Pathophysiology of Ischaemia and Infarction

Question 1

What is hypoxic hypoxia?

Answer 1

Either :
A) Low inspired oxygen levels or,
B) Normal inspired oxygen but low PaO2

Question 2

What is anaemic hypoxia?

Answer 2

Hypoxia where the inspired oxygen levels are normal but the blood itself is abnormal

Question 3

What is stagnant hypoxia?

Answer 3

Hypoxia where there is normal inspired oxygen levels but abnormal delivery which is either local e.g. occlusion of a vessel or systemic e.g. shock

Question 4

What is cytotoxic hypoxia?

Answer 4

When the inspired oxygen levels are normal but oxygen levels are abnormal at the tissue level

Question 5

What factors affect oxygen supply?

Answer 5

Inspired oxygen levels, pulmonary function, blood constituents, blood flow, integrity of vasculature and tissue mechanisms

Question 6

What factors affect oxygen demand?

Answer 6

The requirement of the tissue itself and activity of the tissue above the baseline value

Question 7

What are the functional effects of ischaemia?

Answer 7

Blood/oxygen supply fails to meet the demand due to a decrease in supply; an increase in demand or both

Question 8

What are the clinical effects of ischaemia?

Answer 8

Dysfunction, pain and physical damage (specialised cells)

Question 9

What are the possible outcomes of ischaemia?

Answer 9

No clinical effect, resolution, therapeutic intervention or infarction

Question 10

What is infarction?

Answer 10

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

Question 11

What are the causes of infarction?

Answer 11

Thrombosis, embolism, strangulation e.g. gut and trauma - cut/ruptured vessel

Question 12

What factors determine how much damage the ischaemia/infarction will cause?

Answer 12

The time period, tissue/organ affected, pattern of blood supply and previous disease

Question 13

What are the two types of necrosis?

Answer 13

Coagulative necrosis e.g. heart or lungs and colliquitive necrosis e.g. brain

Question 14

How does a myocardial infarction progress?

Answer 14

Coronary artery obstruction leads to a decrease in blood flow to a region of the myocardium. This causes ischaemia, rapid myocardial dysfunction and then myocyte death

Question 15

What will the appearance of an infarct be within 24hrs?

Answer 15

No changes will be visible on a visual inspection. After a few hours swollen mitochondria may be seen on an electron microscopy

Question 16

How will an infarct appear between 24-48hrs after the event?

Answer 16

In solid tissues e.g. myocardium, spleen and kidneys the infarct will be pale.
In loose/previously congested tissues/second or continuing blood dupply/venous occlusion e.g. lungs and liver the infarct will appear red
Microscopically: Acute inflammation initially at the edge of the infarct and loss of specialised cell features

Question 17

How will an infarct appear from 72hrs onwards?

Answer 17

Pale infarct - yellow/white with red periphery
Red infarct - little change
Microscopically: Chronic inflammation, macrophages remove debris, granulation tissue and fibrosis

Question 18

What will be the end result of the appearance of an infarct?

Answer 18

A scar will replace the area of tissue damage

Question 19

What is a transmural infarction?

Answer 19

Where the ischaemic necrosis affects the full thickness of the myocardium

Question 20

What is a subendocardial infarction?

Answer 20

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

Question 21

What are the complications of an MI?

Answer 21

Sudden death, arrhythmias, angina, cardiac failure, cardiac rupture - ventricular wall, septum, papillary muscle, reinfarction, pericarditis, pulmonary embolism secondary to DVT, papillary muscle dysfunction - necrosis/rupture, mitral incompetence, mural thrombosis, ventricular aneurysm and Dressler’s syndrome