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Year 1-Cardiovascular System > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

Define ischaemia

A

Lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue/organ

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2
Q

What do we also have if we have ischaemia?

A

Hypoxia

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3
Q

What are the four types of hypoxia?

A
  1. Hypoxic
  2. Anaemic
  3. Stagnant
  4. Cytotoxic
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4
Q

When may you get hypoxic hypoxia?

A
  • Low inspired O2 level
    or
    -Normal inspired O2 but low PaO2
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5
Q

When may you get anaemic hypoxia?

A

Normal inspired O2 but blood abnormal

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6
Q

When may you get stagnant hypoxia?

A

Normal inspired oxygen but abnormal delivery

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7
Q

When may you get cytotoxic hypoxia?

A

Normal inspired O2 but tissue cannot use the oxygen being delivered to it

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8
Q

How can oxygen delivery be abnormal?

A

Local delivery due to occlusion of vessel
Systemic due to shock

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9
Q

List some factors which can affect oxygen supply

A
  1. Inspired O2
  2. Pulmonary function
  3. Blood constituents
  4. Blood flow
  5. Integrity of vasculature
  6. Tissue mechanisms
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10
Q

What are some factors which affect oxygen DEMAND?

A
  1. Tissue itself - different tissues have different requirements
  2. Activity of tissue above baseline value
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11
Q

For ischaemic heart disease, what may cause issues with oxygen supply?

A

Coronary artery atheroma
Cardiac failure (flow)
Pulmonary function
Pulmonary oedema (LVF)
Anaemia
Previous MI

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12
Q

What is the key issue with oxygen demand?

A

Heart already has high intrinsic demand but will be higher under exertion/stress

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13
Q

RECAP- what is an atheroma?

A

Localised accumulation of lipid and fibrous tissue in intima of arteries

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14
Q

What can a established atheroma in a coronary artery lead to?

A

Stable angina

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15
Q

What can an complicated atheroma in a coronary artery lead to?

A

Unstable angina

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16
Q

What ca ulcerated/fissured plaques lead to?

A

Thrombosis which can in turn lead to ischaemia/infarction

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17
Q

What can an atheroma in the aorta lead to?

A

Aneurysm

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18
Q

What are some of the clinical consequences of ischaemia?

A

MI
TIA (transient ischemic attack)
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure

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19
Q

Describe the common pathway of heart related conditions.

A

Coronary artery disease -> thrombosis -> MI -> Cardiac failure

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20
Q

What are the functional affects of ischaemia?

A

-Blood/O2 supply fails to meet demand due to decreased supply, increased demand, or both

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21
Q

What are the functional affects of ischaemia related to?

A

Rate of onset

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22
Q

What are the biochemical affects of ischemia?

A

Anaerobic metabolism due to lack of oxygen-

Less ATP produced
Lactate produced
Little ATP produced needed to removed the lactate

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23
Q

When there is less/no oxygen supply to a cell, what can happen?

A

Anaerobic metabolism leading to cell death

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24
Q

Discuss how cells with different metabolic rates get affected by ischaemia.

A

Cells w high metabolic rate get affected at a faster rate

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25
Q

Give some examples of cells with high metabolic rates which can lead to fast affects of ischaemia.

A

Muscle cells
Liver cells
Renal tubular epithelial cells

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26
Q

Give examples of cells with a low metabolic rate and will not be affected by ischaemia as quickly.

A

Fat cells
Bone cells
Connective tissue

27
Q

What are some of the clinical effect you might see with someone with ischaemia?

A

Dysfunction
Pain
Physical damage- specialised cells

28
Q

Describe how there can be dysfunction in a patient with ischaemia?

A

In the heart, the effects of ischaemia may cause an arrhythmia

29
Q

What are some of the outcomes for a patient with ischaemia?

A

No clinical effect
Resolution- either w therapeutic intervention or not
Infarction

30
Q

What is infarction?

A

Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage

31
Q

What is the cause of infarction?

