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Cardiovascular System > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

Ischaemia

A

Relative lack of blood supply to tissue/organ leading to hypoxia

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2
Q

Factors affecting oxygen supply

A 
Inspired oxygen
Pulmonary function
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms
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3
Q

Factors affecting oxygen demand

A

Tissue itself

Activity of tissue above baseline value

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4
Q

Ischaemic heart disease supply issues

A

Coronary artery atheroma
Cardiac failure
Pulmonary oedema or disease
Previous MI

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5
Q

Ischaemic heart disease demand issues

A

Heart has high intrinsic demand

Exertion/stress

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6
Q

Clinical consequences if ischaemic heart disease

A 
MI
Transient ischaemic attack
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure
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7
Q

Functional effects of ischaemia

A

Blood/oxygen supply fails to meet demand due to decrease in supply and increase in demand

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8
Q

Biochemical effects of ischaemia

A

Decrease in oxygen leads to anaerobic metabolisms, change in acid base balance due to build up of lactate, cell death

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9
Q

Clinical effects of ischaemia

A

Dysfunction
Pain
Physical damage to specialised cells

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10
Q

Outcomes of ischaemia

A

No clinical effect
Resolution vs therapeutic intervention
Infarction

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11
Q

Infarction

A

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

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12
Q

Aetiology of infarction

A

Thrombosis
Embolism
Strangulation
Trauma

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13
Q

Scale of damage of ischaemia/infarction depends on

A

Time period
Tissue/organ
Pattern of blood supply
Previous disease

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14
Q

Coagulative necrosis occurs in

A

Solid organs e.g. heart, lung

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15
Q

Colliquitive necrosis occurs in

A

Loose organs e.g. brain

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16
Q

Colliquitive necrosis

A

Transformation of the tissue into a liquid viscous mass

17
Q

Coagulative necrosis

A

The architecture of dead tissue is preserved for at least a couple of days. If enough viable cells are present around the affected area regeneration will usually occur.

18
Q

Severe ischaemic damage is irreversible at what time

A

20-30 mins

19
Q

Sequence of events following myocardial infarction

A 
Anaerobic metabolisms, onset of ATP depletion 
Loss of myocardial contractility
Ultrastructural changes
Myocyte necrosis
injury to the microvasculature
20
Q

Appearance of infarct at less than 24 hours

A

No change

21
Q

Appearance of infarct at 24-48 hours to naked eye

A

Solid tissues - pale infarct

Loos tissues - red infarct

22
Q

Appearance of infarct at 24-48 hours microscopically

A

Acute inflammation at edge of infarct

Loss of specialised cell features

23
Q

Appearance of infarct at 72 hours onwards to the naked eye

A

Pale infarct - becomes yellow/white with red edges

Red infarct - no change

24
Q

Appearance of infarct at 72 hours onwards microscopically

A

Chronic inflammation
Macrophages remove debris
Granulation tissue
Fibrosis

25
Q

Appearance of infarct end result

A

Scar replaces area of tissue damage

Shape depends on territory of occluded vessel

26
Q

Reparative process of myocardial infarction

A 
Cell death
Acute inflammation 
Macrophage phagocytosis of dead cells
Granulation tissue
Fibrosis (collagen deposition)
Scar formation
27
Q

Transmural infarction

A

Ischaemic necrosis affects full thickness of the myocardium

28
Q

Subendocardial infarction

A

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

29
Q

Effects of infarction depend on

A

Site within body and organ
Size of infarct
Contribution of previous disease/infarction

30
Q

Effects of infarction

A

Death
Dysfunction
Pain

31
Q

Complications of myocardial infarction

A 
Sudden death
Arrhythmias
Angina
Cardiac failure or rupture
Pericarditis
Thrombosis or embolism

Cardiovascular System (27 decks)

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