Ischemic syndromes

Wednesday, November 19, 2008
Ischemic syndromes
Stable angina vs. unstable
Stemi vs. nonstemi
A stemi, plaque rupture rapid thrombus formation through the whole wall. A much bigger infarcton. This is something you have on page 146.
They all relate to atherosclerotic plaque
If it’s stable, it sticks way out into the vessel
Unstable plaques tho, might be completely flat. Pts may have no symptoms at all until they rupture. We go to acute coronary syndromes. If it’s sustained it leads to MI which is stemi and nonstemi. Page 143. We are only looking at part of this picture. Left main divides into the LAD and left cirq.
Right coronary comes off the aortic valves and perfuses the right ventrical and the nodes and wraps around in the inferior part of the heart. SA nodes. Responsible as the pacemaker of the heart and controlling conduction in the heart. IF you had an infarction that damaged your nodes you might not generate an adequate heart rate. Right coronary disease can cause bradycardia. And if conduction can’t go from the av node you call it heart block. Obstruction to right coronary artery affects the inferior heart and is associated with bradycardia and heart block.
The left coronary artery perfuses the major heart muscle which is required for normal ventricular function. When you have an infarction involving the distributino of the LAD you worry about tachyrhythmias. Morelikely to result in heart fialure.
In men of middle age, the symptoms of ischemic heart disease are extremely predictable. Nausia diaphorses, anxiety, substantial pain chest pain radiating to arm and neck, dypnea.
Women often present with atypical symptoms most commonly the sudden onset of extreme fatigue. Elderly pts and pts with diabetes frequently have silent ischemia. Just know they feel bad. The absence of classis symptoms does not rule out someone having a heart attack.
Stable plaque partially obstructs flow. Increase demand by some form of exercise. Pain is predictable and relieved with rest. Measuring something called cardiac iso enzymes. Troponin. CPKMB. Not elevated during stable angina. ST depression which returns to normal with cessation of pain. Treat with antithrombitcs like aspirin and treating risk factors like statins and PCI or CABBG.
Changes on the ECG.
Lactic acidoses stimulates the autonomic nervous system and the sympathetic nerves enter thes pine in the same place as the arm and the jaw. Arm is getting enough flow, its just a cross stimulation of nerves.
Krebs cycle requires oxygen and sugar to make ATP and if you don’t have nough it releases lactate which is an acid and an acidic environment is bad for tissue function and it hurts.
Coronary stenting. You probably don’t have just one problem. You must deal with it systemically. Get nitrates to deal with vasospasms. May be beta blockers and calcium channel blockers. And Every one with atherosclerotic heart disease will get STATINS. They help to stabalize plaques.
Coronary Artery bipass graph: used to be more common than anything. Pypass the obstruction.
Acute Coronary Syndromes: all characterized by the rupture of an unstable plaque. How long did that clot stick there? If they have ST elevaation, we know what they have. ST depression of ischemia with exercise. Lesion may not obstruct the vessel very much. Thin cap and vulnerable to rupture. IF that clot is big enough and stays a long time, we see ST elevation and stemie. So we just did stable plaque and stable angina. Alteration of rupture. Sustained ischemia infarction. Fabulus artists rendition.
The plaque ruptures. Stress and Cold weather, so it may have to do with SNS. Also more in moring when theres a busrt of cortical. Unstable angina often occurs at rest. So the thing just ruptures and once it rupture it exposes all this damaged tissue and we see them stick until they obstruct the vessel. If we have spontaneous dissolution of this clot, which does happen, then less than 20 mins perfusion is restored and we have unstable angina. If it was to stay there more than 20 minutes then we would see noontime or stemie depending on whow long it stuck there./
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Next step. Understnaidng anatomy of coronary perfusion. Whqat we have is across section of the ventricle. Clot forms an area of ischemia. If clot dissolves in more than 20 minutes then is this unstable angina a prescursor to ? No heart damage to eleveation fo cardiac is enzymes. If a clot stays longer, you get infarction. Yellow part is infarction. Because of anatomy of coronary vessels. Infarction stays near the . Sub endocardial MI = non stemie.
Watching desperate housewives and gets tremendous chest pain. Rushes to Er and gets there in 20 minutes. ST deprssion and no elevation of cardiac is enzymes: Unstable angina
ST depression and cardiac enzymes elevated. If didn’t get there till 40 minutes…
Later…transmural
And when that occurs we see .
Chest pain at rest, ECG shoes transient changes relieved with rest: unstable angina.
Review thse stemie things.