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34 Cards in this Set
- Front
- Back
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Acute MI
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WA present AT REST however bc Acute wall thickness will still be normal
-BUT systolic wall thicken endocardial motion decrease -hypokinetic/Akinetic |
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CHRONIC MI
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thinning wall
-increase echo wall affected segments does not mean entire wall bc 2ndary to scar tissue or fibrosis - abnormal wall motion -absent wall thickening |
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What is Ischemia
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lack of o2 imbalance myocardial o2 supply and demand ratio
-supply does not meet demand |
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When narrowing greater than 70% of cross sectional area of vessel
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ISCHEMIA
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Myocardial infarction
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irreversible injury to myocardim
-2ndary prolong ischemia -not enough o2 to the tissue over significant period time usually bc pt had: - atherosclerosis, piece of plaque broke off, bleed thrombosis, and occlude CA |
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Immediately Post MI
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akinetic area
-wall thickens normal |
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damage more 50% wall
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transmural
BIG Q WAVES wall thinning def area Akinesis |
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Stunned Myocardium
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is reversible WMA after reperfusion of transient CA occulusion
-reperfusion can occur spontaneously or after thrombolytic therapy or angioplasty it can take from days-weeks |
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Hibernating Myocardium
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chronically depressed myocardial function resulting from chronic myocardial ischemia
-Recovery of myocardial function after coronary revascularization -pet scan remains the gold standard for detecting myocardial viability |
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Complications of post MI
Acute phase |
-LV systolic dysfunction - rupture
-MR -LV thrombosis -Tamponade/PE -RV infarct -LVOT obstruction |
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Complications of Post MI
Chronic Phase |
infarction expansion
ventricular aneurysm LV thrombus |
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FREE Wall rupture
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!% pt with MI
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why pt dies? (rupture)
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basically sudden hemodynamic collapse bc muscle tears blood leaks out LV travels around the heart = instant tamponade
- NO blood going to AO |
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Most ruptures occur
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1st week in infarct - elderly women
-electromechanical disassociation -not going to have regular contraction |
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May present in sub acute phase
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hyptension recurrent chest pain vomitting
HX: - MI -CAD present hyptension =Rule out free wall rupture |
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Pseudo aneurysm with free wall rupture
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usually happens inferiolateral wall
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Ventricular septal rupture
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pt can develop spontaneous VSD
- 1-3% with infarct within 1st week -more common elderly women -single vessel CAD |
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Clinical presentation of VSD
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sudden hemodynamic deterioration
murmur- systolic |
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What causes shunts
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pressure causes shunting
-when is LT and RT pressure biggest? during systole |
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Systolic murmur POSt MI
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-pm dysfunction/rupture
-free wall rupture -pericardial rub= pericarditis Acute LVOT obsturction -VSD rupture |
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POST MI VSD
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defect always found thin area of the myocardium that s why its torn
=with dyskiniesis motion - not only tissue dead wrong direction |
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PM Rupture
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MV cant close blood will leak back
- severe Regurgitation immediate repair - replacement serious complication MV small infarct RT or circumflex artery |
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Which PM most likely to rupture
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PMPM - most like to rupture bc feed by 1 CA
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3 Scenarios that can cause severe MR
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1. PM RUPTURE
2. PM DYSFUNCTION 3. LV CH MITRAL ANNULUS DIaLATION |
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PM dysfunction
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not getting perfused enough
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mintral annulus dilatation
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if CH dilates the annulus stretches
-PT MI if wall damaged it stretches not contracting LV dilates |
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Tamponade/PE
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larger eff- worry about rupture of free wall
- common to see PE post MI |
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RV infarct
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frequently with MI
but hemodynamically significant infarct of RV not common - |
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INferior wall MI associated with
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RV INFARCT
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PT with hypotensive RV dilated
(hypo -Akinetic) |
RA enlarged
TR dilated TRicuspid annulus |
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Infarction expansion
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area that is damaged spreads
-when tissue is scared thin and wall stretches -wall not movin or moving opposite direction what happens? develop ventricular aneurysm |
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Ventricular aneurysm
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most common apex
2nd most common inferobasal |
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True aneurysm
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myocardial thinning
bulging motion systole Aneurysm formation related transmural -MI freq apex |
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Thrombus
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behind abnormal wall motion
Akinetic dyskinetic heterogenous |
