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CVS * > S10 Heart Failure > Flashcards

S10 Heart Failure Flashcards

1
Q

What is heart failure?

A

The inability of the heart to meet the demands (deliver a blood volume that allows the body tissues to function as required) of the body.

A clinical syndrome of reduced CO, tissue hypoperfusion, increased pulmonary pressures and tissue congestion

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2
Q

What is a syndrome?

A

A collection of signs and symptoms

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3
Q

What 3 things allow the heart to work as an effective pump?

A
  • one way valves
  • the chamber size
  • functioning muscle
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4
Q

Conditions that impair what 3 things could lead to impairment of cardiac function?

A
  • one way valves
  • the chamber size
  • functioning muscle
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5
Q

What is the most common cause of heart failure?

A

Ischaemic heart disease

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6
Q

Apart from ischaemic heart disease, what are some other causes of heart failure?

A
  • hypertension
  • aortic stenosis
  • cardiomyopathies
  • arrhythmias
  • valvular/myocardial structural diseases
  • pericardial diseases
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7
Q

What is the rarest cause of heart failure?

A

Highly increased demand on CO due to sepsis, severe anaemia or thyrotoxicosis - high output heart failure

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8
Q

Why does myocardial dysfunction occur with ischaemic heart disease?

A

Dysfunction occurs through fibrosis and remodelling of the muscle

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9
Q

How does hypertension result in heart failure?

A

There’s increased afterload on the ventricles and increased risk of atherosclerosis (can lead to IHD)

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10
Q

How does aortic stenosis result in heart failure?

A

There’s increased afterload on the L ventricle

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11
Q

How does cardiomyopathies result in heart failure?

A

Muscles could be hypertrophic/dilated - can lose elasticity - harder to pump effectively and the walls are thickened - issue with filling

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12
Q

What is the stroke volume?

A

The volume of blood ejected by a ventricle in a single beat

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13
Q

What is the CO?

A

The volume delivered to tissues, etc

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14
Q

How do you calculate ejection fraction (EF)?

A

SV/EDV x 100

SV = EDV - ESV

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15
Q

What factors influence stroke volume?

A 
Increase SV:
* preload
* myocardial contractility 
Decrease SV:
* afterload
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16
Q

What is Frank-Starling’s Law?

A

The more the ventricles are filled/stretched during diastole, the greater volume (SV) ejected during systole - the greater the cardiac myocytes are stretched, the greater their force of contraction.

However does reach a point when the cells are overstretched and then SV decreases.

This is an intrinsic mechanism

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17
Q

How does the influence of the sympathetic nervous system effect the Frank-Starling curves? Why?

A

Curve is shifted upwards and to the left

Positive inotropic effect - the contractility of the heart increases with increased sympathetic activity - there’s a greater CO for a given EDP

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18
Q

Why is CO reduced in heart failure?

A
  • there’s a reduced preload (EDV)
  • there’s reduced myocardial contractility
  • there’s an increase afterload

These all reduce SV, hence CO is reduced

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19
Q

What can cause increased afterload in the L side of heart?

A

Aortic stenosis or chronic severe hypertension

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20
Q

What is the most common reason for reduced preload?

A

Due to a problem with the size of the chamber, rather than a problem with venous return

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21
Q

What can caused reduce filling of the heart?

A
  • the ventricular chambers are too stiff/aren’t relaxing enough
  • ventricular hypertrophy
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22
Q

What can caused reduce contractility of the heart?

A
  • thin/fibrosed muscle walls
  • overstretches sarcomeres - enlarged chambers
  • abnormal/uncoordinated myocardial contraction
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23
Q

What is heart failure with reduced ejection fraction (HFrEF)?

What is heart failure with preserved ejection fraction (HRpEF)?

A

Systolic dysfunction - contractility problem - most common

Diastolic dysfunction - filling problem

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24
Q

What is a normal ejection fraction percentage?

A

Normal is 50% or above

Typical is 60% or above

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25
Q

How do you measure ejection fraction?

A

Measure using an echocardiogram

26
Q

At what percentage is the ejection fraction considered reduced?

A

Below 40%

27
Q

How can a heart be failing if the EF is maintained?

A

Because the ventricle is ejecting less volume in systole because diastole is reduced. It’s ejecting the correct percentage, just of a smaller initial volume

28
Q

Which ventricle is most commonly involved?

A

The left ventricle

But the right ventricle will become effected as a result of L ventricular failure

29
Q

What is involvement of both ventricles called?

A

Biventricular (congestive) heart failure

30
Q

When can right ventricular heart failure occur without left ventricular failure?

A

Due to chronic lung diseases - much less common

31
Q

What happens to the Frank-Starling curve in heart failure?

A

CO is reduced

32
Q

How does neuro-hormonal activation, to TRY and correct falling CO, occur?

A
  1. Damaged ventricular tissues
  2. Reduced efficiency of ventricular contraction
  3. Reduced stroke volume
  4. Reduced cardiac output
  5. Neuro-hormonal activation
33
Q

Why are physiological mechanisms to try and correct the falling CO actually bad?

A

Lead to increased cardiac demand and a further reduced SV - so heart failure worsens

“Don’t flog a dying horse”

34
Q

How is the sympathetic nervous system, to TRY and correct falling CO, activated?

A
  1. Reduced CO
  2. Reduced BP
  3. Reduced BP detected by baroreceptors e.g. carotid sinus
  4. Increase in sympathetic drive - increased HR and peripheral resistance
  5. Increased afterload increased cardiac work
35
Q

How is the RAAS, to TRY and correct falling CO, activated?

