heart failure Flashcards

1
Q

What usually leads to impaired cardiac function?

A

Altered chamber size

Altered functioning muscle

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2
Q

Cardiac output (volume delivered per minute) =

A

SV x HR

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3
Q

What is the fraction that gets ejected from the heart? (eg the fraction of total volume available)

A

Ejection fraction

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4
Q

What is ejection fraction?

A

Fraction ejected from heart in a single beat from the total volume available (EDV)

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5
Q

How do you calculate ejection fraction?

A

Stroke volume / end diastolic volume (filled ventricle)N

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6
Q

Normal stroke volume and ventricular capactity

A

SV - 70-75ml

Ventricle capacity - 110-150 ml

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7
Q

Normal ejection fraction

A

> 50%

Usually 60-70% (2/3)

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8
Q

How is stroke volume increased? (made bigger)

A
Increasing preload (increases stretch on ventricle just before contraction)
Increasing myocardial contractility
Decreasing afterload (TPR)
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9
Q

How is an increase in demand met by the heart?

A

Increase HR

Increase stroke volume

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10
Q

How does preload increase stroke volume?

A

Increase EDV increases stretch on ventricles
More stretch during diastole = increase stroke volume in systole

= increase cardiac output

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11
Q

What is an intrinsic property of cardiac myocytes?

A

Greater they are stretched the greater their contractility (force of contraction)
…up to a point

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12
Q

Relationship between myocardial contractility and stroke volume

A

Contractility improves with greater stretch (greater EDV) and increased sympathetic activity

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13
Q

What else occurs during increased sympathetic activity that could affect cardiac output

A

Increased afterload (increased pressure that the heart is pumping against)

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14
Q

What is heart failure?

A

Its a Clinical syndrome of:

reduced cardiac output
tissue hypoperfusion
increased pulmonary pressures
tissue congestion

-arising from problems with ventricular filling and/or emptying

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15
Q

Most common cause of heart failure

A

Ischaemic heart disease

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16
Q

Other causes of heart failure

A

Hypertension
Valvular disease (eg aortic stenosis)
Cardiomyopathies (hypertrophic/dilated)
Arrhythmias

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17
Q

Rare causes heart failure

A

Increased demand of cardiac output (no problem with heart, body is just demanding too much)

eg:
sepsis
thyrotoxicosis

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18
Q

What is important in heart failure?

A

To identify underling cause as this shapes treatment options (eg repair valve etc)

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19
Q

What occurs from these conditions that results in heart failure?

A

Re-modelling of cardiac muscle - loss of myocytes and fibrosis
Changes ventricular function, size/shape

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20
Q

What does remodelling result in?

A

Impairment of ventricular filling (chamber size)

Impairment of ventricular ejection (emptying)

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21
Q

Impairment of filling

A

Ventricles become thick walled and stiff

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22
Q

Impairment of ejection

A

Muscle thin and weak

Cannot contract with enough force/uncoordinated

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23
Q

what type of heart failure is caused by ejection problem?

A

HFrEF (reduced ejection fraction)

Contractility (systolic) problem - cannot pump with enough force

24
Q

Ventricles in HFrEF

A

Muscle walls thin and fibrosed
Chamber space enlarged
Abnormal/un-coordinated myocardial contraction

SPACE NOT REDUCED just POOR contraction

25
Q

What type of heart failure is caused by filling problem?

A

HFpEF (preserved ejection fraction)

Filling (diastolic) problem

26
Q

Ventricles in HFpEF

A

Ventricle volume/capacity for blood is reduced
Ventricle chambers too sniff/not relaxed
Thickened walls

SPACE AVAILABLE REDUCED, EDV reduced

27
Q

How do we determine type of heart failure?

A

Measure ejection fraction (echocardiogram)

28
Q

Ejection fraction in different heart failures

A

HFrEF - ejection fraction reduced LOWER than 40%

HFpEF - ejection fraction greater/equal to 50% (normal ejection)

29
Q

HFrEF and HFpEF meaning

A

HFrEF - Heart failure with REDUCED ejection fraction (ejection problem)

HFpEF - Heart failure with PRESERVED ejection fraction (filling problem)

30
Q

How can a heart be failing if EF is maintained?

A

Filling problem: EDV reduced from smaller chamber size

Fraction still maintained BUT stroke volume is SMALLER = decreased cardiac output

31
Q

Ventricle most commonly involved in heart failure

A

Left

32
Q

Failure of both ventricles

A

Biventricular (congestive) heart failure

33
Q

What can cause isolated right ventricle failure (rare)

A

Chronic lung disease

34
Q

What can failure of one ventricle lead to?

