302 Pathophysiology of heart failure Flashcards

1
Q

What is the definition of heart failure?

A

When the cardiac output does not meet the systemic requirements/demands

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2
Q

What are the causes of heart failure?

A

Ischaemic
hypertensive
arrhythmia related
cardiomyopathy
valvular
congenital

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3
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic: heart muscle is weak, and the ventricle can’t contract normally

Diastolic: heart muscle is stiff, and the left ventricle can’t relax normally

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4
Q

What are the symptoms of right sided heart failure?

A

Fatigue
Increased peripheral venous pressure
Ascites
Enlarged liver and spleen
Distended jugular veins
Anorexia and GI stress
Weight gain
Dependent oedema

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5
Q

What is Cor pulmonale?

A

It causes the right side of the heart to fail

Long-term high blood pressure in the arteries of the lung and right ventricle of the heart can lead to cor pulmonale

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6
Q

What is dependent oedema?

A

Oedema specific to parts of the body that that are influenced by gravity
Eg, arms and legs

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7
Q

What are the symptoms of left sided heart failure?

A

Paroxysmal nocturnal dyspnoea
Pulmonary congestion
-Cough, crackles, wheeze, bloody sputum
Restlessness
Orthopnoea
Tachycardia
Fatigue
Cyanosis

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8
Q

What is end Systolic volume?

A

The amount left in the heart after a heart beat

This is dependent on contractility and resistance to flow out of the heart

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9
Q

What is preload?

A

Volume of blood left after diastole

Increases in:
Hypovolaemia
Regurgitation
Heart failure

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10
Q

How do the kidneys impact cardiac output and blood pressure?

A

The kidneys help regulate blood volume and total peripheral resistance

Low arterial pressure reaching the afferent arteriole in the renal glomerulus causes the release of renin from juxtaglomerular (JG) cells.

Beta adrenoreceptors on the JG cells respond to sympathetic nerve stimulation by releasing renin.

Additionally Macula densa cells of the distal tubules sense the concentration of sodium and chloride ions in the tubular fluid. If this is reduced this leads to renin release by the JG cells.

Renin acts on the angiotensinogen which is converted to angiotensin I.
The enzyme Angiotensin converting enzyme converts this to angiotensin II

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11
Q

What is the role of Angiotensin II?

A

-Causes arterial vasoconstriction increasing TPR and arterial pressure
-Stimulates sodium transport (resorption) in the renal tubules increasing sodium and water retention
-Acts at the adrenal glands to release aldosterone which also acts at the kidneys to increase sodium and water retention
-Stimulates the release of vasopressin (antidiuretic hormone) from the posterior pituitary also increasing sodium and water retention
-Enhances sympathetic activity
-Stimulate cardiac hypertrophy and vascular hypertrophy

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12
Q

What is the role of ANP and BNP?

A

-They both cause venous dilatation (increasing venous compliance) and reduce venous return and preload.
-They act at the kidneys to increase glomerular filtration increasing sodium and water excretion.

This is a counter regulatory system to the RAAS

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13
Q

What is the difference between ANP and BNP?

A

ANP signals in an endocrine and paracrine manner to decrease blood pressure and cardiac hypertrophy

BNP acts locally to reduce ventricular fibrosis

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