A
  1. Decreased CO
  2. Decreased BP
  3. Decreased BP leads to decreased renal perfusion
  4. This activated the renin-angiotensin-aldosterone pathway
  5. Angiotensin II increases circulating volume due to Na+/water retention (via aldosterone), stimulates ADH, leads to vasoconstriction, enhances sympathetic activity
  6. This all increases the preload and afterload
  7. Increased afterload increases cardiac work
36
Q

What are the clinical signs and symptoms of heart failure?

A
  • fatigue/lethargy
  • breathlessness due to pulmonary oedema
  • leg swelling due to peripheral oedema
37
Q

If the heart is failing, what happens to the venous pressure? What does this mean for hydrostatic pressures in capillaries and formation of tissue fluid?

A

Venous pressure increases

This means there’s increased hydrostatic pressure at the venule end of the capillary bed so more fluid moves out of the capillaries/less fluid moves back into capillaries at venule end leading to formation of tissue fluid

38
Q

What does a chest x-ray look like when someone has pulmonary oedema?

A

There’s accumulation of fluid in the lung interstitium - white splotches

39
Q

How can you tell there’s accumulation of fluid in the interstitium of peripheral tissues?

A

Push on area of swelling - will leave an indent - pitting

40
Q

What are the signs/symptoms of left ventricular heart failure?

A

Causes pulmonary congestion

  • fatigue/lethargy
  • breathlessness on exertion
  • orthopnoea (breathless when lying flat)
  • paroxysmal nocturnal dyspnoea (waking up due to shortness of breath/coughing)
  • basal pulmonary crackles
  • cardiomegaly - displaced apex beat to the left - sign of enlarged LV
41
Q

What are the signs/symptoms of right ventricular heart failure?

A

Causes peripheral congestion

  • fatigue/lethargy
  • breathlessness
  • peripheral oedema
  • raised jugular venous pressure
  • tender, smooth enlarged liver - liver congestion
42
Q

What is raised jugular venous pressure a sign of?

A

Increased pressures in the right side of the heart

43
Q

How is heart failure classified?

A

NYHA functional classification

  • class I - asymptotic limitation of activity
  • class II - slight limitation or activity, asymptomatic at rest
  • class III - limitation of activity, asymptomatic at rest
  • class IV - inability to do activity without symptoms, symptoms at rest, discomfort increases with activity
44
Q

What are the 3 key questions to consider when carrying out investigations linked to heart failure?

A
  • do they have heart failure?
  • what sort of heart failure do they have?
  • what is causing the heart failure?
45
Q

What imaging can be carried out?

A
  • ECG
  • CXR
  • transthoracic echocardiogram
46
Q

Why do you give IV furosemide in heart failure?

A

A diuretic that has immediate venodilatory effects

47
Q

What blood tests do you carry out when investigating heart failure?

A
  • NTpro-BNP
  • FBC
  • U&Es
  • LFTs
  • clotting
  • thyroid function, vitamin D levels, CRP
48
Q

What is NTpro-BNP blood test?

A

Natriuretic peptide is released in response to atrial/ventricular stretch due to fluid overload

The normal range varies wit age/gender

49
Q

Why do you do a FBC for heart failure?

A

Patients with heart failure and usually anaemic - helps explains some of the symptoms?

50
Q

Why do you do a U&Es for heart failure?

A

Renal function often deteriorates in heart failure and knowing the Na+/K+ levels are important for knowing which medications to give

51
Q

Why may LFTs be elevated?

A

Due to hepatic congestion (R sided failure)

52
Q

Why do you carry out thyroid function tests, vitamin D levels and CRP levels?

A

To explore alternative explanations for the symptoms

53
Q

What 3 systems are activated in heart failure? Which are positive, which are negative?

A
  • sympathetic nervous system/the RAAS/ - HR, contractility and preload increase - negative
  • ANP and BNP secretion - natriuresis, diuresis, vasodilation increase, RAAS decreases - positive
54
Q

What are the main treatments for heart failure?

A
  • ACE inhibitors/ ARB (angiotensin receptor blocker)
  • beta blockers - used with caution
  • mineralocorticoid receptor antagonist e.g. spironolactone - aldosterone inhibitor
  • biventricular ICD - pacemaker
55
Q

When myocardial damage occurs, the sympathetic nervous system is activated. What are the outcomes of this?

A
  • activation of the RAAS - decreased contractility and myocardial hypertrophy
  • vasoconstriction - decreased contractility and myocardial hypertrophy
  • increased heart rate and contractility - decreased contractility
  • direct cardiotoxicity - myocyte damage
56
Q

Why does increased HR and contractility lead to decreased contractility?

A

Because the increase means there’s increased myocardial oxygen demand which can’t be obtained/maintained

57
Q

How is the sympathetic nervous system mediated?

A

By baroreceptors

58
Q

What are the physiological effects of beta-blockers on heart failure?

A
  1. They reduce heart rate
  2. This reduces BP and CO
  3. So myocardial oxygen demand is reduced
  4. There’s reduced mobilisation of glycogen
  5. Work against the unmanaged effects of catecholeamines - adrenaline/NA
59
Q

Why do you initiate beta blocker treatment for heart failure at low doses?

A

Because if you give too much, could make the heart failure worse

60
Q

Where do the leads go with a biventricular pacemaker?

A
  • lead in right atrium
  • lead in right ventricle
  • lead in coronary sinus vein
61
Q

What is the approach to a patient with heart failure with reduced ejection fraction (HFrEF)?

A
  1. Have a multidisciplinary team
  2. Cardiac rehabilitation
  3. Use evidence based treatments - ACE/ARB, beta blocker, pacemaker, mineralocorticoid receptor antagonists (MRAs)
  4. Palliative care, heart transplant
  5. Patient education

This is a cycle

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