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36 Cards in this Set
- Front
- Back
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What are some of the clinical manifestations of ischemic heart disease?
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angina pectoris
MI Chronic IHD with heart failure Sudden cardiac death |
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What are some of the causes of the ischemia?
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Fixed coronary obstruction
acute plaque change - platelet aggregation coronary thrombus vasospasm |
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Fixed coronary obstruction
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90% of patients
beginning of LAD and LCX entire length of RCA secondary epicardial branches rare in intramural branches |
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Acute plaque change
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rupturing or fissuring
erosion or ulceration can be triggered by adrenergic stimulation moderately stenotic are most dangerous |
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Coronary thrombus
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can cause partial to total occlusion
vessel mural thrombus can embolize - cause partial occluusion and can embolism activate smooth muscle growth related signals |
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Vasoconstriction
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adrenergic agonists
platelet contetnts impaired secretion of NO mast cells causing inflamation |
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What is the cause of stable angina? Unstable?
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Stable - decreased perfusion on exertment
Unstable - increasing in frequency, often at rest, due to distruption of atherosclerotic plaque with superimposed occluding thrombus harbinger of acute MI |
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What is Prinzmetal angina?
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due to coronary artery spasm
episodic, at rest treat with Ca channel blocker and nitroglycerin |
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What are some common risk factors with MI?
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Male, age,
females - after menopause blacks same risk as whites |
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What is the pathogenesis of MI?
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Active plaque disruption (hemorrhage, erosion, rupture)
platlets adehere to plaque site and release aggregators vasospasm extrinsic coagulation pathway |
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What is the myocardial response to ischemia?
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cesssation of glycolysis
accumulation of breakdown products loss of contractility injury and arrhythmias |
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Transmural vs. subendocardial infarction
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Most MI's are transumural
transmural - associated with coronary athersclerosis acute plaque change causes ST elevation on EKG Subendocardial inner walls difuse stenosing coronary atherosclerosis NO plaque disruption NO superimpsed thrombus from early lysed thrombus from severe prolonged hypotension Non ST elevated MI |
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What is the morphology process after an infarct?
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12-24 hrs red-blue from trapped blood (necrosis and neutrophil infiltrate)
10 days - soft yellow 2 weeks - yellow zone inside red zone past 8 weeks - scarring past this - can't tell |
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What are some treatments for MI?
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Thrombolysis
Angioplasty with possible stent placementCoronary bypass graft |
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What is thrombolytic therapy and PTCA?
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reestablishes flow through the occluded coronary artery salvages ischemic myocytes
PTCA + stent improves stenosis CABG helps perfuse tissue past plaque |
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What is the morphology of a reperfused myocardium?
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hemorrhagic
microscopic contraction bands (eosinophillic bands in sync with sarcomere's) can have free radical damage myocardium may be "stunned" - take several days to regain strength |
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What are some Lab tests done to diagnose MI?
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CK: MM - muscle; BB - brain lungs; MB - myocardium
starts 2-4 hrs/ peaks at 24/ returns by 72 (CK-MB not myocardium specific, could be skeletal) Troponins - cardiac specific rise similar to CK-MB, but may remain elevated for a week |
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What are some imaging studies done to dianose MI?
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ECHO
Radionucleotide angiography |
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What might post MI contractile dysfunction lead to?
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hypotension
pulmonary congestion cardiogenic shock |
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What arrhythmias or dysrhythmia are common post MI?
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sinus brady
asystole tachy V-vib premature Ventr. V-tach heart block |
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Consequences and Complications: Myocardial rupture
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3-7 days after MI
rip in necrotic/inflamed tissue Ventricular wall - most common IV septum - causes shunting papillary musce - causes mitral regurg |
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Consequences and Complications: Pericarditis
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2-3 days
fibrous/hermorrhagic tissue overlying the myocardium |
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What are some infarct related complications post MI?
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Right ventricular infarcts
infarct extension infarct expansion Mural thrombus ventricular aneurysm |
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What complications arise from large transmural infacts?
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cardiogenic shock
arrhythmias late CHF |
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What complications arise from anterior transmural infarcts?
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free wall rupture, mural thrombi, aneurysm
More severe clinical course |
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What are the complications of inferior transmural infarcts?
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conduction blocks, right ventricular involvement
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What is ventricular remodeling?
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necrotic area thins - can aneurysm
non-infarcted area hypertrophys - seems good, but may lead to impairment Goal is to minimize remodeling with medication |
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WHat are the most important factors in determining prognosis post MI?
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quality of LV function
area necrosed |
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What are the preventative measures for MI?
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aggressive risk factor modification
prevent reinfarction |
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Chronic Ischemic Heart Disease
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often elderly
progressive heart failure history of MI or bypass surgery cardiac decompensation of hypertrophied myocardium severe obstruction of coronary artery |
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What is the morphology of chronic ischemic heart disease?
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heart is enlarged and heavy
coronary arteries severly stenosed healed infarcts usually present |
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What is the clinical picture of someone with chronic ischemic heart disease?
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previous MI
Angina CHF some patients are previously silent - only present with CHF accounts for 1/2 of transplants |
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What are some causes of sudden cardiac death?
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IHD
Congenital abnormalities valvular problems myocarditis cardiomyopathy |
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What is the MOA of suden cardiac death?
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formation of a lethal arrhythmia (v-fib)
#3 coronary syndrome (#1 - unstable angina, #2 MI) |
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What is the morphology of sudden cardiac death?
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most have high great stenosis (>75%)
some have previous MI prognosis improved with implantation of defibrilator |
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What is the common pathophysiology of the acute coronary syndromes?
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atherosclerotic plaque disruption with thrombus formation
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