Session 9-Pathophysiology Of Heart Failure

Question 1

What is the definition of heart failure relating to its pathophysiological state?

Answer 1

Pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolising tissues

Question 2

What is the definition of heart failure relating to it being a clinical syndrome?

Answer 2

Clinical syndrome caused by an abnormality of the heart and recognised by characteristic pattern of haemodynamic, renal, neural and hormonal responses

Question 3

What is the other definition of heart failure?

Answer 3

State in which heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

Question 4

What is the primary cause of systolic heart failure?

Answer 4

Ischaemic heart disease

Question 5

What is the approximate cardiac output of the heart?

Answer 5

~5 litres/min

Question 6

What is the approximate ejection fraction of the heart?

Answer 6

50-60%

Question 7

Which factors influence the cardiac output of the heart?

Answer 7

1) heart rate
2) venous capacity (LV preload)
3) aortic and peripheral impedance (after load)
4) myocardial contractility

Question 8

What does Starling’s Law of the heart say?

Answer 8

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

Question 9

What is the most common cause of heart failure?

Answer 9

Left ventricular systolic dysfunction

Question 10

What happens to the myocardial wall in left ventricular systolic dysfunction?

Answer 10

Thins due to:

• fibrosis and necrosis of myocardium
• activity of matrix proteinases

Question 11

Why does left ventricular systolic dysfunction lead to mitral valve incompetence?

Answer 11

Gap forms between the cusps due to dilatation of the ventricle

Question 12

What structural heart changes occur in left ventricular systolic dysfunction?

Answer 12

1) loss of muscle
2) uncoordinated or abnormal myocardial contraction
3) changes to extra cellular matrix: increase in collagen
4) change of cellular structure and function:
- sarcoplasmic reticulum dysfunction
- changes to calcium availability
- myocyte hypertrophy

Question 13

What are the long-term deleterious effects of an increased level of noradrenaline after heart failure?

Answer 13

1) beta-adrenergic receptors are down-regulated
2) noradrenaline induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha receptors
3) noradrenaline induces up-regulation of RAAS
4) reduction in heart rate variability (reduced parasympathetic and increased sympathetic nervous system)

Question 14

How does sympathetic activation in heart failure lead to myocardial hypertrophy?

Answer 14

1) myocardial damage
2) activation of sympathetic nervous system
3) RAAS -> fluid retention -> increased wall stress -> myocardial hypertrophy

OR

3) vasoconstriction -> increased wall stress -> myocardial hypertrophy

Question 15

How does sympathetic activation in heart failure lead to decreased contractility?

Answer 15

1) myocardial damage
2) activation of sympathetic nervous system
3) vasoconstriction -> increased wall stress -> increased myocardial oxygen demand -> decreased contractility

OR

3) increased heart rate and contractility -> increased myocardial oxygen demand -> decreased contractility

Question 16

How does sympathetic activation in heart failure lead to myocyte damage?

Answer 16

1) myocardial damage
2) activation of sympathetic nervous system
3) direct cardiotoxicity -> myocyte damage

Question 17

What effects does elevated angiotensin II have?

Answer 17

• potent vasoconstrictor
• promotes left ventricular hypertrophy and myocyte dysfunction
• promotes aldosterone release
• promotes Na+/H20 retention
• stimulates thirst by central action

Question 18

True or false: natriuretic hormones work in the same way as angiotensin

Answer 18

FALSE - opposite way

Question 19

What effect does atrial natriuretic hormone have on arterioles?

Answer 19

Constricts afferent and vasodilates efferent arterioles

Question 20

What effect does atrial natriuretic hormone have on Na+ reabsorption?

Answer 20

Decreases Na+ reabsorption in collecting duct

Question 21

What causes the release of natriuretic peptides?

Answer 21

Stretch or increase in cardiac chamber volume

Question 22

What can cause hypo-natraemia?

Answer 22

• increased water intake

- action of anti-diuretic hormone on V2 receptors in collecting duct

Question 23

True or false: normally, hypo-natraemia/hypo-osmolality inhibits anti-diuretic hormone release but its levels are increased in heart failure

Answer 23

TRUE

Question 24

Which cells secrete endothelin?

Answer 24

Vascular endothelial cells

Question 25

What is endothelin?

Answer 25

Potent system and renal vasoconstrictor acting via autocrine activity thus activating RAAS

Question 26

What happens to the level of endothelin in patients with heart failure?

Answer 26

Increases

Question 27

What stimulates prostaglandins E2 and I2?

Answer 27

Noradrenaline and RAAS

Question 28

What do prostaglandins E2 and I2 act as?

Answer 28

Vasodilators on afferent renal arterioles to attenuate effects of noradrenaline/RAAS

Question 29

Which cells produce nitric oxide?

Answer 29

Endothelial cells via nitric oxide synthase

Question 30

What does bradykinin promote?

Answer 30

Natriuresis and vasodilation | Production of prostaglandins

Question 31

What happens to the level of tumour necrosis factor in heart failure?

Answer 31

Increases

Question 32

What is net filtration pressure equal to?

Answer 32

Hydrostatic pressure - osmotic pressure

Question 33

How does heart failure affect capillary hydrostatic pressure?

Answer 33

Increases pressure

Question 34

What changes in skeletal muscle can alterations in vascular tone lead to?

Answer 34

- reduced skeletal muscle blood flow - reduction in skeletal muscle mass (cachexia) - abnormalities of structure and function - contribute to fatigue and exercise intolerance

Question 35

What renal changes can alterations in vascular tone lead to?

Answer 35

-increased Na+/water retention due to neuro--hormonal activation

Question 36

What are the cardiomyocytes like in heart failure with preserved ejection fraction (HFpEF)?

Answer 36

Thicker and shorter

Question 37

What can heart failure be divided into in clinical practice?

Answer 37

- left sided heart failure - right sided heart failure - biventricular (congestive) cardiac failure - LVSD (pump failure) - HFpEF (failure of LV relaxation)

Question 38

What are the signs/symptoms of left heart failure?

Answer 38

- fatigue - exertional dyspnoea - Orthopnoea - paroxysmal nocturnal dyspnoea (PND) - tachycardia - cardiomegaly - 3rd or 4th heart sound - functional murmur of mitral regurgitation - basal pulmonary crackles - peripheral oedema

Question 39

What can cause right heart failure?

Answer 39

- chronic lung disease - pulmonary embolism/pulmonary hypertension - left-to-right shunts - isolated right ventricular cardiomyopathy - pulmonary/tricuspid valvular disease

Question 40

What are the signs/symptoms of right heart failure?

Answer 40

- fatigue - dyspnoea - anorexia - nausea - increased jugular venous pressure - tender, smooth hepatic enlargement - dependent pitting oedema - ascites - pleural effusion

Question 41

What is left ventricular systolic dysfunction?

Answer 41

Increased LV capacity but reduced LV cardiac output

Question 42

What is heart failure with preserved ejection fraction?

Answer 42

Ejection fraction is normal, LV relaxation decreases, leading to impaired LV filling

Question 43

What are the risk factors for HFpEF?

Answer 43

``` Obesity Elderly Female Hypertension Diabetes ```

Question 44

Why is peripheral oedema seen in left heart failure?

Answer 44

Increased hydrostatic pressure in vessels