9- Heart Failure Flashcards

1
Q

Define heart failure

A

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

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2
Q

What are the main causes of heart failure?

A
Ischaemic heart disease 
Hypertension 
Congenital/ valvular disease 
Arrhythmia 
Dilated cardiomyopathy (pregnancy/alcohol/bacteria)
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3
Q

Explain the classification of heart failure

A

Class I- no symptomatic limitation
II - normal physical activity results in symptoms
III - less than normal physical activity results in symptoms, marked limitation of physical activity
IV- unable to do any physical activity without symptoms, symptoms at rest

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4
Q

Explain heart failure in terms of starlings law

A

The heart cannot produce the same amount of force for a given level of filling (stretch of fibres)

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5
Q

What happens to the heart in left ventricular systolic dysfunction?

A

Increased left ventricular capacity
Reduced LV output
Myocardial wall thins due to fibrosis/necrosis and matrix proteinases destroying collagen
Mitral valve incompetence as LV dilates
Weakened heart adversely affected by adrenaline surges
Cardiac arrhythmias

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6
Q

What structural changes can lead to heart failure?

A

Bundle branch blocks: change in contractility
Extracelluar matrix protein changes, increased collagen III
Cellular structure/function changes (myocyte hypertrophy, sER dysfunction)

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7
Q

Describe the two main pathways to heart failure

A

High BP, LV hypertrophy, increased afterload, global thinning of wall
MI, remodelling, scar tissue forms and thins area of infarct
Both increase LV size and capacity, reducing cardiac output

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8
Q

What does the sympathetic nervous system do in heart failure and what effect does this have?

A

Up-regulates RAAS - leading to fluid retention and LV hypertrophy
Vasoconstriction - increases wall stress, LV hypertrophy and decreased contractility
Increases heart rate and contractility - increases myocardial demand for oxygen leading to decreased contractility
Beta adrenergic receptors down regulated
Noradrenaline induces hypertrophy/necrosis via alpha receptors

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9
Q

How is RAAS activated in heart failure?

A

Reduced renal blood flow

Sympathetic stimulation releasing renin from macula densa

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10
Q

What are the effects of increased angiotensin II?

A

Vasoconstriction
Aldosterone release, leading to Na and H2O retention, which increases blood volume, increasing afterload, LV hypertrophy
Organ damage

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11
Q

What receptor does Angiotensin II bind to?

A

AT1 receptor

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12
Q

What effect does angiotensin II have on the brain?

A

Atherosclerosis
Vasoconstriction
Leading to stroke

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13
Q

What effect does,angiotensin II have on vasculature?

A

Vascular hypertrophy
Endothelial dysfunction
Leading to hypertension

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14
Q

What effect does angiotensin II have on the heart?

A
LV hypertrophy 
Fibrosis 
Remodelling 
Apoptosis 
Leading to heart failure and MI
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15
Q

What effect does angiotensin II have on the kidneys?

A

Decreased glomular filtration rate
Increased proteinuria
Increased aldosterone release
Renal failure

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