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

Pathophysiology of Ischaemia and Infarction Flashcards

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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
Give some examples of cells with high metabolic rates which can lead to fast affects of ischaemia.
Muscle cells Liver cells Renal tubular epithelial cells
26
Give examples of cells with a low metabolic rate and will not be affected by ischaemia as quickly.
Fat cells Bone cells Connective tissue
27
What are some of the clinical effect you might see with someone with ischaemia?
Dysfunction Pain Physical damage- specialised cells
28
Describe how there can be dysfunction in a patient with ischaemia?
In the heart, the effects of ischaemia may cause an arrhythmia
29
What are some of the outcomes for a patient with ischaemia?
No clinical effect Resolution- either w therapeutic intervention or not Infarction
30
What is infarction?
Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage
31
What is the cause of infarction?
Cessation of blood flow
32
What could cause cessation of blood flow, and therefore, infarction?
1. Thrombosis 2. Embolism 3. Strangulation e.g. gut 4. Trauma - cut/ruptured vessel
33
The scale of damage caused by ischemia/infarction is dependant on many factors. List some of them.
Time period Tissue/organ Pattern of blood supply Previous disease
34
What type of necrosis occurs in most tissues like the heart and lungs?
Coagulative necrosis
35
What type of necrosis occurs in the brain?
Colliquitive necrosis
36
How how coronary artery obstruction lead to myocyte death?
Decreased blood flow to region of myocardium -> Ischaemia, rapid myocardial dysfunction -> Myocyte death
37
In myocardial ischaemia, how long does it take for the depletion of ATP due to anaerobic metabolism?
Seconds
38
In myocardial ischaemia, how long does it take for the loss of myocardial contractibility?
< 2 mins
39
How long do you have to have severe ischemia for it to cause irreversible damage?
20-30 mins
40
How long does it take in myocardial ischaemia for there to be myocyte necrosis?
20-40 mins
41
How long does it take in myocardial ischaemia for there to be injury to the microvascular?
>1 hour
42
Describe what the appearance of infarcts will look like in less than 24hrs.
No change on visual inspection A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy
43
Describe what the appearance of infarcts will look like in 48hrs.
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
Describe what the appearance of infarcts will look like in 72hrs.
Macroscopically: Pale infarct - yellow/white and red periphery Red infarct - little change Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis
45
What is the end result of infarcts?
Scars replaces area of tissue damage
46
What is reperfusion injury?
Damage that occurs after blood supply is restored to a tissue or organ after a period of ischemia.
47
What happens in reperfusion injury?
Absence of oxygen and nutrients in restored bloodstream causes inflammation and oxidative damage
48
Describe the reparative process which occurs in MI.
1. Cell death 2. Acute inflammation 3. Macrophage phagocytosis of dead cells 4. Granulation tissue forming 5. Collagen deposition (fibrosis) 6. Scar formation
49
What happens in 4-12hrs of MI?
Early coagulation necrosis, oedema, haemorrhage
50
What happens in 12-24hrs of MI?
Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
51
What happens in 1-3 days of MI?
Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate
52
What happens in 3-7 day of MI?
Disintegration of dead myofibres, dying neutrophils, early phagocytosis
53
What happens in 7-10 days of MI?
Well developed phagocytosis, granulation tissue at margins
54
What happens in 10-14 days of MI?
Well established granulation tissue with new blood vessels and collagen deposition
55
What happens in 2-8 weeks of MI?
Increased collagen deposition, decreased cellularity
56
What happens in >2 months of MI?
Dense collagenous scar
57
Therefore, how long does it take from development of MI to a scar?
At least two months
58
Where does transmural infraction affect?
Ischaemic necrosis affects full thickness of the myocardium
59
Where does subendocardial infarction affect?
Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
60
What are acute infarctions classified by?
Whether there is elevation of the ST segment on the ECG
61
What is it called if there is no elevation of the ST segment on ECG but a significantly elevated serum troponin level?
Non-STEMI
62
There are lots of complications with MI but list a few
Sudden death Arrhythmias Angina Cardiac failure Cardiac rupture - ventricular wall, septum, papillary muscle
63
What type of infarct is a non-STEMI thought to correlate with?
Subendocardial infarction

Year 1-Cardiovascular System (41 decks)

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