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Heart Failure > Heart Failure Case Introduction > Flashcards

Heart Failure Case Introduction Flashcards

1
Q

Definition

A
  • Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired
  • Having heart failure means that for some reason, your heart is not pumping blood around the body as well as it used to
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2
Q

Causes of heart failure(10)

A

• Ischaemic heart disease
– Previous N/STEMI is the most common cause in the UK
• Hypertension
• Valve disease – e.g. aortic stenosis, mitral regurgitation • Diabetes
• Cardiomyopathies
– Hypertrophic Obstructive Cardiomyopathy (HOCM)
– Dilated cardiomyopathy (DCM)
– Arrhythmogenic Right ventricular cardiomyopathy (ARV) – Restrictive cardiomyopathy
• Alcohol, drugs, pregnancy

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3
Q

Ejection fraction

A
  • Measure of how well the heart is pumping blood
  • The lower this figure, the worse the pumping ability of the heart
  • Normal ejection fraction: 60-65%
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4
Q

Left ventricular systolic dysfunction (LVSD)

A

most common
– Impaired LV contraction (systolic)
– Associated with a reduced ejection fraction
– Most treatment evidence is for heart failure due to LVSD: also known as heart failure
with reduced ejection fraction (HFrEF)

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5
Q

Heart Failure with preserved ejection fraction (HFpEF)[3]

A

– Impaired LV relaxation (diastolic)
– Preserved ejection fraction
– Common in hypertension particularly in the elderly (females)

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6
Q

Systolic dysfunction:

A
  • Ventricles fill a lot but only pump out 40-50%
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7
Q

Diastolic dysfunction

A

-Ventricles don’t fill enough

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8
Q

Precipitants of heart failure(8)

A

• Non- compliance
– Medication
– Fluid intake
• Infection
– E.g. Chest ( HR and demand on heart) • Arrhythmias
– Tachyarrhythmia’s (e.g. AF) – loss of atrial component to cardiac output
– Bradyarrhythmias – rate too slow to provide enough cardiac output • XS Etoh / fluid
– Fluid / Cardiomyopathy
• Anaemia
• Check thyroid and renal function

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9
Q

Signs(7)

A 
• Hypotension
• Cold peripheries
• Raised JVP
• 3rd heart sound
• Lung crackles/ wheeze • Fluid retention
– L-lung
– R-peripheral /ascites
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10
Q

Incidence & prevalence(8)

A

• Nearly 1 million people in the UK have heart failure • Prevalence increasing
– Ageing population
– More pts surviving N/STEMI but left with LVF
• Incidence increasing
– 1 new case per 1000 population / yr – Rising about 10% / yr
– Median age presentation is 76
– Male: female - 2:1

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11
Q

Prognosis

A
  • Poor survival rates (worse than many cancers)
  • 30-40% patients diagnosed die within one year
  • Difficult to define prognosis due to high risk of sudden cardiac death (SCD)
  • 6000 deaths / yr due to heart failure caused by IHD
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12
Q

Increasing blood returning to the heart

A

Increases Stroke volume and cardiac output

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13
Q

Another heart failure definition:

A

The inability of the heart to meet the circulatory demands of the body Or
The ability to do so only at abnormally high cardiac filling pressures

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14
Q

If you increase the amount blood returning to the heart

A

then stroke volume and cardiac output will increase

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15
Q

HFpEF

A

heart failure with preserved ejection fraction

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16
Q

HFrEF

A

heart failure with reduced ejection fraction

17
Q

Ejection fraction

A

Percentage of the blood that is removed from the ventricles during a single beat. In a healthy heart, typically 60-70% of the blood gets removed per beat

18
Q

HFpEF?

A
  • In somebody with heart failure with preserved ejection fraction (HFpEF), they are still able to remove 60-70% of the blood per beat
  • So why do they still have heart failure?
  • The problem is that in HFpEF the volume of the ventricles is reduced
  • This is because the left ventricle muscle cells have become larger (left ventricular hypertrophy) and there is also fibrosis (excess connective tissue)
  • Since the ventricles are smaller and therefore the ventricle holds less blood, even though the ejection fraction is preserved, a much smaller volume of blood is getting pumped out and therefore not meeting the circulatory needs of the body
19
Q

HFrEF?

