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PATH: Ischemic Heart
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| Question | Answer |
|---|---|
| cause of coronary ischemia | 1) atherosclerosis 2) Platelet problems 3) Hemodynamic abnormalitites 4) coronary artery spasms 5) syphilis 6) Kawaski's (arteritis) 7) coronary artery embolism |
| what is the initiating even of an infarct | rupture of a plaque (already 75% occluded) resulting in thrombis |
| what do EXPOSED platelets release to aggregate | adenosine DIphosphate |
| what does the tissue release to encourage coagulation | thromboplastin |
| what do activated platelets release | thromboxan A2, serotonin, and platelet factor 3 and 4 |
| Activated platelets (via tissue thromboxane favor? | vasospasm and coagulation |
| besides thrombus how can an MI be initiated | increased demand, decresed flow (sleep), cocain, syphilis, emboli, odd anatomy, arteritis |
| Most MIs involve? | LV, Septum and conducting system |
| when do you see an infarct of the RV | when there is a massive LV infarct |
| what is implied when you see an MI that is non-confluent (in a strange place | Collaterals |
| LAD supplies? | ant wall of LV and ant 2/3 of septum |
| what percent of MIs are LAD | 50% |
| RCA supplies? | posterior wall LV and post 1/3 of septum |
| LCCA supplies? | Lateral wall LV |
| what percent of MIs are RCA in origin | 30% |
| what percent of MIs are LCCA in origin | 20% |
| what part of the myocardial wall is most vulnerable | subendocardium (least well perfused) especially inner 1/3 of LV wall |
| where is clinically significant disease with the LCA | poximal 2-4 cm |
| where is clinically significant disese with the LCCA | proximal 2-4 cm |
| where is clinically significnt disease with the RCA | proximal and distal 1/3s |
| what mediates vasospasms | histomine and thromboxane |
| how long do you see prominant hemorrhage with reperfusion | through day 3-5 |
| you see mummified fibers and granulation what day is it post MI | 6-10 |
| when does collagen start to deposit post MI | day 10-14 after mummified fibers with no reperfusion and day 3-5(early collagen) with reperfusion |
| do you get granulation tissue with reperfusion and without | no only without |
| final appearance with reperfusion and without | with you have white intermingled with red myocardium without you have gelatinous to greywhite scar and greater healing at the borders |
| when do you get a tan yellow with soft center with no reperfusion | day 3-5 |
| how do you diagnose MI | 1) pain 2) increased CK, LDH, Troponin 3) systemic changes (acute phase) and fever and electrocardial changes |
| what electrocardial changes are seen with an MI | inverted T, elevated ST, and abnormal Q |
| what percent of MIs have arrhythmias | 70% within the first few hours |
| what type of ectopic arrhythimas are noted | extopics (extra ventricular systole), vtach, and vfib |
| what are the arrythmias noted with MI | 1. ectopics 2. heart block 3. autonomic stim |
| what artery supplies SA and AV nodes | RCA |
| what supplies the bundle of his an LBB | LAD |
| what is autonomic stim | symp and parasymp |
| what happens when there is LV failure following and MI | cardiogenic shock or severe pulmonary edema |
| what types of pericarditis can occur due to an MI | hemorrhagic and fibrinous |
| when does pericarditis occur | first 2-3 days |
| what are the top three complications of MI | 1) arrythmia (70%) 2) Systemic Emboli (50%) 3) Pericarditis (30%) |
| systemic emboli from Mi is due most often to? | mural thrombi |
| when is the maximum weakness of the heart | 5-7 days after you can have a rupture |
| what can happen when there is a rupture | 1) hemopericardium (tamponade) 2) intraventricular septal rupture (RV failure) 3) ruptured papillary muscle (mitral regurge) |
| when can you see a ventricular aneurysm | 2 weeks to several months after |
| what EKG change is noted with stable angina | ST depression maybe (subendothelial) |
| do enzymes elevate with angina | no |
| what do you see on EKG of prinzmetal angina | ST elevation (transmural) |
| sudden cardiac death occurs when? | within 1 hour of symptoms |
| what is noted with chronic ischemic heart disease | often post MI decompensation that results in a 4 chamber dilation with perivascular fibrosis |