Ischaemia And Infarction Flashcards
Hypoxic hypoxia
Low inspired O2
Or normal inspired O2 but low PaO2
Anaemic hypoxia
Normal inspired O2 but blood is abnormal
Stangnant hypoxia
Normal inspired O2 but abnormal delivery from local occlusion of vessel or systemic effects eg shock
Cytotoxic hypoxia
Normal inspired O2 but abnormal at tissue level
Factors affecting oxygen supply
Inspired O2 Pulmonary function Blood constituents Blood flow Integrity of vasculature Tissue mechanisms
Factors affecting oxygen demand
Different types of tissue
Activity of tissues above baseline value
Causes of supply issues in is ischaemic heart disease
Coronary artery atheroma, cardiac failure, pulmonary disease or oedema (LVF), anaemia, previous MI
Cause of demand issues in is ischaemic heart disease
Heart has high Intrinsic demand, exertion/stress
Atheroma types in coronary artery
Established - stable angina(on exertion)
Complicated - unstable angina (at rest)
Ulcerated/fissured - thrombosis then ischaemia/infarction
Clinical consequences of ischemia
MI TIA Cerebral infarction Abdominal aortic aneurysm Peripheral vascular disease CF
blood flow formula
Q= difference in Pressure over resistance
Resistance is worked out with radius and constants and length and viscosity
Biochemical effects of ischemia
Only anaerobic respiration so less ATP
Lactate produces and the acid damages tissue
Clinical effects/symptoms of ischemia
Dysfunction
Pain
Physical damage
Outcomes of ischemia
No clinical effects
Resolution with or without therapeutic intervention
Infarction
Causes of infarction
Thrombosis
Embolism
Strangulation eg gut
trauma
Occlusion of either arterial supply or venous drainage
what is coagulative necrosis and where does it happen
Goes hard eg heart, lung
Colliquitive necrosis
Eg brain, draws fluid
Onset time of anaerobic metabolism and ATP depletion in MI
Seconds
Onset of loss of myocardial contractility (heart failure) in MI
Less than 2 minutes
Onset of loss of myocardial contractility (heart failure) in MI
Less than 2 minutes
Onset of ultrastructural changes in MI eg myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling
A few minutes
When does severe ischaemia become irreversible in MI
20-30 minutes
Onset of myocyte necrosis (disruption of sarcolemmal membrane and leakage of cell contents) in MI
20-40 minutes
Onset of injury to microvasculature in MI
Over an hour
Changes of appearance of infarcts at under 24 hours
No visual but under EM swollen mitochondria at under 12 hours
Changes of appearance of infarcts at 24-48 hours
Pale infarct eg myocardium, spleen , kidney (solid tissues)
Or
Red infarct eg lung, liver (loose tissues, previously congested tissue, second/continuing blood supply, venous occlusion
Microscopically, acute inflammation initially at edges, loss of specialised cell features
Changes in appearance of infarcts at 72hours
Pale infarct with red periphery
Red little change
Chronic inflammation, MQ to remove debris, granulation tissue, fibrosis
End result appearance of infarcts
Scar replaces tissue damage
Reparative processes in myocardial infarction
Cell death Acute inflammation Macrophages phagocytosing dead cells Granulation tissue Collagen deposition (fibrosis) Scar formation
4-12 hours of myocardial infarction
Early coagulation necrosis, odema and haemorrhage
12-24 hours of myocardial infarction
Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
1-3 days of myocardial infarction
Coagulation necrosis again, loss of nuclei and striations, brisk neutrophilic infiltrate
3-7 days of myocardial infarction
Disintegration of dead myofibres, dying neutrophils, early phagocytosis
7-10 days of myocardial infarction
Well developed phagocytosis, granulation tissue at margins
10-14 days of myocardial infarction
Well established granulation tissue with new blood vessels and collagen deposition
2-8 weeks of myocardial infarction
Increased collagen deposition, decreased cellularity
> 2 months of myocardial infarction
Dense collagenous scar
Transmural infarction
Ischemic necrosis affects full thickness of myocardium
Subendocardial infarction
Ischemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
What type of infarct correlates with Non-stemi
Subendocardial
