention
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38
Q

What does natriuretic peptide system do? (ANP/BNP)

A
  • enhances beneficial hormonal changes
  • potent vasodilators and natriuretic agents
  • metabolised by neutral endopeptidases
39
Q

What is the effect of Neprolysin on ANP/BNP natriuretic peptides? (2)

A
  • prevents metabolism

- enhances ANP/BNP actions

40
Q

What is a drug that is a positive inotrope?

A

Digoxin

41
Q

What do positive inotropes do?

A
  • improve ability of the heart to pump and so improve cardiac status
42
Q

What are common vasodilators which reduce preload and afterload which improve cardiac function? (2)

A
  • isosorbide mono or di nitrate

- hydralazine (arterial dilator)

43
Q

Does mortality for chronic heart failure remain high with therapy?

A

Yes, despite risk reduction therapies, mortality rates remain very high (risk reduction with ACEIs and beta blockers only reduce mortality by 35%)

44
Q

Which cancers have a better prognosis that heart failure? (4)

A
  1. bladder
  2. uterus
  3. prostate
  4. breast
45
Q

Describe the function of the most commonly used loop diuretic, furosemide.

A
  • removes excess salt and water
  • induce profound diuresis (urination)
  • inhibit Na-K-Cl transporter in the loop of henle
  • work at very low glomerular rates
  • prevent reabsorption of 20% filtered na and water
46
Q

What are common loop diuretics which work on the loop of Henle? (3)

A
  1. furosemide
  2. bumetanide
  3. ethacrynic acid
47
Q

What diuretics work on proximal tubule of nephron? (3)

A
  1. triamterene
  2. amiloride
  3. spironolactone
48
Q

What diuretics work on distal tubule of nephron? (3)

A
  1. thaizides
  2. metolazone
  3. indapamide
49
Q

What can be done for diuretic resistant patients?

A

diuretics can be given with thazide diuretics to improve outcome (powerful combo)

50
Q

What are adverse drug reactions to diuretics? (5) HYPOs

A
  1. dehydration
  2. gout
  3. hypokalaemia, hyponatraemia
  4. impaired glucose tolerance, diabetes
  5. hypotension
51
Q

What does a drug interaction between furosemide and aminoglycoside produce?

A

aural and renal toxicity

52
Q

What does drug interaction between furosemide and lithium, NSAIDs and vancomycin produce?

A

renal toxicity

53
Q

What does a drug interaction between furosemide and antihypertensives produce?

A

profound hypotension

54
Q

Overall, furosemide should NOT be mixed with which drugs to avoid dangerous drug-drug interactions? (5)

A
  1. NSAIDs
  2. lithium
  3. vancomycin
  4. aminoglycoside
  5. antihypertensives
55
Q

Therefore what drugs reduce mortality from chronic heart failure? (4)

A
  1. angiotensin blockade
  2. beta blockers
  3. aldosterone blockade
  4. ANP/BNP enhancement
56
Q

What is an alternative enzyme in heart tissue which can convert angiotensin 1 to angiotensin 2 without ACE?

A

chymase (it cannot be blocked by ACEIs)

57
Q

Damage to which body structures does angiotensin 2 cause organ damage to? (4)

A
  1. brain
  2. blood vessels
  3. kidneys
  4. heart
58
Q

What organ damaging effect does angiotensin 2 have on the brain and blood vessels? (4)

A
  1. atherosclerosis
  2. vasoconstriction
  3. vascular hypertrophy
  4. endothelial dysfunction
59
Q

What organ damaging effect does angiotensin 2 have on the heart? (4)

A
  1. l. ventricular hypertrophy
  2. fibrosis
  3. remodelling
  4. apoptosis
60
Q

What organ damaging effect does angiotensin 2 have on the kidneys? (4)

A
  1. decrease in glomerular filtration rate
  2. increase in proteinuria
  3. increase in aldosterone release
  4. glomerular sclerosis
61
Q

What are the most commonly used ACEIs? (3)

A
  1. ramipril
  2. enalapril
  3. lisinopril
62
Q

What effect do ACEIs have?

A
  • competitively block ACE (angiotensin converting enzyme)
  • prevent conversion of angiotensin 1 into angiotensin 2
  • reduce preload and afterload on heart
63
Q

What beneficial effect do ACEIs have on post MI patients and heart failure patients?

