What are the characteristics of an MI
Site, radiation
-diffuse, ant chest, l arm, neck
Character
-tight, pressure, dull, weight
Triggers
Relief
-rest, GTN
Duration
Why do we get pain in MIs
Stenosis > 80% => ischemia as demand > supply
Increase in metabolites (bradykinin, adenosine) => visceral pain
Why do we get breathless in MIs
Decreased CO => increased LVEDP => net mv of fluid into lungs => decreased gas exchange
How would you diagnose an MI
ECG
-ST elevation or no ST elevation
Troponin
-significantly increased
What are the 2 types of MI
STEMI
-transmural, complete occlusion
NSTEMI
-subendocardial, partial occlusion
How does atherosclerotic plaque rupture lead to MI
Foam cells induce SM death => protease release
=> soften collagen in cap
Platelets gather at rupture side => thrombus => stenosis
How would you treat the thrombus
Drugs
Mechanical
-PCI => increase perfusion, decrease stroke and bleed risk
How would you treat the decreased coronary flow
Why would you use these drugs
Antianginals
Decrease the cardiac load and strain
Increase the amount of coronary perfusion
How would you prevent future MIs
-2 methods
What drugs would you use
Reduce effect of stenosis
Reduce wall stress from dilation