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25 Cards in this Set
- Front
- Back
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pathogenesis of MI
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85-90% due to trhombotic occlusion of coronary artery due to primary plaque rupture
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most dangerous plaques - factors
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are not the ones that occlude more of the lumen
the noncalcified ones with thin fibrous cap key factors that increase vulnerability: low smooth muscle cell count thin cap high macrophage content large lipid core |
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T/F Red clots give thrombolytics
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True
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T/F White clots give thrombolytics
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False: gives platelet inhibitors
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T/F red clots are associated with non-ST elevation MI
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False; associated with ST elevation MI
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T/F white clots are associated with ST elevation MI
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False; associated with non-ST elevation MI
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etiology of heart block
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anterior MI - damages septum and infranodal conduction system
inferior MI - activates CV reflexes or damages AV node |
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1st degree AV block
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longer PR segment
>0.2s usually asymptomatic |
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2nd degree Mobitz 1 (wenckenbach)
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PR segment gets progressively longer until a dropped QRS complex
usually asymptomatic or mild symptoms impairment is usually at the AV node |
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2nd degree Mobitz II
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PR segment remains constant until a dropped QRS complex
more symptoms than Mobitz I, need to monitor closely - can convert to complete heart block impairment usually below the AV node |
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3rd degree heart block
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P waves and QRS complex do not correspond to each other - complete disassociation
very dangerous |
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premature ventricular contraction
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see a random QRS copmlex with no associated p wave and a compensatory pause
asymptomatic...don't treat...test electrolytes |
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Accelerated Idioventricular Rate (AIVR)
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ventricular rhythem between 60-125
see with patients with anterior MI 2 days after short lasting an terminate on its own, likely a good sign of reperfusion related to automaticity of purkinfe fibers |
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ventricular tach
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sustained is >3 or more beats lasting for more than 30s - requires intervention
nonsustained >3 beats lasting less than 30 seconds polymorphic indicates bigger infarct - worse monomorphic - focal need to defibrilate...VT and Vfib are bad |
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premature atrial contraction
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premature heart beat originating in atria
can set off Afib or Aflutter - but usually not an issue on hemodynamic system |
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torsades de pointes
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a type of polymorphic ventricular tachycardia with characteristic sine wave pattern on EKG
associated with low Magnesium certain drugs can cause |
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mitral insufficiency/regurgitation
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usually due to rupture of papillary muscle
most often the posterior papillary muscle (due to inferior MI) rare but can be fatal see 2-7 days after MI get increases in LA pressure because of increased volume to pump against due to regurg also see rise in pulmonary arteries - get pulm edema |
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septal rupture
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2% of acute MI
5-7 days after MI either anterior or inferior hard to differentiate from mitral regurg |
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LV free wall rupture
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10% of patients who die after MI
1day - 3weeks later elderly, high bp increases risk sudden cardiac tamponade |
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mural thrombus
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found 40% in anterior MI
60% if apex is involved can embolize need anticoagulation |
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RV infarct
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see with inferior MI, RCA occlusion
clear lung sounds because RV damage preventing from pumping to lungs see systemic blood backup JVD kussmaul sign edema in extremities give volume to increase preload and positive inotropic drugs NO DIURETCS |
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pericarditis causes
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infection
post-MI Dressler's syndrome |
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Dressler's Syndrome
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autoimmune etiology
malasise, fever, pain, leukocytosis 1-8 weeks after MI |
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MONA treatment
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morphine
oxygen nitroglycerin aspirin |
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can you use calcium channel blockers to treat MI?
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NO
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