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Semester 2-CVS > Session 9-Pathophysiology Of Heart Failure > Flashcards

Session 9-Pathophysiology Of Heart Failure Flashcards

1
Q

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

A

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

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2
Q

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

A

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

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3
Q

What is the other definition of heart failure?

A

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

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4
Q

What is the primary cause of systolic heart failure?

A

Ischaemic heart disease

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5
Q

What is the approximate cardiac output of the heart?

A

~5 litres/min

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6
Q

What is the approximate ejection fraction of the heart?

A

50-60%

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7
Q

Which factors influence the cardiac output of the heart?

A

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

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8
Q

What does Starling’s Law of the heart say?

A

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

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9
Q

What is the most common cause of heart failure?

A

Left ventricular systolic dysfunction

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10
Q

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

A

Thins due to:

  • fibrosis and necrosis of myocardium
  • activity of matrix proteinases
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11
Q

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

A

Gap forms between the cusps due to dilatation of the ventricle

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12
Q

What structural heart changes occur in left ventricular systolic dysfunction?

A

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

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13
Q

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

A

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)

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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

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

A

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

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17
Q

What effects does elevated angiotensin II have?

A
  • potent vasoconstrictor
  • promotes left ventricular hypertrophy and myocyte dysfunction
  • promotes aldosterone release
  • promotes Na+/H20 retention
  • stimulates thirst by central action
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18
Q

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

A

FALSE - opposite way

19
Q

What effect does atrial natriuretic hormone have on arterioles?

A

Constricts afferent and vasodilates efferent arterioles

20
Q

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

A

Decreases Na+ reabsorption in collecting duct

21
Q

What causes the release of natriuretic peptides?

A

Stretch or increase in cardiac chamber volume

22
Q

What can cause hypo-natraemia?

A
  • increased water intake

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

23
Q

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

A

TRUE

24
Q

Which cells secrete endothelin?

A

Vascular endothelial cells

25
Q

What is endothelin?

A

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

26
Q

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

A

Increases

27
Q

What stimulates prostaglandins E2 and I2?

A

Noradrenaline and RAAS

28
Q

What do prostaglandins E2 and I2 act as?

A

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

29
Q

Which cells produce nitric oxide?

A

Endothelial cells via nitric oxide synthase

30
Q

What does bradykinin promote?

A

Natriuresis and vasodilation

Production of prostaglandins

31
Q

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

A

Increases

32
Q

What is net filtration pressure equal to?

A

Hydrostatic pressure - osmotic pressure

33
Q

How does heart failure affect capillary hydrostatic pressure?

A

Increases pressure

34
Q

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

A
  • reduced skeletal muscle blood flow
  • reduction in skeletal muscle mass (cachexia)
  • abnormalities of structure and function
  • contribute to fatigue and exercise intolerance
35
Q

What renal changes can alterations in vascular tone lead to?

A

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

36
Q

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

A

Thicker and shorter

37
Q

What can heart failure be divided into in clinical practice?

A
  • left sided heart failure
  • right sided heart failure
  • biventricular (congestive) cardiac failure
  • LVSD (pump failure)
  • HFpEF (failure of LV relaxation)
38
Q

What are the signs/symptoms of left heart failure?

A
  • 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
39
Q

What can cause right heart failure?

A
  • chronic lung disease
  • pulmonary embolism/pulmonary hypertension
  • left-to-right shunts
  • isolated right ventricular cardiomyopathy
  • pulmonary/tricuspid valvular disease
40
Q

What are the signs/symptoms of right heart failure?

A
  • fatigue
  • dyspnoea
  • anorexia
  • nausea
  • increased jugular venous pressure
  • tender, smooth hepatic enlargement
  • dependent pitting oedema
  • ascites
  • pleural effusion
41
Q

What is left ventricular systolic dysfunction?

A

Increased LV capacity but reduced LV cardiac output

42
Q

What is heart failure with preserved ejection fraction?

A

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

43
Q

What are the risk factors for HFpEF?

A 
Obesity
Elderly
Female
Hypertension
Diabetes
44
Q

Why is peripheral oedema seen in left heart failure?

A

Increased hydrostatic pressure in vessels

Semester 2-CVS (18 decks)

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