Term
| can vasoconstriction reduce blood flow to the heart and cause ischemia? what else can it affect? |
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Definition
| yes, vasoconstriction can reduce blood flow to the heart - which can potentially lead to infarcts/arrhythmia. it can also cause changes in plaque morphology |
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Term
| what can cause vasoconstriction? |
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Definition
| adrenergic agents, released platelet contents, impaired secretion of endothelial cell relaxing factors, and mediators released from perivascular inflammatory cells (inflammation is becoming increasingly more recognized in the pathogenesis of CAD) |
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Term
| can can develop with slowly progressing CAD? |
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Definition
| collateral circulation (a kind of "auto-bypass") |
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Term
| are most hearts usually L or R dominant, and what does this mean? |
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Definition
| most hearts are L dominant systems - meaning the L coronary artery is providing most of the blood flow to the posterior ventricle |
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Term
| what does the location of the atherosclerotic lesion determine? |
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Definition
| where the ischemia is, what the EKG changes look like, how much myocardium is involved, |
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Term
| where are the majority of lethal atherosclerotic lesions found? |
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Definition
| in the proximal LAD (closest to the L main and the aorta - several cm from its origin) |
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Term
| the more proximal an atherosclerotic lesion the less __________ and more ____________ ? |
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Definition
| the more proximal an atherosclerotic lesion the less blood will go to the area beyond and more ischemia will occur |
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Term
| what is myocardial bridging? why is this a potential risk? |
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Definition
| when a portion of the coronary artery dips down into the myocardium. this is a potential risk, b/c when the myocardium contracts - it may compress the artery. scar tissue will often form around these spots |
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Term
| what happens within 10 min of an MI? |
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Definition
| 50% of ATP are reduced from normal |
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Term
| what happens within 40 min of an MI? |
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Definition
| only 10% from normal ATP levels remain |
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Term
| at what point does irreversible cell injury occur after an MI? |
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Definition
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Term
| how long does it take for microvascular injury to occur after an MI? |
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Definition
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Term
| what do the location, size and morphology of an MI depend on? |
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Definition
| the location/severity (degree of obstructino)/rate of development of coronary atherosclerotic obstructions (younger = worse, less time to collateralize), the size of the vascular bed perfused by the obstructed vessels, the duration of the occlusion, the metabolic/O2 needs of the myocardium at risk (hypertrophic hearts require more), the extent of the collateral blood vessels, the presence/site/severity of the coronary arterial spasm, and other factors (alterations in BP, HR, cardiac rhythm) |
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Term
| between 1/2-4 hrs after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| there are not usually any gross changes in heart tissue, microscopically; variable waviness of fibers at the border and sarcolemmal disruption consisting of mitochondrial amorphous densities is seen |
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Term
| between 4-12 hrs after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically the beginning of coagulation necrosisis (coagulation of the cell, but the outline is still maintained) seen w/edema and hemorrhage - appearing grossly as occasionally dark mottling |
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Term
| between 12-24 hrs after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically; ongoing coagulation necrosis, pyknosis of nuclei (pinkish), myocyte hypereosinophilia, marginal contraction band necrosis, beginning *neutrophilic infiltrate* occur - grossly appearing as dark mottling |
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Term
| between 1-3 days after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically; ongoing coagulation necrosis w/loss of nuclei and striations and interstitial infiltrate of neutrophils occurs - grossly appearing as mottling w/yellow-tan infarct centers |
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Term
| between 3-7 days after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically; beginning disintegration of dead myofibers w/dying neutrophils, early phagocytosis of dead cells by *macrophages* at the infarct border occurs - grossly appearing as a hyperemic border with central yellow-tan softening |
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Term
| between 7-10 days after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopially, there is well developed-phagocytosis of dead cells; early formation of fibrovascular *granulation tissue* at margins - grossly appearing as maximally yellow-tan and soft, w/depressed red-tan margins |
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Term
| between 10-14 days after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically, there is now well established granulation tissue with new blood vessels and collagen deposition - grossly appearing as red-gray depressed infarct borders |
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Term
| between 2-8 wks after an MI, what are the microscopic and gross changes in heart tissue? |
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Definition
