Pathophysiology of Ischaemia and Infarction Flashcards
Ischaemia
Relative lack of blood supply to tissue/organ leading to hypoxia
Factors affecting oxygen supply
Inspired oxygen Pulmonary function Blood constituents Blood flow Integrity of vasculature Tissue mechanisms
Factors affecting oxygen demand
Tissue itself
Activity of tissue above baseline value
Ischaemic heart disease supply issues
Coronary artery atheroma
Cardiac failure
Pulmonary oedema or disease
Previous MI
Ischaemic heart disease demand issues
Heart has high intrinsic demand
Exertion/stress
Clinical consequences if ischaemic heart disease
MI Transient ischaemic attack Cerebral infarction Abdominal aortic aneurysm Peripheral vascular disease Cardiac failure
Functional effects of ischaemia
Blood/oxygen supply fails to meet demand due to decrease in supply and increase in demand
Biochemical effects of ischaemia
Decrease in oxygen leads to anaerobic metabolisms, change in acid base balance due to build up of lactate, cell death
Clinical effects of ischaemia
Dysfunction
Pain
Physical damage to specialised cells
Outcomes of ischaemia
No clinical effect
Resolution vs therapeutic intervention
Infarction
Infarction
Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either arterial supply or venous drainage
Aetiology of infarction
Thrombosis
Embolism
Strangulation
Trauma
Scale of damage of ischaemia/infarction depends on
Time period
Tissue/organ
Pattern of blood supply
Previous disease
Coagulative necrosis occurs in
Solid organs e.g. heart, lung
Colliquitive necrosis occurs in
Loose organs e.g. brain
Colliquitive necrosis
Transformation of the tissue into a liquid viscous mass
Coagulative necrosis
The architecture of dead tissue is preserved for at least a couple of days. If enough viable cells are present around the affected area regeneration will usually occur.
Severe ischaemic damage is irreversible at what time
20-30 mins
Sequence of events following myocardial infarction
Anaerobic metabolisms, onset of ATP depletion Loss of myocardial contractility Ultrastructural changes Myocyte necrosis injury to the microvasculature
Appearance of infarct at less than 24 hours
No change
Appearance of infarct at 24-48 hours to naked eye
Solid tissues - pale infarct
Loos tissues - red infarct
Appearance of infarct at 24-48 hours microscopically
Acute inflammation at edge of infarct
Loss of specialised cell features
Appearance of infarct at 72 hours onwards to the naked eye
Pale infarct - becomes yellow/white with red edges
Red infarct - no change
Appearance of infarct at 72 hours onwards microscopically
Chronic inflammation
Macrophages remove debris
Granulation tissue
Fibrosis
Appearance of infarct end result
Scar replaces area of tissue damage
Shape depends on territory of occluded vessel
Reparative process of myocardial infarction
Cell death Acute inflammation Macrophage phagocytosis of dead cells Granulation tissue Fibrosis (collagen deposition) Scar formation
Transmural infarction
Ischaemic necrosis affects full thickness of the myocardium
Subendocardial infarction
Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
Effects of infarction depend on
Site within body and organ
Size of infarct
Contribution of previous disease/infarction
Effects of infarction
Death
Dysfunction
Pain
Complications of myocardial infarction
Sudden death Arrhythmias Angina Cardiac failure or rupture Pericarditis Thrombosis or embolism
