Ischaemia and Infarction Flashcards
What is ischaemia
Relative lack of blood supply to tissue/organ leading to inadequate oxygen supply to meet demands of tissue/organ
Name the four types of hypoxia
Hypoxic hypoxia
Anemic hypoxia
Stagnant hypoxia
Cytotoxic hypoxia
How does hypoxia arise in hypoxic hypoxia
Low inspired oxygen level or normal inspired oxygen but low PaO2
How does anaemic hypoxia arise
Abnormal blood
How does stagnant hypoxia arise
Abnormal delivery of oxygen either locally (eg occlusion) or systemic (eg shock)
How does cytotoxic hypoxia arise
Abnormal at tissue level
What 6 factors affect oxygen supply
Inspired oxygen Pulmonary function Blood constituents Blood flow Integrity of vasculature Tissue mechanisms
2 factors affecting oxygen demand
Tissue itself - some require more oxygen than others
Activity of tissue above baseline
In terms of the factors that affect oxygen supply, what specific problems can lead to ischaemic heart disease?
Coronary artery atheroma Cardiac failure (flow) Pulmonary function - disease/pulmonary oedema (LVF) Anaemia Previous MI
What demand issues may lead to ischaemic heart disease
Heart has high intrinsic demand, especially on exertion or stress
What is an atheroma
Localised accumulation of lipid and fibrous issue in intima of arteries
What do the following lead to clinically:
- established atheroma
- complicated atheroma
- ulcerated/fissured plaques
- atheroma in aorta
- stable angina
- unstable angina
- thrombosis and then ischaemia or infarction
- aneurysm
6 clinical consequences of atheroma throughout the body
MI - cardiac failure Transient ischaemic attack Cerebral infarction Abdominal aortic aneurysm Peripheral vascular disease
What are the 6 categories for effects of ischaemia
functional general biochemical cellular clinical outcome
What are the functional effects of ischaemia
Blood oxygen supply fails to meet demand
What are the three ways the general effects of ischaemia can be described
Can be acute, chronic or acute on chronic
What are the biochemical effects of ischaemia
Aerobic metabolism changes to anaerobic metabolism. Increased lactate and pyruvate. Not enough oxygen for cells and cells die.
What are the cellular effects of ischaemia?
Different cells have variable oxygen requirement so are variably susceptible to ischaemia eg those with high metabolic rate
Three clinical effects of ischaemia
Dysfunction
Pain
Physical damage
Three possible outcomes of ischaemia
No clinical effect
Resolution versus therapeutic intervention
Infarction
Definition of infarction
Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage
Four examples of aetiology of infarction
Thrombosis
Embolism
Strangulation
Trauma
What four factors is the scale of damage of ischaemia/infarction dependent on
time period
tissue/organ
pattern of blood supply
previous disease
What are the two types of necrosis
Coagulative necrosis
Colliquitive necrosis
What organs experience coagulative necrosis
Heart
Lung
What organ has colliquitive necrosis
brain
What happens in seconds in myocardial ischaemia
anaerobic metabolism
onset of ATP depletion
What happens in less than 2 minutes
Loss of myocardial contractility
How long until myocyte necrosis
20-40 minutes
How long until injury to microvasculature
over an hour
What is the appearance of the infarct in less than 24 hours
no change on visual inspection
swollen mitochondria on electron microscopy
What is the appearance of the infarct 24-48 hours
Pale infarct
red infarct
microscopically - acute inflammation at edge of infarct, loss of specialised features
What kind of tissues appear as pale infarcts
Solid tissues eg. myocardium, spleen, kidney
What kind of tissues appear as red infarcts
Loose tissue eg. lung, liver
Previously congested tissue
Second, continuing blood supply
Venous occlusion
What changes to pale infarct 72 hours onwards
Yellow/white and red periphery
What changes to red infarct 72 hours onwards
little change
What changes microscopically 72 hours onwards
Chronic inflammation, macrophages remove debris, granulation tissue, fibrosis
6 steps of reparative process of myocardial infarction
- cell death
- acute inflammation
- macrophage phagocytosis dead cells
- granulation tissue
- collagen deposition
- scar formation
What are the two types of infarction
Transmural - affects full thickness of myocardium
Subendocardial - limited to zone under endocardial lining
Complications of myocardial infarction (there are many)
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 Dressler's syndrome