| microscopically, there is increased collagen deposition, w/decreased cellularity - grossly appearing as a gray-white scar; progressive from the border toward the core of the infarct |
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Term
| at >2 mo, what is the morphology of an MI? |
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Definition
| microscopically, the scarring is complete and grossly the area affected appears as a dense collagenous scar |
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Term
| what are the general complications in the first couple of hours after an MI? |
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Definition
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Term
| what is significant about days 3-7 after an MI? |
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Definition
| there is danger of the myocardium rupturing, during the phagocytosis of the dead myocytes and before the scar tissue can be laid down |
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Term
| why is the endocardium most susceptible to ischemia? how does it correlate with the zone of necrosis? |
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Definition
| b/c it is the farthest away from the arteries. the zone of necrosis starts from the endocardium and can either remain a subendocardial infarct - or it may progress to transmural infarct that involves the entire wall |
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Term
| what is in danger of rupturing at between 7-10 days after an MI? |
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Definition
| where still living myocytes meet granulation tissue there is a high susceptibility to shearing forces at systole |
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Term
| can reperfusion after ischemia damage the heart? |
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Definition
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Term
| what are possible complications of an MI? |
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Definition
| contractile dysfunction, arrhythmias, papillary muscle dysfunction and rupture, ventricular/septal rupture, mural thrombi (potential for systemic emboli), acute pericarditis, and ventricular aneurysms (bulging of fibrous myocardium) |
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Term
| after an MI, how might resultant contractile dysfunction manifest itself? |
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Definition
| as left ventricular failure, hypotension, vascular congestion, pulmonary edema (due to backng up of blood), and cardiogenic shock (heart stops beating completely) |
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Term
| after an MI, how might resultant an arrythmia manifest itself? |
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Definition
| as a conduction disturbance, myocardial irritability, sinus bradycardia, asystole, PVC, and/or a heart block |
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Term
| when does papillary muscle dysfunction and rupture occur usually occur post MI? |
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Definition
| 3 days - as indicated by a murmur |
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Term
| when is the heart at highest risk for ventricular/septal rupture post-MI? |
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Definition
| @ 4-7 days, when dead myocardium are being phagocytized - but no fibrous tissue is being laid down. it may easily tear at its junction w/still intact myocardium |
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Term
| when is the heart at risk for mural thrombi post-MI? what is another potential risk with this? |
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Definition
| very early on to later, mural thrombi can be due to arrythmic change to blood flow. mural thrombi can also give off systemic emboli causing a change in mental status if the brain is involved. |
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Term
| when are pts at highest risk for acute pericarditis post MI? |
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Definition
| 2-4 days - this can contribute to cardiovascular decline esp with friction rub |
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Term
| when are pts at highest risk for ventricular aneurysms post MI? how do they appear? |
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Definition
| months to years. they appear as bulging fibrous tissue that has replaced active myocardium, and therefore makes the heart less pliable, affecting its contractility as well as more likely to form thrombi |
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Term
| what are the clinical feature of an MI? |
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Definition
| substernal chest pain radiating to the L arm, neck, jaw. |
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Term
| what pts are particularly at risk for slient MIs? |
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Definition
| diabetics (may not have pain due to neuropathy) and pts with HTN |
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Term
| how is lactate dehyrogenase good for lab evaluation of MIs? is there a specific form of it that is more related to the heart? |
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Definition
| total lactate dehydrogenase rises within 24 hrs of an MI, it peaks at 72 hrs and persists for a week. LD-1 is present on the myocardium and is more specific to cardiac damage |
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Term
| how is creatine kinase good for lab evaluation of MIs? does it have different dimers that behave differently? |
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Definition
| total creatine kinase rises 2-4 hrs post MI, peaks at 24, and returns to normal by 72 hrs. CK-MB is released 2-4 hrs post MI, peaks at 18 hrs and disappears by 48 hrs (if there is no change in CK-MB levels 2 days post chest pain, you can r/o an MI - good initial indicator) |
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Term
| how are troponin levels used to help dx MIs? is there one isomer that is more effective for MI dx? |
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Definition
| cardiac troponins cTnT and cTnI both rise at the same time as CK-MB (2-4 hrs post MI) and peak at 48 hrs, but their levels remain elevated for 4-7 days post MI. *cTnI is more cardiospecific* |
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