A

Failure of the other ventricle

35
Q

Symptoms of HFrEF and HFpEF

A

Very similar:

Dyspnoea (breathlessness)
Fatigue (limiting exercise tolerance)
- due to hypoperfusion

Tissue fluid retention (pulmonary/peripheral oedema)

36
Q

Why perform an echocardiogram for heart failure?

A

Confirm diagnosis (identify structural/functional issues)
Identify potential cause (valve problem)
Implicates prognosis and treatment

37
Q

How does type of heart failure impact treatment?

A

HFrEF treatments have no effect on mortality/morbidity of patients with HFpEF

(only helps symptoms eg reduced oedema)

38
Q

what is HFrEF known as in left ventricle?

A

Left ventricular systolic dysfunction

39
Q

50% cases of heart failure

A

HFrEF of left ventricle (left ventricular systolic dysfunction)

40
Q

What happens to FranK starling curve in left ventricular systolic dysfunction?

A

LV pre load (EDV) increase leads to little increase in CO (shallow gradient curve)
Eventually increase filling = worsening CO (curve dips)
Develop pulmonary congestion

41
Q

What does reduced cardiac output trigger?

A

Neurohormonal activation to ‘correct’

42
Q

How is reduced cardiac output sensed and neurohormonal activation activated?

A

Reduced blood pressure

  • baroreceptors sense less stretch
  • Decreased renal perfusion
43
Q

Blood pressure =

A

cardiac output x TPR

44
Q

Neuro part

A

Baroreceptors sense drop in BP (low CO)
Increase sympathetic drive = increased heart rate and peripheral resistance
= increased afterload
= increased cardiac work

MAKES WORSE

45
Q

Hormonal activation

A

Decreased renal perfusion (from low BP) =
activation of renin-angiotensin-aldosterone system:

  • increased volume (Na+ and water reabsorption kidney, ADH release)
  • Vasoconstriction
46
Q

What does RAAS do?

A
Increases volume = increase pre load
Increases resistance (vasoconstriction) = increase afterload

= increase cardiac workload

47
Q

What happens due to neurohormonal activation?

A

Increased afterload + increased circulating volume

Increase pressures within ventricle (failing to eject volume, low CO)
Increased tissue fluid in interstitium - lungs and peripheries mostly
Cardiotoxic effects from long term activation of sympathetic nervous system

48
Q

How does pulmonary oedema occur?

A

Increase LV pressure (cannot eject volume sufficiently)
Increased pulmonary circulation pressure (venule end)
Increased hydrostatic pressure at venule end of capillary beds
No favourable gradient (hydrostatic and oncotic) for fluid to return to capillaries
Increased fluid volume in pulmonary interstitium

= pulmonary oedema (+/-peripheral oedema)

49
Q

Which failure = pulmonary oedema

A

left sided ventricular heart failure

50
Q

How does pulmonary oedema present?

A
Fluid in lungs on CXR
Dyspnoea 
Basal pulmonary crackles (auscilation)
Orthopnoea (dyspnoea worse at night)
Paroxysmal nocturnal dyspnoea (waking suddenly at night gasping for air)
51
Q

What happens in right ventricular heart failure? or left

A

Increased pressure RV
Increased systemic pressure (venule end)
Increased central venous pressure = increased jugular venous pressure
Increase hydrostatic pressure at venule end of systemic capillaries
Non favourable (hydrostatic and oncotic) gradient for return of fluid to capillaries
Tissue fluid accumulates in interstitial tissues (gravity dependent eg legs)

= peripheral oedema

52
Q

Peripheral oedema signs

A
Pitting oedema (legs)
(LV or RV heart failure can cause)

Raised jugular venous pressure (ONLY in RV failure)

53
Q

what can be used to indicate RV pressure?

A

Jugular venous pressure (right jugular vein)

54
Q

LV vs RV heart failure

A

Both:
Fatigue/lethargy
Breathlessness

LV:
pulmonary oedema and all symptoms +/- peripheral oedema
Cardiomegaly (displaced apex beat enlarged LV)

RV:
peripheral oedema
raised jugular venous pressure
tender, smooth and enlarged liver (congestion)

55
Q

How can peripheral oedema occur in LV failure?

A

Activation of RAAS due to lack of perfusion of kidney