A
  1. reduce mortality
  2. reduce morbidity
  3. reduce onset of heart failure (in post MI patients)
64
Q

What are adverse drug reactions to ACEIs? (6)

A
  1. first dose hypotension
  2. cough
  3. angioedema
  4. renal impairment
  5. renal failure
  6. hyperkalaemia
65
Q

What does a drug interaction of ACEI with NSAIDs cause?

A

acute renal failure

66
Q

What does a drug interaction of AEI with pottasium supplements and potassium sparing diuretics cause?

A

hyperkalaemia

67
Q

Overall, what drugs should NOT be used with ACEIs? (3)

A
  1. NSAIDs
  2. potassium supplements
  3. potassium sparing diuretics
68
Q

What do ARBs block?

A

block the angiotensin 2, AT1 receptor

69
Q

When are ARBs give to patient?

A
  • only when patient intolerant to ACEIs

- they are not as effective as ACEIs

70
Q

What are two angiotensin 2 receptors?

A
  1. AT1

2. AT2

71
Q

What does activation of AT1 receptor do? (5)

A
  1. vasoconstriction
  2. vascular proliferation
  3. aldosterone secretion
  4. cardiac myocyte proliferation
  5. increased sympathetic tone
72
Q

What does activation of AT2 receptor do? (3)

A
  1. vasodilation
  2. antiproliferation
  3. apoptosis
73
Q

Why is AT1 receptor blocked?

A
  • more selective and specific blockade of angiotensin 1 at At1 receptor rather than non-specific blockade by ACEIs for example
74
Q

What is Valsartan- Sacubitril (ARNI)?

A
  • combined valsartan and ARB and neprilysin
  • ARB blocks AT1 receptor
  • Neprilysin stops breakdown of ANP and BNP by neutral endopeptidases
75
Q

What type of drug is spironolactone?

A
  • Aldosterone antagonist
  • K sparing diuretic
  • inhibits actions of aldosterone
76
Q

On which part of the nephron does spironolactone act on?

A

distal tubule

77
Q

What is spironolactone used in combination with?

A

with loop diuretics and ACEIs

78
Q

What is spironolactone useful for treating?

A

resistant oedema

79
Q

What are 3 most commonly used beta blockers?

A
  1. Carvedilol
  2. Bisoprolol
  3. Metoprolol
80
Q

When should beta blockers be used?

A
  • only in STABLE patients and not during an acute presentation stage
  • they block actions of sympathetic system and may cause severe deterioration of chronic heart failure
  • specialist use only since can be hazardous
81
Q

What is Ivabradine an inhibitor of?

A
  • specific inhibitor of the I current in sinoatrial (SA) node
  • no action on other channels in the heart or vascular system
82
Q

Does Ivabradine modify myocardial contractility?

A
  • it doesn’t modify heart contractility or intracardiac conduction even in impaired systolic function
83
Q

When is it recommended to give patients Ivabradine?

A
  • stable chronic patients who are receiving stabdard therapy including beta blockers at max. tolerated dose
  • patients in sinus rhythm with heart rate at 70bpm or greater at rest
84
Q

What sort of drug is Digoxin?

A

positive inotrope

85
Q

What is the mechanism of digoxin?

A
  • increases availability of calcium in the myocyte

- no effect on mortality

86
Q

Why does digoxin have to be administered carefully?

A

has a narrow therapeutic index

87
Q

What are adverse side effects of digoxin? (3)

A
  1. arrhythmias
  2. nausea
  3. confusion
88
Q

What anticoagulant can be used to treat chronic heart failure?

A

Warfarin

89
Q

Why is Warfarin used in patients with heart failure?

A
  • dilated ventricle gives rise to thrombus formation and thromb-embolic events
  • Warfarin prevents these events from causing problems
90
Q

What is the therapeutic regime for treating chronic heart failure? (9)

A
  1. furosemide +/- thiazide
  2. furosemide +pulsated metolazone
  3. ACEI
  4. ARB
  5. ARNI; angiotensin receptor neprilysin inhibitor
  6. beta blocker +/- Ivabradine
  7. MRA spironolactone
  8. digoxin
  9. warfarin
91
Q

What are symptomatic reliefs seen in heart failure patients after therapy administered? (3)

A
  1. dyspnoea
  2. tiredness
  3. lethargy
92
Q

What clinical relief is seen in heart failure patients after therapy administered? (3)

A
  1. peripheral oedema
  2. ascites
  3. weight
93
Q

What should be monitored in a heart failure patient? (3)

A
  1. symptoms and clinical signs
  2. weight
  3. patient education

2. Cardiovascular System (42 decks)

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