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CVS Pathology > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Definition of heart failure

A

A clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation

A state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can only do so from high pressures

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2
Q

What does HF stand for?

A

Heart failure

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3
Q

Types of HF

A

Heart failure due to LVSD due to IHD

Heart failure due to severe aortic stenosis

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4
Q

What does LVSD stand for?

A

Left ventricular systolic dysfunction

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5
Q

Examples of myocardial injury in the pathology of HF

A 
Coronary artery disease
HTN
DM
Cardiomyopathy 
Valvular disease
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6
Q

What does myocardial injury lead to?

A

Neurohormonal stimulation

Myocardial toxicity

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7
Q

What is involved in ventricular remodelling?

A

Fibrosis and scarring and myocytes healing

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8
Q

Pathology of systolic dysfunction

A

If failing or damaged heart - as circulatory volume increases, the heart dilates, the force of contraction weakens and CO drops further.
Decreased CO then activates RAAS further (which increases salt and water retention)
This is then viscous cycle of RAAS activation, circulatory volume increases and cardiac performance deteriorates further.
As heart starts to dilate, the cardiac myocytes undergo hypertrophy and then fibrosis and thus the heart is further weakened

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9
Q

When does HF usually occur?

A

Following sustained HTN (diastolic dysfunction/preserved ejection fraction HF)
Following myocardial damage i.e. an MI (i.e. systolic dysfunction)

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10
Q

What happens when CO falls?

A

Body registers this as loss in circulatory volume - vasoconstrictor system activation (sympathetic systems)
Salt and water retaining system (RAAS)

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11
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone system

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12
Q

What does RAAS cause the release of?

A

Angiotensin II

Aldosterone

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13
Q

What does RAAS result in?

A

Salt and water retention
Vasoconstriction
Hypertrophy and fibrosis of cardiac myocytes

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14
Q

What does activation of the sympathetic system cause activation of?

A

Noradrenaline

Adrenaline

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15
Q

What does the release of noradrenaline and adrenaline result in?

A

Vasoconstriction
Stimulates renin release which feeds into RAAS system
Myocyte hypertrophy

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16
Q

What causes salt and water excretion and vasodilation?

A

Natriuretic peptide system ANP/BNP (weaker than RAAS)

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17
Q

What do ANP and BNP stand for?

A

Atrial natriuretic peptide

Brain natriuretic peptide

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18
Q

What do ANP and BNP do?

A

Potent vasodilators and natriuretic peptides

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19
Q

Does the body have a weak or strong system to excrete and retain salt and water?

A

Retain - very strong

Excrete - weak

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20
Q

Risk factors for HF

A 
Age
HTN (LVH)
Chronic heart disease
Obesity
DM
Hyperlipidaemia
Coronary artery disease
Valvular heart disease
Alcoholism 
Infection (viral)
Congenital heart defects
Smoking
High or low haematocrit level 
OSA
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21
Q

What does OSA stand for?

A

Obstructive sleep apnoea

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22
Q

What is the number 1 risk factor for heart failure?

A

HTN

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23
Q

If sufficiently severe, almost any structural cardiac abnormality will cause HF; e.g.

A

LVSD
Valvular heart disease
Pericardial constriction or effusion
LV diastolic dysfunction/HF with preserved systolic dysfunction/HF with normal ejection fraction
Cardiac arrythmias; tachy or brady
Myocardial ischaemia/infarction (usually with LVSD)
Restrictive cardiomyopathy e.g. amyloid
Right ventricular failure; primary or secondary to pulmonary HTN

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24
Q

Causes of LVSD

A

Ischaemic heart disease (usually MI)
Dilated cardiomyopathy (DCM)
Severe aortic valve disease or mitral regurg

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25
Q

Explain DCM further

A

An umbrella term - means LVSD not due to IHD or secondary to another lesion i.e. valves/VSD

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26
Q

Causes of DCM

A

Inherited
Toxins e.g. alcohol, catecholamines (pheochromocytoma or stress cardiomyopathy)
Viral; acute myocarditis or chronic DCM
HIV, Lyme’s disease, Chagas disease
Sarcoidosis, hemochromatosis, SLE, mitochondrial disease
Muscular dystrophies
Peri partum cardiomyopathy
HTN
Isolated non compaction
Tachycardia related cardiomyopathy
Right ventricular pacing induced cardiomyopathy
End stage hypertrophic cardiomyopathy
End stage arrhythmogenicity RV cardiomyopathy

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27
Q

How does HF affect neurohormonal factors?

