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Cardiovascular system SA > Pathophysiology of ischaemia + infarction > Flashcards

Pathophysiology of ischaemia + infarction Flashcards

1
Q

Define ischaemia

A

Relative 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 are the factors affecting 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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3
Q

What are the factor affecting oxygen demand

A
  1. Tissue itself - different tissues have different requirements
  2. Activity of tissue above baseline value
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4
Q

What are examples of conditions that causes ischaemia

A

Hypoxia - Low oxygen
Anaemia - abnormal delivery
Stagnant - abnormal delivery
Cytotoxic - abnormal tissue

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5
Q

What are the potential oxygen supply issues that can cause myocardial ischaemia

A 
coronary artery atheroma, 
cardiac failure (flow),
 pulmonary function – other disease 
pulmonary oedema (LVF), 
anaemia, 
previous MI
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6
Q

What are the potentially oxygen demand issue that can cause myocardial ischaemia

A

heart has high intrinsic demand, exertion/stress

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7
Q

What is the clinical consequences of ischaemia due to atheroma

A 
MI 
TIA - symptoms of a stroke that are resolved 
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure
Stable/unstable angina
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8
Q

How does atheroma cause ischaemia

A

Atheroma causes vessels radius to decrease, decreasing the flow of blood, decreasing oxygen delivery resulting in decreased supply of oxygen to an organ - ischaemia

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9
Q

What is the biochemical effect of ischaemia

A

Decreased oxygen results in anaerobic respiration which promotes cell death

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10
Q

What cells are more susceptible to ischaemia

A

Cells with a high metabolic rate

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11
Q

What is the clinical effects of ischaemia

A

(a) Dysfunction - e.g. abnormal heart rhythms
(b) Pain

(c) Physical damage
Specialised cells

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12
Q

What is the there possible outcomes of ischaemia

A

No clinical effect

Resolution versus therapeutic intervention

Infarction

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13
Q

Define infarction

A

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

cessation of blood flow

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14
Q

What are examples of the aetiology of infarction

A
  1. Thrombosis
  2. Embolism
  3. Strangulation e.g. gut
  4. Trauma - cut/ruptured vessel
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15
Q

What does the scale of damage in infarction depend upon

A

Time period
Tissue/organ
Pattern of blood supply
Previous disease

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16
Q

What is the pathology of infarction

A

Anaerobic metabolism cell death liberation of enzymes breakdown of tissue

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17
Q

What is the two types of necrosis

A

Coagulative necrosis e.g. heart, lung

Colliquitive necrosis e.g. brain

18
Q

How long does it take in myocardial ischaemia for anaerobic metabolism to occur/ ATP depletion

A

few seconds

19
Q

How long does it take in myocardial ischaemia for loss of myocardial contractility i.e. heart failure

A

< 2 minutes

20
Q

After a few minutes in a myocardial ischameia what ultrasound changes can be seen

A

myofibrillar relaxation,
glycogen depletion,
cell and mitochondrial swelling

21
Q

At what timing and stage does the affect of myocardial infarction become irreversible and why is this

A

Severe ischaemia 20-30 mins

As myocyte necrosis is occurring

22
Q

What occurs in myocyte necrosis

A

disruption of integrity of sarcolemmal membrane resulting in leakage of intracellular macromolecules

23
Q

What happens after one hour into a myocardial infarction

A

Injury to the microvasculature

24
Q

What is the appearance of infarcts in less than 24 hours

A

No change on visual inspection

A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy

25
Q

What is the microscopic appearance if infarcts from 24-48 hours

A

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

26
Q

What is classified as pale infarct

A

Solid tissues

myocardium, spleen, kidney

27
Q

What is classified as red infarct

A

Loose tissue - previously congested

Lung, liver

28
Q

72 hours onwards into MI what is the appearance of pale and rd infarcts

A

Pale infarct - yellow/white and red periphery

Red infarct - little change

29
Q

72 hours onward into MI what can be seen microscopically

A

chronic inflammation;
macrophages remove debris;
granulation tissue;
fibrosis

30
Q

What is Reperfusion injury

A

tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen

31
Q

What is the reparative process of MI and what is the end result

A 
Cell death
Acute inflammation
Macrophage phagocytosis of dead cells
Granulation tissue
Collagen deposition (fibrosis)
Scar formation
As Scar replaces area of tissue damage
32
Q

What is two different type of MI

A

Subendocardial infarction

transmural infarction

33
Q

What is the affect of Subendocardial infarction

A

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

34
Q

What is the affect of transmural infarction

A

ischaemic necrosis affects full thickness of the myocardium

35
Q

What is the similarity and differences in reparative process in subendocardial and transmural

A

They have the same histological features but granulation tissue stage followed by fibrosis - in subendocardial infarct possibly slightly shortened compared to transmural infarct

36
Q

How is acute infarcts classified in investigation with ECG

A

according to whether there is elevation of the ST segment on the ECG

37
Q

What does it mean If no ST segment elevation but a significantly elevated serum troponin level:

A

non-STEMI

38
Q

What kind of infarct is is non STEMI thought to correlate with

A

a subendocardial infarct

39
Q

Why is it Difficult to carry out detailed studies to show link between ECG changes seen with an infarct and exact pathological features

A

because declining post mortem rates

people don’t stick around long enough for us to see the pathology

40
Q

What is the complications of myocardial infarction

A

Sudden death;

arrhythmias - abnormal heart rhythm

angina;

cardiac failure;

cardiac rupture - ventricular wall, septum, papillary muscle;

reinfarction - repeat infarction

pericarditis;

pulmonary embolism secondary to DVT;

mural (bv/cavity) thrombosis;

ventricular aneurysm;

Dressler’s syndrome

Cardiovascular system SA (43 decks)

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