Pathophysiology of IHD Jeeves

Causes Obstruction of blood flow Decrease in flow of oxygenated blood Increased oxygen demand

Obstruction of blood flow Atherosclerosis Thrombosis Embolism CA Vasospasm- Called variant angina. The exact cause is unknown. Usually happens at rest in the morning. Coronary ostial stenosis- Narrowing of the mouths of the coronary arteries as a result of syphilitic aortitis or atherosclerosis Coronary arteritis- In inflammatory conditions like SLE

Decrease in flow of oxygenated blood Anaemia Carboxyhaemoglobinaemia- When CO binds to haemoglobin it does so irreversibly and remains bound to it until the red cell is broken down. CO poisoning occurs due to car exhaust (attempted suicide), smoke from a fire and tobacco smoke. Hypotension- cardiac perfusion is impaired when BP drops in shock.

Increased oxygen demand Thyrotoxicosis- Causes increased heart rate and can cause CA vasospasm. Myocardial hypertrophy- When the myocardium hypertrophies the coronary arteries may not be able to supply the increased thickness of the muscle resulting in ischaemia during exertion.

Atherosclerosis Fatty streaks Atheroma formation Lipid accumilates in the tunica intima Macrophages invade, phagocytose the lipids and develop a foamy appearance. Atheroma formation The underlying smooth muscles proliferates. The atheroma may grow slowly and gradually occlude the vessel or its protrusion into the vessel lumen may cause sufficient turbulence to wears away the endothelium and exposes the underlying collagen. A thromus forms on the exposed surface. This has the potential to embolise. A 50% reduction in CA lumen diameter causes a haemodynamically significant reduction in flow and ischaemia occurs on exertion.

Acute Coronary Syndromes Include STEMI, NSTEMI and unstable angina. Unstable angina- Worsening myocardial ischaemia which occurs at rest. It is due to thrombosis resulting from the rupture of a fibrous cap on an atheromatous plaque. This is a grey area between stable angina and AMI and is differentiated from a NSTEMI by negative cardiac enzymes. Pts are at high risk of AMI.

AMI Obstruction of a coronary artery can lead to myocardial necrosis within 15-30 minutes. The sub endocardial myocardium is the first to be affected (as it is the furthest away from the arteries). With continued ischaemia the necrosis spreads all the way to the sub epicardial myocardium producing a transmural MI. The aim of Tx is to re-perfuse the myocardium and reduce the thickness of the necrosis.

AMI Histology Normal Acute AMI Fibrosed myocardium several months post AMI