A 
RAAS 
- salt and water retention 
- adverse haemodynamics
- LV hypertrophy / remodelling and fibrosis 
- hypokalaemia and hypomagnesia
SNS 
- arrhythmogenic
- adverse haemodynamics 
- increases renin etc
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28
Q

Overall effects of neurohormonal activation

A

Vasoconstriction
Endothelial dysfunction
Renal sodium retention

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29
Q

Mean age for HF

A

74 y/o

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30
Q

What is a potent predictor of death in HF?

A

Left ventricular systolic dysfunction

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31
Q

Presentation of HF

A 
Breathlessness
Fatigue
Oedema
Reduced exercise capacity 
Tachycardia
Raised JVP
Chest crepitations or effusions
3rd heart sound
Displaced or abnormal apex beat
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32
Q

What classification is used for HF?

A

New York Association (NYHA) classification

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33
Q

What does NYHA look at in HF?

A

Exercise tolerance

Symptoms

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34
Q

NYHA class I

A

No limitation of exercise, no symptoms during usual activity

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35
Q

NYHA class II

A

Mild limitation of exercise, Comfortable with rest or symptoms with mild exertion

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36
Q

NYHA Class III

A

Moderate limitation, comfortable only at rest

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37
Q

NYHA Class IV

A

Severe limitation, any physical activity brings on discomfort and symptoms occur at rest

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38
Q

Investigations for LVSD

A 
Antibodies / viral serology 
Ferritin 
FBC
RFTs, TFTs
Consider causes and exclude them 
ECG
CXR
ECHO
Coronary angiography 
Cardiac MRI
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39
Q

What would a cardiac MRI show?

A

Infarction
Inflammation
Fibrosis

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40
Q

What is needed to diagnose HF?

A

Symptoms and signs of HF (rest or exercise)
AND
Objective evidence of cardiac dysfunction
AND
Response to therapy i.e. diuretics (in doubtful cases)

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41
Q

What are ways of obtaining objective evidence of cardiac dysfunction?

A

ECHO
Radionucleotide ventriculography (RNVG/MUGA)
MRI
Left ventriculography

42
Q

Potential screening tests for HF

43
Q

BNP in HF

A

Elevated in heart failure

44
Q

What does BNP stand for?

A

Brain (b-type) natriuretic peptide

45
Q

What is BNP and where is it found?

A

Amino acid peptide

Blood

46
Q

Low BNP does what?

A

Excludes HF

47
Q

Is BNP produced in a healthy heart?

A

Yes at low levels

When the heart is stressed it produces more

48
Q

How long is BNP stable for?

A

Up to 72 hours

49
Q

What can BNP predict in HF?

A

Mortality

Morbidity

50
Q

What can ECHO identify?

A 
LVSD
Valvular dysfunction 
Pericardial effusion/tamponade
Diastolic dysfunction 
LVH
Atrial/ventricular shunts/complex congenital heart defects
Pulmonary HTN/ Right heart dysfunction 
Atrial dilatation
51
Q

What may ECHO not identify?

A

Constriction

Shunts

52
Q

Different stages of LV ejection fraction dysfunction

A

Normal 50-80%
Mild 40-50%
Moderate 30-40%
Severe <30%

53
Q

Treatment of HF (due to LVSD)

A

Diuretics
ACEIs or ARBs
BBs
Aldosterone receptor blockers

54
Q

What characterises HF?

A 
Progressive cardiac dysfunction 
SOB
Tiredness
Neurohormonal disturbances
Sudden death
55
Q

Types of HF

A

Systolic HF
Diastolic (or relaxation) HF
Chronic HF

56
Q

What happens in systolic HF?

A

Heart failure reduced ejection fraction (HFrEF)

Decreased pumping function of the heart, which results in fluid back up in the lungs and HF

57
Q

What happens in diastolic HF?

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 HF

58
Q

What % of the population has chronic HF?

59
Q

Prognosis of chronic HF

A

5 year mortality 50% - poor

60
Q

Which gender has more HF?

61
Q

Aims of treatment of HF and how they do so

A 
To improve symptoms
- Diuretics
- digoxin
To improve symptoms and survival 
- ACEIs/ARBs
- spironolactone 
- valsartan-sacubitril
To improve survival
- BBs
- Ivabradine
62
Q

What does spironolactone do?

