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Cardiovascular System > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

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1
Q

What is hypoxia?

A

Relative lack of blood supply to the tissue/organ, leading to inadequate oxygen supply to meet the needs of that tissue/organ

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2
Q

What are the main types of hypoxia?

A

Hypoxic
Anaemic
Stagnant
Cytotoxic

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3
Q

What is seen in hypoxic hypoxia?

A

Low inspired O2 level
or
Normal inspired O2 but low PaO2

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4
Q

What is seen in anaemic hypoxia?

A

Normal inspired O2 but abnormal blood

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5
Q

What is seen in stagnant hypoxia?

A

Normal inspired O2 but abnormal delivery, either local e.g. occlusion of a vessel or systemic e.g. shock

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6
Q

What is seen in cytotoxic hypoxia?

A

Normal inspired O2 but abnormal at tissue level

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7
Q

What factors affect oxygen supply?

A 
Inspired O2
Pulmonary function 
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms
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8
Q

What factors affect oxygen demand?

A

The tissue itself - different tissues have different requirements
Activity of the tissue above baseline value e.g. in exercise

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9
Q

What is ischaemia?

A

Inadequate blood supply to an organ or tissue

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10
Q

What is infarction?

A

Obstruction of the blood supply to an organ or tissue resulting in local cell death
Ischaemic necrosis within a tissue or organ in the living body

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11
Q

What is atheroma?

A

A localised accumulation of lipid and fibrous tissue in the intima of arteries

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12
Q

What does established atheroma in coronary arteries result in?

A

Stable angina

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13
Q

What does complicated atheroma in coronary arteries result in?

A

Unstable angina

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14
Q

What do ulcerated or fissured atheromatous plaques result in?

A

Thrombosis, causing ischaemia or infarction

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15
Q

What can atheroma in the aorta result in?

A

Aortic aneurysm

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16
Q

What are the clinical consequences of atheroma?

A 
MI 
TIA
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure
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17
Q

What is the effect of atheroma on blood flow, according to Poiseuille’s formula?

A

Atheroma leads to narrowing of the vessel lumen due to occlusion or thrombus
A reduction in vessel radius in an atheromatous vessel results in a 16 fold reduction in blood flow
This reduced blood and therefore oxygen flow leads to ischaemia or infarction

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18
Q

What are the functional consequences of ischaemia?

A

Blood/O2 supply fails to meet demand due to low supply, high demand or both

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19
Q

What are the general consequences of ischaemia?

A

Acute - obvious signs and symptoms
Chronic - may go unnoticed over a long period of time, insidious onset
Acute on chronic - acute signs/symptoms on already compromised tissues

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20
Q

What are the biochemical consequences of ischaemia?

A

Normal aerobic metabolism affected

Anaerobic metabolism occurs, causing cell death

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21
Q

What are the cellular consequences of ischaemia?

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A

Different tissues have variable O2 requirements so are variably susceptible to ischaemia
Cells with high metabolic rate e.g. cardiac cells and neurons are greatly and quickly affected by ischaemia
Cells with low metabolic rate e.g. fat cells are much less affected by ischaemia

22
Q

What are the clinical consequences of ischaemia?

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A

Dysfunction
Pain
Physical damage of specialised cells

23
Q

What are the potential outcomes of ischaemia?

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A

No clinical effect
Resolution
Therapeutic intervention
Infarction

24
Q

What might result in supply issues in IHD?

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A 
Coronary artery atheroma
Cardiac failure
Pulmonary function due to another disease causing pulmonary oedema e.g. left ventricular failure
Anaemia
Previous MI
25
What results in demand issues?
Increased exertion and stress
26
What causes infarction?
Occlusion of the arterial supply or the venous drainage
27
What might cause the cessation of blood flow?
Thrombosis Embolism Strangulation Trauma
28
What does the scale of damage resulting from ischaemia or infarction depend on?
Time period Tissue/organ affected Pattern of blood supply Previous disease
29
What is the basic process of infarction?
``` Anaerobic metabolism Cell death Liberation of enzymes Breakdown of tissue Coagulative necrosis e.g. heart, lung Colliquitive necrosis e.g. brain ```
30
What occurs in myocardial ischaemia?
Anaerobic metabolism - within seconds Loss of myocardial contractility - in under 2 minutes Ultrastructural changes - within a few minutes Severe ischaemia - within 20-30 minutes Myocyte necrosis - within 20-40 minutes Injury to microvasculature - over 1 hour
31
What is transmural infarction?
Ischaemic necrosis which affects the full thickness of the myocardium
32
What is subendocardial infarction?
Ischaemic necrosis which is mostly limited to a zone of myocardium under the endocardial lining of the heart
33
What is the difference in the histological features of a transmural and subendocardial infarction?
Histological features are the same | Repair time, granulation tissue stage followed by fibrosis, is possibly slightly shorter in a subendocardial infarct
34
What are acute infarcts classified according to?
Whether there is elevation of the ST segment on the ECG
35
What is the class of acute infarct if there is no ST elevation but significantly elevated serum troponin level?
Non-STEMI
36
What are NSTEMIs thought to correlate with?
Subendocardial infarct
37
What is the appearance of an infarct at < 24 hours?
No change on visual inspection | From a few hours - 12 hours post-insult you will see swollen mitochondria on electron microscopy
38
What is the appearance of an infarct at 24-48 hours?
Pale infarct will develop in tissues such as myocardium, spleen and kidneys Red infarct will develop in more solid tissues such as liver and lungs Continuing blood supply and venous occlusion occurs in loose tissues or previously congested tissues Acute inflammation initially at the edge of the infarct, loss of specialised cell features, and death/breaking apart of nuclei seen microscopically
39
What is the appearance of an infarct at 72 hours onwards?
Pale infarct develops a yellow/white and red peripheral (hyperaemic rim) Red infarcts show little change Microscopically there is chronic inflammation, macrophages remove the debris and granulation tissue and fibrosis develops
40
What is the effect of an infarct dependent on?
Site Size Death/dysfunction Contribution of previous disease/infarction
41
What is the basic reparative process which occurs following myocardial infarction?
``` Cell death Acute inflammation Macrophage phagocytosis of dead cells Granulation tissue formation Collagen deposition, fibrosis Scar formation ```
42
What occurs in the reparative process of MI from 4-12 hours post-insult?
Early coagulation necrosis Oedema Haemorrhage
43
What occurs in the reparative process of MI from 12-24 hours post-insult?
Ongoing coagulation necrosis Myocyte changes Early neutrophilic infiltrate
44
What occurs in the reparative process of MI from 1-3 days post-insult?
Coagulation necrosis Loss of nuclei and striations Brisk neutrophilic infiltrate
45
What occurs in the reparative process of MI from 3-7 days post-insult?
Disintegration of dead myofibrils Dying neutrophils Early phagocytosis
46
What occurs in the reparative process of MI from 7-10 days post-insult?
Well-developed phagocytosis | Granulation tissue at margins
47
What occurs in the reparative process of MI from 10-14 days post-insult?
Well-established granulation tissue with new blood vessels and collagen deposition
48
What occurs in the reparative process of MI from 2-8 weeks post-insult?
Increased collagen deposition | Decreased cellularity
49
What occurs in the reparative process of MI from over 2 months post-insult?
Dense collagenous scar forms
50
What are the complications of myocardial infarction?
``` Sudden death Arrhythmias Angina Cardiac failure Cardiac rupture Reinfarction Pericarditis Pulmonary embolism secondary to DVT Papillary muscle dysfunction Mural thrombosis Ventricular aneurysm Dressler's syndrome ```

Cardiovascular System (40 decks)

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