CVS - heart failure Flashcards

1
Q

Define ‘heart failure’:

A

A state in which the heart fails to maintain an adequate circulation for the needs of the body, despite an adequate filling pressure.

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2
Q

What is the primary cause of systolic heart failure?

A

Ischaemic heart disease.

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3
Q

What can cause dilated cardiomyopathy?

A
  1. Bugs (viral, bacterial, mycobacteria)
  2. Alcohol/ drugs/ posioning
  3. Pregnancy
  4. Idiopathic
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4
Q

What is dilated cardiomyopathy?

A

A condition in which the heart’s ability to pump blood is decreased because the heart’s main pumping chamber, the left ventricle, is enlarged and weakened. In some cases, it prevents the heart from relaxing and filling with blood as it should.

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5
Q

What is restrictive cardiomyopathy?

A

A rare form of heart muscle disease that is characterised by restrictive filling of the ventricles. In this disease the contractile function of the heart and wall thicknesses are usually normal, but the relaxation or filling phase of the heart is very abnormal.

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6
Q

How is progression of heart failure measured?

A

New York Heart Association (NYHA) functional classification. Class 1 (asymptomatic) to Class IV (inability to carry out any physical activity without symptoms).

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7
Q

What is the mortality of Class IV heart failure?

A

It is 80% in 3 years. This is the same as Stage 3 lung cancer. Therefore palliative care has a large role to play in these individuals.

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8
Q

What is the normal ejection fraction of the heart?

A

50% plus (LV end diastolic volume is ~150ml, LV end systolic volume is ~75ml, stroke volume is therefore ~75ml).

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9
Q

What factors affect the cardiac ouput?

A
  1. HR
  2. Venous capacity (LV preload)
  3. Aortic and peripheral impedance (after-load)
  4. Myocardial contractility
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10
Q

What is Starling’s Law of the heart?

A

That the force developed in a muscle fibre depends on the degree to which it is stretched (e.g. the greater the preload the greater the contractility).

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11
Q

What happens to a Starling’s curve in mild heart failure?

A

The cardiac output at each end diastolic pressure is decreased compared to normal. E.g. at a given preload the contractility is decreased.

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12
Q

What happens to Starling’s curve in congestive heart failure? What are the implications for this on the treatment of congestive heart failure?

A

A point is reached where increasing the preload further can actually decrease the cardiac output. This is important as patients with cardiac failure tend to get fluid overload. Therefore have to get the diuretic treatment just right to get the optimum cardiac output.

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13
Q

What happens to the left ventricle capacity in systolic dysfuction? What effect does this have on cardiac output?

A

It is increased. This reduces the left ventricle cardiac ouput.

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14
Q

What causes thinning of the myocardial wall in systolic dysfunction?

A

Fibrosis and necrosis of myocardium (e.g. from a MI) and activity of matrix proteinases.

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15
Q

Why does mitral valve incompetence occur in systolic dysfunction?

A

Thinning of the myocardial wall and enlarging of the left ventricle pulls the cusps of the valves apart from each other.

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16
Q

Why can systolic dysfunction lead to sudden death?

A

It predisposes to cardiac arrhythmias, particularly ventricular arrhythmias, which can lead ventricular fibrillation and death.

17
Q

Why does water retention occur with systolic dysfunction?

A

because it activates neuro-hormonal mechanisms such as the RAAS system.

18
Q

What general structural heart changes occur in heart failure?

A
  1. Loss of muscle
  2. Uncoordinated or abnormal myocardial contraction
  3. Changes to the extracellular matrix
  4. Changes to cellular structure and function
19
Q

What changes to the extracellular matrix occur in heart failure?

A
  1. Increase in collagen 3 cf. to collagen I (from 5-25%)

2. Slippage of myocardial fibre orientation.

20
Q

What changes to cellular structure and function occur in heart failure?

A
  1. Myocytolysis and vacuolation of cells
  2. Myocyte hypertrophy
  3. SER dysfunction
  4. Changes to Ca2+ availability and/ or receptor regulation
21
Q

What happens to the structure of the heart after a MI?

A
  1. The initial infarct occurs
  2. Expansion of infarct (hours to days)
  3. Global remodelling -> ventricle dilation (days to months)
22
Q

Describe the broad ventricular modelling that occurs in diastolic heart failure:

A

The heart hypertrophies (this is usually in response to hypertension).

23
Q

Describe the broad ventricular modelling that occurs in systolic heart failure:

A

The heart dilates - this is often caused by MI or coronary disease.

24
Q

How does heart failure activate the RAAS?

A
  1. SNS induction of renin from macula densa (kidney)
  2. Decrease in renal perfusion causes juxtaglomerular cells to release the enxyme renin, which converts angiotensin to angiotensin I.
25
Q

What early compensatory affects does the sympathetic nervous system have on heart failure?

A

In a baroreceptor-mediated response, there is an early compensatory mechanism to improve cardiac ouput:

  1. Increased cardiac contractility
  2. Arterial and venous vasoconstriction
  3. Tachycardia
26
Q

What are the long-term deleterious effects of the sympathetic nervous system on heart failure?

A
  1. Beta-adrenergic receptors are down-regulated/ uncoupled.
  2. Noradrenaline induces:
    (i) cardiac hypertrophy/ myocyte apoptosis and necrosis via alpha-receptors
    (ii) induce up-regulation of RAAS
27
Q

What are the effects of elevated angiotensin II?

A
  1. Vasoconstriction
  2. Promotes LVH and myocyte dysfunction
  3. Promotes aldosterone release
  4. Promotes Na+/water retention
  5. Stimulates thirst by central action?
28
Q

What causes the release of natriuretic peptides? What is their function?

A

Stretch or increase in cardiac chamber volume leads to their release. They cause vasodilation and increased urinary sodium excretion which balances the effects of the RAAS on the vascular tone and water balance.