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CAR > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Hydrostatic pressure

A
  • Outward filtration pressure
  • Exerted against the inner capillary wall
  • Promotes the formation of tissue fluid
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2
Q

Colloid osmotic pressure

A
  • Inward absoprtion pressure
  • Exerted by plasma proteins which are too big to leave the capillary
  • Promotes fluid reabsorption into the circulatory system
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3
Q

How does capillary hydrostatic pressure change over the course of the capillary?

A
  • It is higher at the arterial around (~32mmHg) than the venous end (~15mmHg)

*Do not need to memorise numbers*

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4
Q

Describe the two main categories for heart failure causes

A
  • Congenital (rare)
  • Acquired
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5
Q

What are some causes of heart failure?

A
  • Degenerative valve disease
  • Cardiomyopathy
  • Valve/endocardial infection
  • Pericardial disease
  • Rate/rhythm abnormalities
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6
Q

Cardiomyopathy

A

Disease of the heart muscle. The muscle function is poor and the heart does not pump effectively.

It develops later in life.

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7
Q

True/false: there are inherited forms of cardiomyopathy in cattle.

A

True.

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8
Q

What is the most common form of cardiomyopathy in dogs?

A

Dilated

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9
Q

What is the most common form of cardiomyopathy in cats?

A

Restrictive. This is due to hypertrophy of the walls of the heart.

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10
Q

How does hypertrophy, as seen with restrictive cardiomyopathy in cats, affect heart function?

A
  • The heart becomes thick-walled
  • There is hardly any lumen for the blood to be in during diastole (thus filling of the heart between beats is compromised)
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11
Q

What type of hypertrophy is shown here?

A

Concentric hypertrophy

The external diameter of the heart in unchanged, but the internal diameter has narrowed due to deposition of additional muscle within the ventricle lumen.

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12
Q

Differentiate between eccentric and concentric hypertrophy

A
  • Eccentric hypertrophy: both internal and external diameter increase (heart = like balloon). This occurs with volume loading e.g. dilated cardiomyopathy, valve incompetence.
  • Concentric hypertrophy: external diameter of heart unchanged, internal diameter (lumen) narrows. Occurs with pressure loading e.g. hypertension and aortic/pulmonic stenosis.
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13
Q

What is valve stenosis?

A

Type of valvular heart disease where the valve narrows and doesn’t open fully.

Aortic stenosis → reduces blood flow from left ventricle to aorta

Pulmonic stenosis → reduces blood flow from right ventricle to pulmonary artery

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14
Q

What is the cardiovascular system’s main aim (the one that tends to take priority over all others)?

A

Maintenance of blood pressure

This is very important as some tissue have very particular perfusion pressure requirements e.g kidneys

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15
Q

Why might preload fall in an animal with a very high heart rate?

A

The heart rate may be so high that the heart does not have time to fill.

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16
Q

This diagram shows how different causes of heart failure can all have the downstream impact of less forward flow.

Fill in the blanks.

A
17
Q

1 and 2

A
18
Q

3

A
19
Q

4

A
20
Q

Describe the incidence and causes of acute heart failure

A
  • Acute heart failure is common in people but rare in animals
  • In people, acute heart failure is caused by vascular disease/acute myocardial infarct
21
Q

What mechanisms are activated to restore blood pressure when it falls?

What is the eventual consequence of these mechanisms being continually employed?

A
  1. Sympathetic nervous system activation
  2. Renin Angiotensin Aldosterone System (RAAS)

Eventually, this will result in cardiac enlargement.

22
Q

What are the clinical signs of heart failure?

A

Case/species dependent. Broadly:

  • Coughing
  • Panting
  • Dyspnoea/elevated respiratory rate even at rest
  • Exercise reluctance
  • Tiring faster with previously-tolerated exercise
  • Fatigue
  • Blue-tinged gums (cyanosis)
23
Q

Describe how sympathetic nervous system activation increases blood pressure.

Include: neurotransmitter involved, receptors involved, location, effect.

A
24
Q

Which works faster: SNS activation or RAAS?

A

SNS activation

RAAS is still reasonably quick though.

25
Q

Describe how the Renin Angiotensin Aldosterone System (RAAS) responds to low blood pressure.

A
26
Q

What does ACE represent in this diagram?

A

Angiotensin-converting enzyme.

It converts Angiotensin I to Angiotensin II.

27
Q

Aldosterone causes renal sodium retention. How does this affect blood pressure?

A

Renal sodium retention → fluid retention

Fluid retention → increase in BP

28
Q

Where is aldosterone released from? What stimulates its release?

A

Angiotensin II stimulates the release of aldosterone from the Zone glomerulosa in the adrenal cortex (adrenal glands).

29
Q

What are the effects of Angiotensin-II?

A
  • Systemic vasoconstriction
  • Increased blood volume
  • Renal sodium and fluid retention
30
Q

Describe the vicious cycle by which the body’s compensatory mechanisms can worsen heart failure.

A
  • Compensatory mechanisms result in increased preload and afterload at a cost of even greater oxygen needs
  • This means the sick heart must cope with increased preload and afterload.
31
Q

How does oedema develop in heart failure?

A
  • Sodium and fluid retention occurs due to RAAS
  • Volume of fluid in the blood vessels, esp. veins, increases
  • Pressure in capillaries increases
  • Excess interstitial fluid (=oedema) develops
32
Q

Why is a patient’s respiratory rate elevated in heart failure?

A
  • To restore blood pressure, heart rate increases, meaning the sick heart must work harder, and thus it demands more oxygen.
  • SNS activation leads to increased contractility, meaning the sick heart must work harder, and thus demands more oxygen.
  • Cardiac enlargement results in increased leakiness of AV valves. Therefore, more oxygen is required to provide the body with the same amount as before.
  • Increased oxygen needs → increased respiratory rate.
33
Q

Why does AV valve regurgitation increase in the vicious cycle of heart failure? What effect does this have on cardiac output?

A
  • SNS activation causes peripheral vasoconstriction
  • Peripheral vasoconstriction increases afterload
  • Increased afterload increases AV valve regurgitation

Increased afterload and valve leakiness results in a fall in cardiac output

34
Q

Outline how heart failure leads to feelings of weakness and fatigue.

A
  • SNS activation causes peripheral vasoconstriction.
35
Q

True/false: the lower the patient’s SNS activation and plasma noradrenaline levels, the less chance they have of surviving heart failure.

A

False.

Lower SNS activation and plasma noradrenaline levels = better chance of survival.

High NA plasma levels = bad news :(

36
Q

1

A

Increased venous return

37
Q

2

A

Peripheral vasoconstriction

38
Q

3

A

Increased peripheral resistance

39
Q

4

A

Increased rate and force of myocardial contraction

CAR (17 decks)

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