A

Cessation of blood flow

32
Q

What could cause cessation of blood flow, and therefore, infarction?

A
  1. Thrombosis
  2. Embolism
  3. Strangulation e.g. gut
  4. Trauma - cut/ruptured vessel
33
Q

The scale of damage caused by ischemia/infarction is dependant on many factors.
List some of them.

A

Time period
Tissue/organ
Pattern of blood supply
Previous disease

34
Q

What type of necrosis occurs in most tissues like the heart and lungs?

A

Coagulative necrosis

35
Q

What type of necrosis occurs in the brain?

A

Colliquitive necrosis

36
Q

How how coronary artery obstruction lead to myocyte death?

A

Decreased blood flow to region of myocardium ->
Ischaemia, rapid myocardial dysfunction ->
Myocyte death

37
Q

In myocardial ischaemia, how long does it take for the depletion of ATP due to anaerobic metabolism?

A

Seconds

38
Q

In myocardial ischaemia, how long does it take for the loss of myocardial contractibility?

A

< 2 mins

39
Q

How long do you have to have severe ischemia for it to cause irreversible damage?

A

20-30 mins

40
Q

How long does it take in myocardial ischaemia for there to be myocyte necrosis?

A

20-40 mins

41
Q

How long does it take in myocardial ischaemia for there to be injury to the microvascular?

A

> 1 hour

42
Q

Describe what the appearance of infarcts will look like in less than 24hrs.

A

No change on visual inspection
A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy

43
Q

Describe what the appearance of infarcts will look like in 48hrs.

A

Pale infarct in solid tissues, like spleen, kidney, heart.
Red infarct in loose tissues, like lungs and liver.

Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features

44
Q

Describe what the appearance of infarcts will look like in 72hrs.

A

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

Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis

45
Q

What is the end result of infarcts?

A

Scars replaces area of tissue damage

46
Q

What is reperfusion injury?

A

Damage that occurs after blood supply is restored to a tissue or organ after a period of ischemia.

47
Q

What happens in reperfusion injury?

A

Absence of oxygen and nutrients in restored bloodstream causes inflammation and oxidative damage

48
Q

Describe the reparative process which occurs in MI.

A
  1. Cell death
  2. Acute inflammation
  3. Macrophage phagocytosis of dead cells
  4. Granulation tissue forming
  5. Collagen deposition (fibrosis)
  6. Scar formation
49
Q

What happens in 4-12hrs of MI?

A

Early coagulation necrosis, oedema, haemorrhage

50
Q

What happens in 12-24hrs of MI?

A

Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate

51
Q

What happens in 1-3 days of MI?

A

Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate

52
Q

What happens in 3-7 day of MI?

A

Disintegration of dead myofibres, dying neutrophils, early phagocytosis

53
Q

What happens in 7-10 days of MI?

A

Well developed phagocytosis, granulation tissue at margins

54
Q

What happens in 10-14 days of MI?

A

Well established granulation tissue with new blood vessels and collagen deposition

55
Q

What happens in 2-8 weeks of MI?

A

Increased collagen deposition, decreased cellularity

56
Q

What happens in >2 months of MI?

A

Dense collagenous scar

57
Q

Therefore, how long does it take from development of MI to a scar?

A

At least two months

58
Q

Where does transmural infraction affect?

A

Ischaemic necrosis affects full thickness of the myocardium

59
Q

Where does subendocardial infarction affect?

A

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

60
Q

What are acute infarctions classified by?

A

Whether there is elevation of the ST segment on the ECG

61
Q

What is it called if there is no elevation of the ST segment on ECG but a significantly elevated serum troponin level?

A

Non-STEMI

62
Q

There are lots of complications with MI but list a few

A

Sudden death
Arrhythmias
Angina
Cardiac failure
Cardiac rupture - ventricular wall, septum, papillary muscle

63
Q

What type of infarct is a non-STEMI thought to correlate with?

A

Subendocardial infarction

Year 1-Cardiovascular System (41 decks)

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