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Cardiovascular > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

What is ischaemia?

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue/organ - hypoxia

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2
Q

Describe what hypoxia can be due to?

A

Low inspired O2 level or
Normal inspired O2 but low PaO2

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3
Q

What is anaemia due to?

A

Normal inspired O2 but blood is abnormal ex. not enough Hb production

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4
Q

What can cause stagnant blood?

A

Normal inspired O2 but abnormal delivery
Due to either local (occlusion of vessel) or systemic (shock)

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5
Q

What causes a patient to become cytotoxic?

A

Normal inspired O2 but abnormal at tissue level
Tissue can not use O2 that has been delivered to it

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6
Q

What are some factors affecting oxygen supply?

A

Inspired O2
Pulmonary function
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms

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7
Q

What are factors affecting oxygen demand?

A

Tissue itself - Different tissues have different requirements
Activity of tissue above baseline value

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8
Q

What are some supply issues that could lead to ischaemic heart disease?

A

Coronary artery atheroma, cardiac failure (flow), pulmonary function like another disease or oedema, anaemia and previous MI

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9
Q

What are some demand issues that could lead to ischaemic heart disease?

A

Heart has high intrinsic demand
On exertion or stress is higher

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10
Q

What is an atheroma?

A

Localised accumulation of lipid and fibrous tissue in the intima of arteries

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11
Q

What does an established atheroma in coronary artery cause?

A

Stable angina - chest pain on exertion

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12
Q

What does complicated atheroma in coronary artery cause?

A

Unstable angina - chest pain at rest

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13
Q

What does ulcerated/ fissured plaques lead to?

A

Thrombosis if ruptured then causes ischaemia and infarction

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14
Q

What does an atheroma in the aorta cause?

A

Aneurysm - dilatation of wall of an artery

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15
Q

What are the clinical consequences of ischaemia?

A

MI, TIA, Cerebral infarction, Abdominal aortic aneurysm, peripheral vascular disease and cardiac failure
Coronary artery disease - MI - cardiac failure

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16
Q

Describe the effects of atheroma on blood flow?

A

If decrease in radius from 4 to 2 - 1/16 reduction in blood flow
Means O2 decreases so ischaemia and infarction
Due to Poiseuille’s formula and blood flow Q = Difference in pressure/resistance

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17
Q

What are the general types of ischaemia?

A

Acute, Chronic and Acute-on-Chronic

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18
Q

What are the functional effects of ischaemia?

A

Blood/O2 supply fails to meet demand due to decreased supply - or increase demand or both
Related to rate of onset

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19
Q

Why is anaerobic metabolism much less efficient?

A

Small amount of ATP produced compared to normal aerobic metabolism
Also energy required to remove lactate as toxic to cells

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20
Q

What does anaerobic metabolism lead to?

A

Cell death
Caused by decrease in O2

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21
Q

What are cellular effects of ischaemia?

A

Cells with high metabolic rate are more greatly and quickly affected
Cells with lower metabolic rate are much less affected - fat, bone or connecting cells

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22
Q

What are some clinical effects of ischaemia?

A

Dysfunction of organ
Pain - angina
Physical damage - specialised cells

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23
Q

What are the outcomes of ischaemia?

A

No clinical effect
Resolution versus therapeutic intervention - can give thrombolytic if no resolution
Infarction

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24
Q

What is infarction?

A

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

25
Q

Describe the aetiology of infarction

A
  1. thrombosis
  2. embolism
  3. strangulation - gut
  4. trauma -cut or rupture of vessel
26
Q

What factors help scale the damage of ischaemia/infarction?

A

Time period
Tissue/Organ - if only one artery supplies there then will be worse outcome
Pattern of blood supply
Previous disease

27
Q

What type of necrosis happens in heart, lung and brain?

A

Heart and lung - coagulation necrosis
Brain - colliquative necrosis

28
Q

Describe colliquative necrosis?

A

Tissue is broken down into very small pieces which draw fluid to that area
Much softer cystic infarct compared to solid organs

29
Q

What does anaerobic metabolism lead?

