Pathophysiology of heart failure Flashcards

1
Q

Main causes of heart failure =

A
Ischemic heart disease
Hypertension
Dilated Cardiomyopathy 
Congenital 
Valvular etc.
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2
Q

New descriptions of HF

A

Acute

Chronic

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3
Q

Pre-load =

A

Venous return.

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4
Q

Filling pressure =

A

the pressure in the ventircles just before it starts to contract

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5
Q

What does increased preload do (Starlings’ law)

A

Stretches myocardial fibres and myocardial contraction increases/is restored

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6
Q

After load =

A

Outflow resistance/peripheral resistance.

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7
Q

What causes outflow resistance?

A

Pulmonary and systemic resistance

Volume of blood ejected

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8
Q

If preload/end diastolic volume increases, what does this do to after load?

A

Increases after load

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9
Q

What is increased in HF, SNS or PNS

A

SNS - originally to provide inotrophic support, chronically increases neurohormonal activation and myocyte apoptosis

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10
Q

What can happen to LV during remodelling

A

Hypertrophy
Intersistial fibrosis
Loss of myocytes

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11
Q

Acute heart failure =

A

Rapid onset of symptoms and signs of HF

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12
Q

Examples of acute HF presenation:

A

Pulmonary oedema
Anasarca
Cardiogenic shock

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13
Q

Starlings law in relation to HF

A

As muscle failures, need to increase preload to get ventricles to work.

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14
Q

What occurs in left ventricular pump failure to increase the BP

A
  • fall in Bp - increased sympathetic - vasoconstriction - increase afterload
  • fall in renal perfusion - RAAS - retention - increased preload
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15
Q

Clinical features of pulmonary oedema:

A
Tachypnoea
Orthopnoea
Crackles
Use of accessory muscles
Pink frothy sputum
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16
Q

O2 sat in pulmonary oedema

A

<90%

17
Q

What can be seen of CXR in pulomonary oedema due to heart failure =

A
Enlarged heart (>50%)
Kerley B lines (straight horizontal lines)
18
Q

Normal pressure in lungs

A

Colloid = hydrostatic. Small amount of fluid leaves and is drained

19
Q

Formation of pulmonary oedema

A

Blood backs up into pulmonary capillaires - increased hydrostatic pressure - more fluid into interstitial space.

20
Q

What is anasarca?

A

Generalied oedema

21
Q

What sided HF does anasarca occur in?

A

Right

22
Q

Features of anasarca:

A

Peripheral oedema
Acities
Pleural effusions

23
Q

Anasarca develops over

A

Days - weeks

24
Q

What might a patient with anasarca notice?

A

Gradual weight gain

25
Q

What causes anasarca?

A

Fall in CO - fall in renal perfusion - increased ADH and aldosterone - Na+ and H2O retention

26
Q

3 features of chronic heart failure =

A

a. symptoms of HF
b. evidence of cardiac dysfunction (imaging, ECG)
c. response to treatment

27
Q

4 models of progression of chronic heart failure =

A
  1. Haemodynamic
  2. Neurohormonal
  3. Peripheral
  4. Metabolic
28
Q

Haemodynamic model:

A
Pump failure results in reduced BP and renal perfusion 
Increased sympathetic and RAAS
Vasoconstriction and Na+/H2O 
Increased afterload and preload
Worsens
29
Q

Neurohormonal:

A
Increased ANP, BNP
Increased ADH
Increased Endothelin
Increased RAAS
Adrenergic activation
30
Q

Endothelin function

A

Vasoconstriction

31
Q

Natriuretic peptides function

A

Vasodilation
Increased Na+/H2O excretion
Inhibit renin, ACE

32
Q

What hormones can cause fibrosis within the heart?

A

Aldosterone

33
Q

ANP =

A

Atrial natriuretic peptide

34
Q

BNP =

A

B-type naturietic peptide

35
Q

What is always raised in HF?

A

BNP

36
Q

In HF there is a switch from what to what (peripheral model)

A

Type 1 slow twitch to type 2 fast twitch skeletal muscle

37
Q

Increased ventilation increases exercise =

A

Ergoreflex

38
Q

In HF there is a shift between (catabolism/anabolism) to (catabolism/anabolism)

A

Anabolism to catabolism

39
Q

Metabolic model:

A

Increased cost/energy cost

Resistance to anabolic hormones