A

Special type of diuretic which antagonises aldosterone

63
Q

What is the mainstay of symptomatic treatment for HF?

A

Loop diuretics

  • furosemide or
  • bumetanide
64
Q

What are used to block the detrimental hormone changes in HF?

A

Carvedilol, bisoprolol, metoprolol

Beta blockers

65
Q

What does angiotensin II do?

A

Potent vasoconstrictor - salt and water retention

66
Q

What drugs block the effects of angiotensin II?

A

ACEIs

Angiotensin antagonists

67
Q

Example of an ACEI

68
Q

Example of angiotensin antagonists

A

Valsartan, losartan

69
Q

What drug blocks effects of aldosterone?

A

Spironolactone

70
Q

What drugs can enhance cardiac function?

A

Positive inotropes

Vasodilators

71
Q

Example of a positive inotrope

72
Q

How do positive inotropes work?

A

Improve the ability of the heart to pump and so can improve cardiac status

73
Q

How do vasodilators work?

A

Reduce preload and improve after load which improves cardiac function

74
Q

Examples of vasodilators

A

Isosorbide mono or dinitrate

75
Q

How do loop diuretics work?

A

Remove excess salt and water
Induce profound diuresis
Inhibit Na-K-Cl transporter in the ascending loop of henle

76
Q

If the patient is diuretic resistant, what can it be used in combination with?

A

Thiazide diuretics

77
Q

S/Es of thiazide diuretics

A 
Dehydration 
Hypotension 
Hypokalaemia
Hyponatraemia
Gout
Impaired glucose tolerance, DM
78
Q

What drugs interact with furosemide

A 
Aminoglycosides (aural and renal toxicity)
Lithium (renal toxicity)
NSAIDs (renal toxicity)
Anti-HTNs (profound HTN)
Vancomycin (renal toxicity)
79
Q

What drugs reduce mortality in HF?

A

Angiotensin blockage
Beta receptor blockade
Aldosterone blockade
ANP/BNP enhancement

80
Q

S/Es of ACEIs

A 
First dose hypotension 
COUGH
Angioedema
Renal impairment
Renal failure
Hyperkalaemia
81
Q

What drugs do ACEIs interact with?

A

NSAIDs (acute renal failure)

Potassium supplements and potassium sparing diruetics (hyperkalaemia)

82
Q

What is spironolactone?

A

Potassium sparing diuretic

83
Q

How does spironolactone work?

A

Inhibits actions of aldosterone
Acts in distal tubule
Used in combination with loop diuretics

84
Q

When is spironolactone particularly useful?

A

Resistant oedema

85
Q

What is ivabradine?

A

Specific inhibitor of the If current in the sinoatrial node

86
Q

How does digoxin work?

A

Increases availability of calcium in the myocyte

87
Q

S/Es of digoxin

A

Narrow therapeutic index - digoxin toxicity
Arrhythmias
Nausea
Confusion

88
Q

In UK, digoxin is only used if the patient has what?

89
Q

What do beta blockers block the action of?

A

Sympathetic system

90
Q

Therapeutic regime summary for HF

A
  1. furosemide (and possibly thiazide)
  2. furosemide (and possibly pulsed metolazone)
  3. ACEI
  4. ARBs
  5. ARNI
  6. BBs
  7. MRA-spironolactone
  8. Digoxin
  9. Warfarin
91
Q

What should be monitored regularly in HF?

92
Q

What is the possible feature to be heard on auscultation of the chest in left sided HF?

A

Third heart sound

93
Q

What may be a S/E of loop diuretics?

A

Ototoxicity

94
Q

NICE guidelines for the management of HF due to LVSD

A
  1. ACEI + BB
  2. If symptoms persist consider
    - ARB
    - Aldosterone antagonist
    - Hydralazine and nitrate
  3. If symptoms persist consider
    - Cardiac resynchronisation therapy
    - Digoxin
95
Q

What should all patients with HF be taking?

96
Q

Name a drug contraindicated in HF

97
Q

What can verapamil not be taken with and why?

A

BB

Risk of complete heart block

98
Q

1st line treatment of a patient with HF with reduced LVEF

A

BB AND ACEI

99
Q

Signs of left sided HF

A 
SOB on exertion 
Orthopnoea
Paroxysmal nocturnal dyspnoea
Wheeze 
Cough
100
Q

Signs of right sided HF

A

Raised JVP
Ankle oedema
Hepatomegaly

CVS Pathology (19 decks)

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