A

Cell death - liberation of enzymes - breakdown of tissue

30
Q

What happens when there is coronary artery obstruction?

A

Decreased blood flow to region of myocardium - ischaemia so rapid myocardial dysfunction leading to myocyte death

31
Q

When does anaerobic metabolism start in myocardial ischaemia?

A

In seconds
Also onset of ATP depletion

32
Q

When does loss of myocardial contractibility occur in myocardial ischaemia?

A

In under 2 mins

33
Q

When are ultrasound changes seen in myocardial ischaemia?

A

A few minutes

34
Q

When does severe ischaemia causing irreversible damage happen?

A

20-30 mins

35
Q

When is myocardial necrosis seen in ischaemia/infarction?

A

20-40 mins

36
Q

When does injury to microvasculature occur in ischaemia/infarction?

A

More than 1 hour

37
Q

What appearances of infarcts are at less than 24 hours?

A

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

38
Q

What are the appearances of infarcts at 24-48 hours?

A

Pale infarct - myocardium, spleen, kidney (solid organs)
Red infarct - Loose tissue like lung and liver or previously congested tissue
Microscope - acute inflammation initially at edge of infarct - loss of specialised cell features

39
Q

What are the appearances of infarcts from 72 hours and onwards?

A

Macroscopically -
Pale infarct - yellow/white and red periphery
Red infarct - little changes
Microscopically -
Chronic inflammation, macrophages removing debris, granulation tissue and fibrosis

40
Q

What is the end result appearance of an infarct?

A

Scar replaces area of tissue damage
Shape depends on territory of occluded vessel

41
Q

What is a reperfusion injury?

A

Damage to the tissue caused when blood supply returns to tissue after period of ischaemia
Absence of O2 and nutrients creates condition where restoration of circulation results in inflammation and oxidative damage from O2 - free radicals

42
Q

What is the reparative process for myocardial infarction?

A

Cell death - Acute inflammation - Macrophage phagocytosis of dead cells - Granulation tissue - Collagen deposition (fibrosis) - Scar formation

43
Q

What happens between 4-12 hours of myocardial infarction?

A

Early coagulation necrosis, oedema and haemorrhage

44
Q

What happens between 12-24 hours of myocardial infarction?

A

Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate at periphery

45
Q

What happens between 1-3 days of myocardial infarction?

A

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

46
Q

What happens between 3-7 days of myocardial infarction?

A

Disintegration of dead myofibrils, dying neutrophils and early phagocytosis

47
Q

What happens between 7-10 days of myocardial infarction?

A

Well developed phagocytosis and granulation tissue at margins

48
Q

What happens between 10-14 days of myocardial infarction?

A

Well established granulation tissue with new blood vessels ad collagen deposition

49
Q

What happens at 2-8 weeks of myocardial infarction?

A

Increased collagen deposition and decreased cellularity

50
Q

When does dense fibrous scar form?

A

After 2 months

51
Q

What is transmural infarction?

A

Ischaemic necrosis affects full thickness of the myocardium

52
Q

What is subendocardial infarction?

A

Ischaemia necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
Histological features the same but repair time could be quicker

53
Q

How are acute infarcts classified?

A

Whether there is elevation of the ST segment on the ECG

54
Q

What is a Non-STEMI?

A

No ST elevation but significantly increased troponin level level
Thought to correlate with a subendocardial

55
Q

What are the effects of infarction dependent on?

A

Site dependant
Size of infarct
Death, dysfunction of organ causing pain
Contribution of previous disease or infarction

56
Q

What are some complications of myocardial infarction?

A

Arrhythmias, angina, cardiac failure, cardiac rupture, pulmonary embolism secondary to DVT, papillary muscle dysfunction, mural thrombosis, ventricular aneurysm and Dressler’s syndrome

57
Q

What is mural thrombosis?

A

Damage to wall so thrombosis forms on inner surface of heart

58
Q

What is ventricular aneurysm?

A

Ventricular wall dilatation as damaged

59
Q

What is Dressler’s syndrome?

A

Inflammation of the sac surrounding the heart
Usually 6 weeks after

Cardiovascular (33 decks)

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