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Cardiovascular System > Session 10- The Pathophysiology of Heart Failure > Flashcards

Session 10- The Pathophysiology of Heart Failure Flashcards

1
Q

What features of the heart have to be affected in order for there to be impairment of cardiac function

A
  • functioning muscle
  • chambers size
  • one-way valves
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2
Q

What is cardiac output

A

Stroke volume x heart rate

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3
Q

Stroke volume

A

Volume of blood ejected by a single ventricle in a single beat

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4
Q

What is ejection fraction

A

Fraction ejection in a single heart beat of total volume available (EDV)

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5
Q

How do you calculate ejection fraction

A

Stroke volume/ end diastolic volume

Amount if blood pumped out of ventricle/ total amount of blood in ventricle

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6
Q

What is ejection fraction typicallly

A

> 50% typically 60-70%

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7
Q

What determines ability to increase stroke volume

A

Pre-load
Myocardial contractility
After-load

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8
Q

What is pre-load

A

Volume in ventricle at end of diastole

The stretch on the ventricle just before contraction

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9
Q

What is after load

A

Force ventricles have to contract against

Total peripheral resistance

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10
Q

What is the relationship between pre-load and stroke volume

A

Increasing blood volume in ventricle at the end of diastole causes increased stretch

More ventricle stretch during diastole = greater stroke volume ejected in systole

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11
Q

Relationship between myocardial contractility and stroke volume

A

Contractility improves with greater stretch afforded by the increase in EDV

Contractility of the heart also improves with increasing sympathetic activity
-greater SV for a give end diastolic volume: if increase in SV so does CO

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12
Q

What is heart failure

A

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

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13
Q

What is the most common cause of heart failure

A

Ischaemic heart disease

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14
Q

Causes of heart failure

A
  • hypertension
  • valvular disease e.g. aortic stenosis
  • cardiomyopathies (e.g. hypertrophic/dilated) - arrhythmias
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15
Q

What is remodelling

A

The loss of myocytes and fibrosis of cardiac tissue in response to these conditions changing ventricular function and ventricular shape/size

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16
Q

What can remodelling lead to

A

Impairment of ventricular filling- chamber size

Impairment of ventricular ejection- emptying

17
Q

What will cause contractility problem

A

Ejection problems

Muscle walls thin/fibrosed

Chamber space enlarged (overstretched sarcomere)

Abnormal or uncoordinated myocardial contraction

18
Q

What will cause a filling problem

A

Diastolic

Ventricular volume/ capacity for blood is reduced

  • ventricular chambers too stiff/ not relaxing enough
  • ventricular walls thickened (Hypertrophied/ concentric remodelling)
19
Q

What is an ejection problem

A

Space available in ventricle not reduced but poor ventricular contraction so unable to empty it as well

20
Q

What is a filing problem

A

Space available in ventricle is reduced therefore EDV is reduced

21
Q

How do you determine if its an ejection issue

A

Drop in ejection fraction
EF<40%
HFrEF

22
Q

How do you determine if its a filling issue

A

EF> 50%

HFpEF

23
Q

Which ventricle s more commonly involved in heart failure

A

Left however failure of one inevitable leads to failure of the other

24
Q

Symptoms of heart failure

A

Dyspnoea
Fatigue
Due to tissue hypoperfusion

As well as tissue fluid retention

25
Q

Frank starling curve in left ventricular systolic heart failure

A

Increased LV filling in failing heart leads to very little increase in CO

Eventually leads to worsening CO

Increase in LVEDP in attempts to increase SV results in failing CO and development of pulmonary congestion

26
Q

How does sympathetic drive affect cardiac work in heart failure

A

Decrease in CO

Decrease in BP

Baroreceptors detect this

Increased sympathetic drive

  • increase heart rate
  • increase peripheral resistance
  • increase after load

Increased cardiac wrk

27
Q

How does the RAAS system affect the heart in hart failure

A

Decrease CO
Decrease BP

Decrease in renal perfusion

activation of renin-angiotensin aldosterone pathway
-increase circulating due to NA+ and water retention via aldosterone
-stimulates ADH
Increase preload

-enhances sympathetic drive
-vasoconstriction
Increase after load

ALL LEAD TO INCREASED CARDIAC WORK

28
Q

How does pulmonary oedema occur

A

Increased pressure within left ventricle as failing to eject volume sufficiently

Increased pressures in pulmonary circulation at venue end- back pressure

Increased hydrostatic pressures at venue end of pulmonary capillary beds

Gradient between hydrostatic and oncotic pressure less favourable for fluid returning to capillary from interstitium ‘

Increased volume of tissue fluid accumulates within pulmonary interstituim

29
Q

How does pulmonary oedema present

A

Breathlessness

Basal pulmonary crackles on auscultation

Orthopnoea

Paroxysmal nocturnal dyspnoea

30
Q

Orthopnoea

A

worsening breathlessness on lying flat

31
Q

Paroxysmal nocturnal dyspnoea

A

Waking in the night from feeling breathlessness

32
Q

How does peripheral oedema occur

A

Increased pressure in right ventricle as failing to eject volume sufficiently

Increased pressures in systemic venous circulation

Increased central venous pressure = increased jugular venous pressure- increased hydrostatic pressures at venule end of capillary beds

Gradient between hydrostatic and oncotic pressures less favourable for fluid returning to capillary from interstitium ‘

Increased volume of tissue fluid accumulates

Peripheral oedema esp in lower limb

33
Q

What does measuring jugular venous pressure le you know

A

Direct indication of pressure in right ventricle

34
Q

What do you get in left heart failure and not in right and vice versa

A

Cardiomegaly (displaced apex beat- indicating enlarged LV) - left

Tender smooth enlarged liver- liver congestion- right

Cardiovascular System (18 decks)

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