A
  • In somebody with heart failure with reduced ejection fraction (HFrEF), there is a dysfunction in the ability of the heart to contract – there is a systolic dysfunction
  • Therefore, they are only ejecting less than 35% of the blood that is present in the ventricles
20
Q

Frank Starling Curves

A
  • As you increased end-diastolic volume, stroke volume also increases
  • A: When we exercise, the curve is shifted up and to the left – predominantly due to the activity of the sympathetic nervous system, because the sympathetic nervous system will increase the force of contraction of the ventricles
  • C: In patients with heart failure, the curve is shifted to the right and the maximum stroke volume that can be achieved is quite low.
21
Q

Rest

A
  • In order to achieve that particular stroke volume that keeps us alive at rest, a normal heart requires a filling pressure (read down to the x-axis where the line cross the rest line).
  • But in patients with heart failure, the heart requires an increased filling pressure in order to obtain the same stroke volume.
  • Patient C’s heart is having to work harder in order to pump out enough blood to supply the needs of this patient at rest
22
Q

Walking

A
  • Now, our patient with heart failure wants to walk around
  • In order to do that, a specific stroke volume has to be achieved
  • In patient C, this can’t be achieved, so the heart is not being able to reach the level at which it can sustain walking activity – the heart is unable to meet the circulatory demands of the body, this patients heart failure is decompensated for walking and is compensated at rest only
23
Q

myosin actin mechanism

A

At rest, when end-diastolic volume is relatively low, there is very little stretch on the muscle fibres in the ventricle and therefore sarcomere length is relatively short and has a high degree of overlap of the myosin and actin filaments in the heart myocytes
• If this heart muscle cell wanted to contract, it can only move a relatively small distance
• As we increase stroke volume, sarcomere length increases and we have a much larger distance that the muscle fibres can contract over
• The more blood that returns to the heart, the more it stretches the sarcomere and therefore the more contraction is possible, allowing the heart to pump out the same amount of blood that enters the heart
• Eventually, these muscle fibres get stretched far too much and therefore the degree of the overlap of the actin and the myosin will not be optimal and you will start to damage the fibres and they will start to lose their efficiency – so the stroke volume will eventually start to decline

24
Q

The other mechanism that is important in allowing the heart to increase stroke volume in response to an increase in end diastolic volume ….

A

based around the sensitivity of troponin C to calcium
• Muscles require calcium to contract because it binds to troponin C, and when troponin C binds calcium, it pulls tropomyosin out of the way of the myosin binding sites – conformational change
• A conformational change is a change in the shape of a macromolecule, often induced by environmental factors
• Therefore the muscle can contract
• As we increase end diastolic volume, troponin C is able to move this tropomyosin at increasingly lower concentrations of calcium – so stretching the muscle fibres sensitizes troponin C to calcium
• So contraction can occur at far lower concentrations of calcium

25
Q

-

A

-

26
Q

Extrinsic mechanisms

A

would be things like sympathetic nervous system and the renin angiotensin system etc.

27
Q

Compensated heart failure:

A

If we increase end diastolic volume, we can increase the same stroke volume as a regular heart – this is an example of compensated heart failure

28
Q

Positive inotropic stimulation:

A

sympathetic stimulation or it could be drug therapy that’s caused that

29
Q

What happens if we increase outflow resistance (afterload)?

A
  • Afterload is the force that the heart has to generate in order to pump blood into the systemic circulation
  • If the blood vessels in the systemic circulation are constricted, then the amount of force the heart has to generate in order to pump the blood out is increased because its pumping it out into a much higher resistance
  • For a normal heart, as afterload increases, theres very little change in stroke volume
  • If we get into the realms of hypertension, there’s still relatively little change in the stroke volume – this is because our heart muscle is healthy and it can generate quite a high degree of force and can compensate for this increase in outflow resistance
  • Compared with a patient that has moderate or severe heart failure, the drop off in stroke volume is far more rapid as afterload goes up, as the heart is struggling to maintain function
  • Uncontrolled hypertension in a patient with heart failure is a real problem

Heart Failure (7 decks)

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