Heart Failure Flashcards

1
Q

What is heart failure?

A

A clinical syndrome of ruduced CO, tissue hypofusion and increased pulmonary pressurs and tissue congestion (oedema)

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2
Q

What is the name for when both the left and right ventricles fail?

A

Congestive heart failure

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3
Q

What are the signs and synptoms of left sided heart failure?

A
  • Fatigue
  • Breathless (around exertion)
  • Orthopnoea (shorting breath laying flat)
  • Paroxysmal nocturnal dysponea (waking up breathless neeing fresh air)
  • Basal pulmonary crackles
  • Cardiomegaly (displaced apex beat)
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4
Q

What are the signs and symptoms of right sidede heart failure?

A
  • Fatigue
  • Breathless
  • Pheripheral oedema (pitting)
  • Raised jugular venous pressure
  • Tender, smooth enlarged liver
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5
Q

What are the key presentations of a patient with heart failure?

A

Dysponea and fatigue (due to tissue hypofusion)

Increased fluid retention
LV failure= pulmonary, RV failure= peripheral

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6
Q

What causes heart failure?

A

Remodelling of cardiac muscle (loss of myoctes/ fibrosis) in response to changing ventricular function and shape/ size

Impairment of filling (decreased chamber size)
Impairment of ejection (decreased contraction)

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7
Q

What are common causes of heart failure?

A

Isceamic heart disease
Hypertension
Valvular disease
(Other)

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8
Q

What is a less common cause of heart failure?

A

High output failure

Increased demand on cardiac output NOT heart function decreasing

Eg, Sepsis

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9
Q

How is heart failure caused by ejection problems?

A

Contractility effected in systolic
Heart cant pump with enough force

Space available for filling NOT reduced just can’t empty ventricles

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10
Q

How is heart failure caused by a filling problem?

A

Less blood into ventricles in diastole
Volume available for blood to fill ventricles is reduced
End diastolic volume decreased

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11
Q

What results in ejection problems?

A

Muscle walls fibrosed
Chamber spaced enlarged (overstretched)
Abnormal myocyte contraction

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12
Q

What results in Filling problems?

A

Chambers stiff

Ventricular walls thickened

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13
Q

How to tell the differnece between ejection/ filling problem?

A

SV/ EDV= ejection fraction (EF)

If less than 50%= ejection (HFrEF)
If normal= filling (HFpEF)

EDV=end diastolic volume
HFrEF= heart failure with reduced ejection fraction
P= preserved

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14
Q

How can a preserved ejection fraction cause heart failure?

A

The contraction is not impaired so 50% of ventricle volume is still ejected but this is a small CO as origionally filled less

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15
Q

How can you determine between if heart failure if HFeEF or HFpEF?

A

Carry out an echocardiogram

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16
Q

What is the normal relationship between CO and end diastolic volume?

A

As EDV increases so does CO

Up to a certain point the CO dips

17
Q

What allows CO to increase with EDV?

A

Properties of cardiac myocytes

  • more stretch in ventricle during diastole= greater SV ejected in systole
  • more myocytes stretched harder they contact
18
Q

How does EDV and CO relationship different in a patient suffering from LV systolic heart failure?

A

Increased filling in failing heart = little increase in CO
(Eventually worsening CO)
Large increases in EDV (to try and increase SV) lead to reduced CO and pulmonary oedema

19
Q

How does the RAAS system contribute to heart failure?

A

Worsens the heart failure by increasing the cardiac work load

Has cardiotoxic effects from long term activation of sympa system and angiotensin 2

20
Q

How does the RAAS increase workload on the heart?

A

Increased the preload (larger EDV)-increased circulating blood volume by stimulating ADH

Increases the afterload- enhances sympathetic activity
-vasoconstriction

21
Q

How does the sympathetic nervous system respond to heart failure?

A

Increases cardiac demand

In response to lower CO and BP, increased sympa drive
Increased afterload

22
Q

How does pulmonary oedemas develop?

A

Increased pressure in LV (failure in ejection)
Increased pressure in pulmonary circulation (backtracks)
Increased pres at venuole end of cap bed
Less favourable hydro/oncotic press gradient
Increased fluid accumulation

23
Q

How do peripheral oedemas develop?

A

Increased pressure in RV (ejection failure)
Increased pressure in systemic circulations
Increased CVP= increased jugular VP
Unfavourable hydro/oncotic gradient at venule end cap beds
Increased volume of tissue fluid= oedema

24
Q

What drugs reduce CO and therefore reduces workload of the heart?

A

B-blockers (reduce BP and CO)
ACE inhibitors (stop effects of angiotensin 2)
Diuretics (reduce blood volume)
Ca channel blockers (reduce peripheral vasoconstriction)
Nitrates (vendodilation)

25
What key drug is given in the general management of heart failure?
Furosemide Immediately vendilatory Later onset diuretic action
26
What is the main blood test used to detect if actually heart failure?
NTpro-BNP | Which is a hormone released in response to stretch/ overfilling of fluid in chambers
27
What is BNP
A natriuretic peptide realised in response to severe heart failure in an attempt to reduce workload on heart
28
What is the sequence of treatments for heart failure?
``` Furosemide O2 (to raise sats) Resp support (cpac can reduce pulmonary oedema) Second line (eg, nitrates) ``` EGC CXR Transthorasic echocardiogram Surgery? (Fix cause is structural/ valve related)
29
How might anaemia effects heart failure?
Could worsen symptoms as heart having to work harder still as o2 carrying capacity reduced
30
How do Biventricular pacemakers aid in heart failure?
In HF right and left sides may not pump together and if out of sync left not able to pump enough Stimulates both sides to contract at the same time
31
How does a biventricular defibrillator work in heart failure treatment?
Detects dangerous/ abnormal rhythms and shocks heart back into normal Prevents life threatening rhythms developing in patients with heart failure
32
Why does prognostic treatment not work for HFpEF?
As due to stiffness of heart not high bp ect | Use only symptomatic treatments