Chest Pain & Breathlessness Flashcards
IHD Syndromes
MI
Angina (stable and unstable)
Sudden cardiac death
Most common cause of IHD
Atheroma of coronary arteries
Causes of IHD
Atheroma of coronary arteries
Coronary artery Vasculitis
Coronary artery vasospasm
RF for IHD
Male Old FH Hyperlipidaemia Hypertension Diabetes Mellitus Smoking Obesity Stress Lack of exercise
Stage 1 of atherosclerosis
Blood flow forms eddies
Loose platelet aggregation
Stage 2 of atherosclerosis
Arterial wall injury at platelet reaction sites Loosened injured endothelium Low grade inflammation Oedema Ruptured internal elastic membrane
Stage 3 of atherosclerosis
Smooth muscle cells proliferate and produce collagen
Stage 4 of atherosclerosis
Blood lipids leak into vessel wall
Smooth muscle cells take up fat and store as droplets
Macrophages take up released fat droplets by phagocytosis
Collagen fibres form
Stage 5 of atherosclerosis
Collagen increases
Cellularity decreases
Stage 6 of atherosclerosis
Acellular plaque with abundant collagen
Stage 7 of atherosclerosis
Necrotic centre and calcified
Stage 8 of atherosclerosis
Calcified necrotic area becomes gruel like
Cholesterol crystals form
Vasa vasorum vessels grow into intima
Complications of atherosclerosis
Ulceration Fissuring Haemorrhage Thrombosis Aneurysm
Stage 9 of atherosclerosis
Risk of massive thrombus formation as exposure of collagen, coagulation and blood flow
Plaque suddenly ruptures
Stage 10 of atherosclerosis
Eddies downstream form plaque stenosis
Platelets thrombus formed = may grow and occlude lumen
Acute MI Types
Transmural
Subendocardial
Transmural Infarction
- involving whole thickness of ventricular wall
- underlying lesion is atheromatous plaque undergone fissuring and occlusive thrombosis
Subendocardial infarction
- inner third or half of myocardium
- from generalised underperfusion of myocardium
MI in L. coronary artery
Massive anterolateral MI
MI in LAD
Anteroseptal MI
MI in L circumflex
Lateral MI
MI in RCA
Posterior MI
0-12hrs MI appearance
No changes
12-24hrs MI appearance
- pale blotchy discolouration
- bright eosinophilia of muscle fibres
24-72hrs MI appearance
- soft, pale, yellow
- loss of nuclei striations
- heavy interstitial neutrophil infiltrate
3-10d MI appearance
- soft yellow/brown
- hyperaemic border
- replacement of infarcted area with granulation tissue
weeks- months appearance
- white fibrous scar
- collagenous scar tissue
ST MI complications
- L ventricular failure
- cardiac dysrhythmias
- ventricular wall rupture
- papillary muscle infarction
- mural thrombus
- fibrinous pericarditis
- DVT -> PE
LT MI complications
- intractable L. ventricular failure
- ventricular aneurysm
- Dressler’s syndrome
- recurrent MI
What do effects of PE depends on?
- size of occluded vessel
- number of emboli
- adequacy of bronchial blood supply
Define large PE
- large embolus coils within 1 pulmonary artery
- saddle embolus blocks both pulmonary artery
= circulatory collapse
Define medium sized PE
- dural blood supply protects lungs from pulmonary artery obstruction
How does a pulmonary infarction occur?
multiple emboli combined with poor bronchial blood supply
Pathogenesis of atheroma
- encrustation (platelets form thrombi over injured endothelium)
- inhibition (inflammation = plasma filtration)
- Reaction to injury (increased permeability and SM accumulation
- Monoclonal hypothesis (SM cells)