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Cardiovascular System > Pathophysiology of Ischaemia & Infarction > Flashcards

Pathophysiology of Ischaemia & Infarction Flashcards

1
Q

What is ischaemia?

A

restriction in blood supply to tissues, causing a shortage of oxygen.

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2
Q

What is hypoxia?

A

a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level.

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3
Q

Describe the four ways that hypoxia can occur?

4

A
  1. Hypoxic = low inspired O2, or inspired O2 normal and PaO2 abnormal.
  2. Anaemic = normal inspired O2, abnormal blood e.g. low Hb
  3. Stagnation = normal inspired O2, abnormal delivery e.g. ischaemia, shock
  4. Cytoxic = normal inspired O2, abnormal at tissue level
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4
Q

What is infarction?

A

tissue death (necrosis) due to inadequate blood supply to the affected area

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5
Q

What are the factors affecting oxygen supply?

6

A
  1. inspired O2
  2. pulmonary function
  3. blood flow (e.g. atheroma)
  4. blood constituents (e.g. Hb level)
  5. integrity of vasculature
  6. tissue mechanisms
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6
Q

Which factors affect oxygen demand?

2

A
  1. tissue itself - different tissues have varying O2 requirements.
  2. activity of tissue e.g. during exercise
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7
Q

What is cytotoxic hypoxia?

A

organelles cannot function properly even though they have adequate oxygen e.g. cyanide poisoning

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8
Q

What are the supply issues that can cause ischaemic heart disease?

(5)

A
  • coronary artery atheroma
  • cardiac failure (flow)
  • pulmonary function: pulmonary oedema (from LVF)
  • anaemia
  • previous MI
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9
Q

What are demand issues that can cause ischaemic heart disease?

(2)

A

heart has high intrinsic demand

exertion/stress

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10
Q

How can atherosclerosis cause stable angina?

3

A
  • established atheroma
  • sufficient O2 supply at rest
  • demand > supply on exertion = angina
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11
Q

How can atherosclerosis cause unstable angina?

4

A
  • complicated atheroma
  • insufficient O2 supply at rest
  • demand > supply at rest = angina
  • worsening pain
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12
Q

What do ulcerated and fissure plaques in the coronary artery lead to?

(2)

A
  • rupture/thrombosis

- ischaemia/infarction

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13
Q

What does atheroma in aorta cause?

How?

A

aneurysm

dilatation of the aorta due to weakening of the vascular wall from inflammation

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14
Q

What conditions can atheromatous plaques lead to?

6

A
  • Coronary artery disease, MI
  • TIA
  • Cerebral infarction
  • Abdominal aortic aneurysm
  • Peripheral vascular disease
  • Cardiac failure
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15
Q

Briefly how would you describe the relationship between flow and radius of vessel?

What clinical problem does this result in?

A

small decrease in radius = large decrease in flow

ischaemia

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16
Q

Give an example of where ischaemia can be chronic?

2

A
  • peripheral vascular disease

- claudication on walking

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17
Q

Give an example of when ischaemia can be acute-on-chronic?

3

A
  • peripheral vascular disease
  • claudication on walking
  • can become an acute incident e.g. CLI
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18
Q

How does ischaemia affect the biochemistry of cells?

5

A
  • reduced aerobic respiration
  • increases anaerobic respiration
  • lactate builds up
  • acid-base imbalance
  • infarction/necrosis
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19
Q

What are the three general clinical effects of ischaemia?

A
  • dysfunction
  • pain
  • physical damage
20
Q

What dysfunction can ischaemia cause in the heart?

A

If it is next to the SA node then there is the chance that it may lead to cardiac arrhythmia.

21
Q

What are the three potential outcomes of ischaemia?

A
  • no clinical effect
  • resolution (normally need therapeutic intervention)
  • infarction
22
Q

What are the 4 possible causes of infarction?

