Ischaemia and infarction Flashcards
ischaemia
relative lack of blood supply to tissue/ organ leading to inadequate oxygen supply to meet needs of tissue/ organ: hypoxia
types of hypoxia
hypoxic, anaemic,
hypoxic hypoxia
low inspired oxygen or normal inspired oxygen but low partial pressure of oxygen
anaemic hypoxia
normal inspired oxygen but blood abnormal
stagnant hypoxia
normal inspired oxygen but abnormal oxygen delivery eg occlusion of vessel (local) and shock (systemic)
cytotoxic hypoxia
normal inspired oxygen but abnormal at tissue level
factors affecting oxygen supply
inspired oxygen, pulmonary function, blood constituents, blood flow, integrity of vasculature, tissue mechanisms
factors affecting oxygen demand
tissue type, activity of tissue above baseline value
ischaemic heart disease
supply issues- coronary artery atheroma, cardiac failure, pulmonary function- other disease or pulmonary oedema, anaemia, previous MI
demand issues- heart has high intrinsic demand, exertion/ stress
clinical correlation between ischaemic heart disease and atheroma
ulcerated/ fissured plaques leads to thrombosis which leads to ischaemia and or infarction
functional effects of ischaemia
blood oxygen supply fails to meet demand due to decreased supply and increased demand or both. related to rate of onset. can be general, chronic, acute on chronic
cellular effects of ischaemia
different tissues have variable oxygen requirement and variably susceptible to ischaemia, neurons, heart cells, renal tubular cells affected more than fat, bone etc
clinical effects of ischaemia
dysfunction, pain, physical damage
outcome of ischaemia
no clinical effect, resolution, infarction
aetiology of infarction
thrombosis, embolism, strangulation eg gut, trauma
scale of damage of ischamia and infarction depends on
time period, tissue organ, pattern of blood supply, previous disease
types of necrosis
coagulative and colliquitive
myocardial ischaemia process and time
anaerobic metabolism and onset of ATP depletion, loss of myocardial contractility, ultrastructural changes eg myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling. all happens within a few mins. 20-30mins means irreversible damage. 20-40 mins myocyte necrosis. 1 hour to injury to microvasculature
appearances of infarcts over time
less than 24 hours swollen mitochondria, 24-48 hours acute inflammation initially at edge of infarct, loss of specialised cell features, 72 hours- chronic inflammation, macrophages remove debris, granulation tissue, fibrosis
pale infarcts occur in
myocardium, spleen, kidney, solid tissues. turn yellow and red periphery after 72 hours
red infarcts occur in
lung, liver loose tissues, previously congested tissue, venous occlusion, secondary/ continuing blood supply. little change after 72 hours
end result of infarct
scar replaces area of tissue damage (more white) and shape depends on territory of occluded vessel
reparative processes of myocardial infarction
cell death, acute inflammation, macrophage phagocytosis of dead cells, granulation tissue, collagen deposition, scar formation
transmural infarction
ischaemic necrosis affects full thickness of the myocardium
acute infarcts are classified according to
whether there is elevation of the ST segments on the ECG.
non stemi
no ST segment elevation but a significantly serum troponin level. thought to correlate with a subendocardial infarct
effects infarction
site of dependent, size of infarct, death, dysfunction, contribution of previous disease/ infarction
complications of myocardial infarction
sudden death, arrhythmias, angina, cardiac failure, cardiac rupture, papillary muscle, reinfarction, pericarditis, papillary muscle dysfunction, pulmonary embolism secondary to deep vein thrombosis, mural thrombosis, ventricular aneurysm, dresslers syndrome
