19. The Pathophysiology of Heart Failure Flashcards Preview

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Flashcards in 19. The Pathophysiology of Heart Failure Deck (40)
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1
Q

What is 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.

2
Q

What is the primary cause of heart failure?

A

Ischaemic heart disease.

3
Q

What are the four classes of heart failure progression according to the NYHA functional classing?

A

Class I - asymtpomatic limitation of physical activity.
Class II - slight limitation of physical activity, normal activity results in symptoms, but none at rest.
Class III - marked limitation of physical activity, less than normal activity results in symptoms, but none at rest.
Class IV - symptoms with any physical activity, even some at rest, discomfort increases with degree of physical activity.

4
Q

What are the 6 year mortality rates for Class I, II, and III heart failure?

A

Class I - 60%.

Class II and III - 40%.

5
Q

What is the 3 year mortality rate for Class IV heart failure?

A

80%.

6
Q

What is Starling’s law for cardiac output and filling?

A

The force developed in a muscle fibre depends on the degree to which the fibre is stretched.

7
Q

What happens to Starling’ curve for cardiac output and filling with mild heart failure and gross heart failure?

A

Mild - output increases with filling, but not to the efficient extent of normal heart function.
Gross - output increases with filling to an extent but then starts to decrease again.

8
Q

What is the pathology of systolic dysfunction?

A

There is an increase left ventricular capacity, but reduced cardiac output. This leads to thinning of the myocardial wall and mitral valve incompetence as the ventricle dilates but the valve is the same size. This can lead to cardiac arrhythmias.

9
Q

What happens structurally to the heart with systolic dysfunction?

A

Loss of muscle which is replaced by scar tissue, that can’t contract. There is uncoordinated contraction of the myocardium. More collagen in the extracellular matrix. Myocyte hypertrophy.

10
Q

What is involved in neuro-hormonal activation on the heart?

A

The sympathetic nervous system, renin-angiotensin-aldosterone system, natriuretic hormones, anti-dieuretic hormone, endothelin, prostaglandins/ nitric oxide, kallikrien system, tissue necrosis factor.

11
Q

What is the early compensatory mechanism to increase CO from the sympathetic nervous system acting on the failing heart?

A

Baroreceptor-mediated response to raise cardiac contractility, cause vasovonstriction of arteries and veins, and also tachycardia.

12
Q

How is the sympathetic nervous system’s compensatory reaction to heart failure deleterious long term?

A

The B-adrenergic receptors are down-regulated/ uncoupled. Noradrenaline induces cardiac hypertrophy/ myocyte apoptosis and necrosis via a-receptors.

13
Q

What happens to angiotensinogen in the RAAS?

A

Angiotensinogen is cleaved to angiotensin I, which is cleaved to angiotensin II, which acts on AT1R and AT2R receptors. Angiotensin I and II are hydrolysed by NEP to angiotensin III.

14
Q

What does an increase in angiotensin II cause in the RAAS?

A

Acts on AT2R receptors which raise nitric oxide levels.

15
Q

What happens to bradykinin in the RAAS?

A

It goes to Bk2R which raises nitric oxide levels.

16
Q

Which receptor does angiotensin II act on to cause damage?

A

AT1R.

17
Q

What can angiotensin II cause damage to?

A

The brain, the vasculature, the heart, and the kidneys.

18
Q

Why is the RAAS activated in heart failure?

A

There is less blood to the kidneys, so SNS induction of renin from macula densa.

19
Q

What are some of the actions of angiotensin II?

A

It is a potent vasoconstrictor, causes left ventricular hypertrophy and myocyte dysfunction, promotes aldosterone release, promotes Na+/H2O retention, and stimulates thirst.

20
Q

What can natriuretic hormone be a marker of?

A

Heart failure, although it is affected by other things too.

21
Q

What do natriuretic hormones balance the effects of?

A

RAAS on the vascular tone and Na+/H2O balance.

22
Q

What does anti-dieuretic hormone being increased in heart failure mean?

A

There is increased H2O retention and tachycardia with reduced systemic resistance resulting in increased cardiac output.

23
Q

What is endothelin secreted by?

A

Vascular endothelial cells.

24
Q

What is the action of endothelin?

A

Renal vasoconstrictor so activates RAAS.

25
Q

How does endothelin suggest prognosis of heart failure?

A

Levels are raised in heart failure, so high levels suggest poor prognosis.

26
Q

What are prostaglandin E2 and I2 stimualted by?

A

NA and RAAS.

27
Q

What do prostaglanin E2 and I2 do?

A

Act as vasodilators on afferent renal arterioles to attenuate effects of NA and RAAS.

28
Q

What is nitric oxide produced by?

A

Endothelial cells via NO synthase.

29
Q

What is the action of nitric oxide?

A

A powerful vasodilator.

30
Q

What does bradykinin promote?

A

Natriuresis and vasodilatation, also production of PGs.

31
Q

How does skeletal muscle change in heart failure?

A

Reduced skeletal muscle blood flow, reduction in skeletal muscle mass, and abnormalities of structure and function.

32
Q

What are the complications in diastolic dysfunction?

A

Reduced LV compliance, impaired myocardial relaxation, impaired diastolic left ventricular filling and pulmonary artery pressures, can’t compensate for cardiac output - so low.

33
Q

What are the five types of heart failure?

A

Right sided heart failure, left sided heart failure, biventricular (congestive) heart failure, systolic heart failure, diastolic heart failure.

34
Q

What are the symptoms of left heart failure?

A

Fatigue, exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea.

35
Q

What are the signs of left heart failure?

A

Tachycardia, cardiomegaly, 3/4th heart sound, functional murmur of mitral regurgitation, basal pulmonary crackles, peripheral oedema.

36
Q

What is the aetiology of right heart failure?

A

Chronic lung disease, pulmonary embolism/ hypertension, pulmonary or tricuspid valvular disease, left-to-right shunts, isolated right ventricular cardiomyopathy.
Most common: secondary to left heart failure.

37
Q

What are the symptoms of right heart failure?

A

Fatigue, dyspnoea, anorexia, nausea.

38
Q

What are the signs of right heart failure?

A

Increased jugular venous pressure, ascites, pleural effusion, tender, smooth hepatic enlargement.

39
Q

How can heart failure be treated?

A

Treat underlying cause, lifestyle modifications, pharmacological, cardiac surgery, implantable pacemakers, and implantable defribillators.

40
Q

How do ACE-inhibitors affect the RAAS?

A

It stops conversion of angiotensin I to angiotensin II so it can’t act on AT1 receptors that would cause vasoconstriction.