Heart failure Flashcards

1
Q

what is heart failure?

A

failure of the heart to meet bodily demands

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2
Q

what factors affect SV (and therefore CO)?

A

increased contractility + pre-load = increased SV
increased after-load = decreased SV

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3
Q

what is the relationship between pre-load and SV?

A

increased blood vol in ventricle at end of dyastole causes ventricles to stretch more during systole so greater force of contraction = increased SV

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4
Q

what factors increase contractility of ventricular myocytes?

A

greater stretch of ventricle = increased contractility
greater sympathetic activity = increased contractility

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5
Q

what are the causes of heart failure?

A

most common = ischaemic heart disease
other causes = hypertension, arrhythmias, valvular disease

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6
Q

how does ischaemic heart disease cause heart failure?

A

remodelling 2 types:
ventricular hypertrophy = reduced filling = decreased pre load = decreased SV = decreased CO
ventricular walls are thinner but cant contract well = decreased contractility = decreased SV = decreased CO

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7
Q

what are the 2 broad types of heart failure?

A

HFpEF = heart failure where filling of the heart is the issue
HFrEF = heart failure where emptying of heart is the issue

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8
Q

how do we measure ejection fraction?

A

using echocardiogram
SV / EDV
normal = > 50%

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9
Q

how does ejection fraction differ in HFpEF and HFrEF?

A

HFrEF = < 40%
HFpEF = > 50%

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10
Q

what are the common symptoms of heart failure?

A

dyspnoea (breathlessness)
fatigue (reduced exercise tolerance)
pulmonary or peripheral oedema

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11
Q

what is the most common type of heart failure?

A

left ventricular systolic dysfunction (left ventricular HFrEF)
* ventricle size is normal or thinner but decreased contractility

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12
Q

what is the impact of increasing pre-load in a failing heart?

A

(first think about why it would be good in a healthy heart)
1. increased pre-load has little effect on increasing CO
2. eventually increasing pre-load decreases CO
3. increased fluid in ventricles = increased pressure
4. increased pressure in pulmonary circulation = pulmonary congestion

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13
Q

what happens when the CO decreases?

A

CO = BP x TPR
1. decreased CO = decreased BP
2. decreased BP activates 2 pathways
3. detected by baroreceptors or decreased renal perfusion
* detected by baroreceptors = increased HR and increased TPR
* decreased renal perfusion activates RAAS = increased Na+ and fluid retention in kidney = increased pre-load

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14
Q

how does left ventricular systolic dysfunction cause pulmonary oedema?

A
  1. increased pressure in LV
  2. increased pressure in pulmonary circulation
  3. increased hydrostatic pressure in venule end
  4. less favourable gradient between hydrostatic and oncotic pressure
  5. increased interstitial fluid accumulation = pulmonary oedema
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15
Q

although less common, how can left ventricular systolic dysfunction cause peripheral oedema?

A
  1. reduced renal perfusion = activation of RAAS
  2. increased Na+ and H20 retention
  3. accumulates in lower extremeties due to gravity
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16
Q

how does right ventricular HFrEF cause peripheral oedema?

A
  1. increased pressure in RV = increased pressure in systemic circulation
  2. increased central venous pressure = increased jugular venous pressure
  3. increased hydrostatic pressure in venule end of capillary
  4. less favourable gradient between hydrostatic + oincotic pressure
  5. increased accumulation of fluid in interstitial space
17
Q

what is the NYHA classification of heart failure?

A

Class I
Class 2
Class 3
Class 4

18
Q

what is class I heart failure?

A

no symptomatic limitations of physical activity

19
Q

what is class II heart failure?

A

slight limitation of physical activity
normal physical activity = symptoms
no symptoms at rest

20
Q

what is class III heart failure?

A

marked limitation of physical activity
less than normal physical activity causes symptoms
no symptoms at rest

21
Q

what is class IV heart failure?

A

inability to carry out any physical activity without symptoms
may have symptoms at rest
discomfort increases with level of physical activity

22
Q

what is heart failure treated?

A

aim is to decrease pre-load:
ACE inhibitors (decreased Na+ and water retention)
beta blockers (decreased contractility and HR)
diuretics (decreased Na+ and water retention)

23
Q

how is acute heart failure managed + treated?

A

manaage: do chest X-ray and look for ABCDE, blood work (NTpro-BNP, FBC, urea + electrolytes)
treat: IV furosemide, O2 + respiratory support

24
Q

what does furosemide do?

A
  1. immediate vasodilating effects
  2. diuretic action roughly 30 min after given
  3. acts to decrease vol + pre load
25
Q

what are the effects of the RAAS in heart failure?

A

ultimately results in:
1. increased Na+ and water retention (increases pre load)
2. vasoconstriction
3. increased sympathetic activity (increases contractility of heart)

26
Q

what is effect of sympathetic activity in heart failure?

A

ultimately results in:
1. myocardial hypertrophy
2. decreased contractility
3. myocyte damage

27
Q

what are the physiological effects of beta blockers?

A

decrease HR
decrease BP
decrease mobilisation of glycogen