A
  1. thrombosis
  2. embolism
  3. strangulation
  4. trauma-cut/ruptured vessel
23
Q

What are the factors that determine the scale of damage from ischaemia or infarction?

(4)

A
  • Time period
  • Tissue/organ
  • Pattern of blood supply
  • Previous disease e.g. MI
24
Q

What is coagulative necrosis?

Give an example of where this may occur?

A

necrosis in which the organ maintains its shape after necrosis

e.g. heart, lung

25
Q

What is colliquitive necrosis?

Give an example of where this may occur?

A

necrosis in which the tissue loses its gross structure as there is loss of connective tissue

e.g. brain

26
Q

Outline the sequence of events in necrosis.

hint: focus on the biochemical processes

(4)

A
  1. anaerobic respiration
  2. cell death
  3. liberation of enzymes
  4. tissue breakdown
27
Q

Outline the sequence of events occurring during ischaemia within coronary arteries.

(4)

A
  1. coronary artery obstruction (atheroma)
  2. reduced blood flow/ischaemia
  3. myocardial dysfunction
  4. myocyte death
28
Q

How long is severe ischaemia in the heart and is it reversible?

A

20-30mins

no - irreversible

29
Q

What happens in the first few seconds of myocardial ischaemia?

(2)

A
  • anaerobic metabolism

- ATP depletion

30
Q

What happens within two minutes of myocardial ischaemia?

2

A
  • loss of myocardial contractility - heart failure
31
Q

What happens after the first two minutes of myocardial ischaemia?

(3)

A

Ultrastructural changes:

  • myofibrillar relaxation
  • glycogen depletion
  • cell/mitochondrial swelling
32
Q

At what time phase of myocardial ischaemia does myocyte necrosis take place?

How is this picked up in blood tests?

A

20-40 minutes

increased troponin levels

33
Q

After how long of ischaemia is there injury to the microvasculature of the heart?

A

> 1 hour

34
Q

How do infarcts appearances change following ischaemic necrosis?

(3)

A
  • mitochondria swells (electron microscopy)

- pale/red colour change

35
Q

In which tissue does an infarct appear red?

3

A

lung, liver, loose tissues

36
Q

In which tissue does an infarct appear pale?

4

A

myocardium, spleen, kidney, solid tissues

37
Q

Under the microscope what can be seen around the edge of infarcts at 24-48 hours?

A

inflammatory cells such as neutrophils

38
Q

Under the microscope what can be seen in infarcts at 72 hours after event?

(colour/microscopy changes)

(5)

A

Pale infarct - yellow/white and red periphery
Red infarct - little change

Chronic inflammation:

  • macrophages remove debris
  • granulation tissue
  • fibrosis
39
Q

What is the end result of infarction?

2

A
  • scar replaces area of tissue damage

- reperfusion injury

40
Q

What is reperfusion injury?

3

A
  • following ischaemic period:
  • blood reperfuses scar tissue
  • causes inflammation and further damage to the tissue (oxidative injury)
41
Q

What are the reparative processes of myocardial infarction?

6

A
  1. Cell death
  2. Acute inflammation
  3. Macrophage phagocytosis of dead cells (chronic inflammation)
  4. Granulation tissue
  5. Collagen deposition (fibrosis)
  6. Scar formation
42
Q

What is a transmural infarction?

A

ischaemic necrosis affects full thickness of the myocardium

43
Q

What is a subendocardial infarction?

A

ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

44
Q

________ thought to correlate with a subendocardial infarct.

A

NSTEMI

45
Q

What are some of the complication of myocardial infarction?

A

C PEAR DROP

Cardiac arrhythmias/shock
Pericarditis
Emboli
Aneurysm
Rupture of free wall
Dresslers syndrome
Rupture of ventricle 
Papillary muscle rupture

SCD,

46
Q

What does papillary muscle dysfunction lead to?

A

mitral regurgitation

Cardiovascular System (37 decks)

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