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18 Cards in this Set
- Front
- Back
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def of acute coronary syndrome
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a spectrum of ischemic myocardial events that share same pathophy.
Unstable angina->NSTEMI->STEMI |
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diagnosis of ACS dependent on (3)
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1. presentation-symptoms and history
2. blood tests-cardiac markers and CBC 3. diag testing-electrocardiogram, echo, nuclear imaging |
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will unstable angina show +/- symptoms, cardiac markers and EKG changes
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+ symptoms
- cardiac markers (normal troponin, CPK, myoglobin) +EKG changes (T wave changes and ST depression) |
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will NSTEMI show +/- symptoms, cardiac markers and EKG changes
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+ symptoms
+cardiac marker changes (raised troponin) +EKG changes (T wave changes and ST depression) |
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will STEMI show +/- symptoms, cardiac markers, and EKG changes
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+symptoms
+cardiac marker changes (raised troponin) +EKG changes (T wave inversion, ST elevation, prominent Q wave) |
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3 cardiac markers
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1. troponin
2. creatine phosphokinase 3. myoglobin |
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when is troponin released?
3 subtypes? how long does it stay elevated? |
1. cardiac specific protein released following cell death. when myocyte doesn't get enough O2, cell becomes leaky and troponin leaves.
2. Troponin T, I & C. T&I used to diag MI 3. elevate w/in 2-4 hrs and persists for 7-14 days |
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when is CPK released?
3 subtypes? how long does it stay elevated? |
1. present in all muscle tissue. CPK-MB released from injured heart muscle.
2. CK-MB (myocardium), CK-MM (skeletal), CK-BB (brain) 3. elevate w/in 4-8 hrs and persists for 72 h |
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def of myoglobin
how long does myoglobin stay elevated? |
1. protein found in cardiac and skeletal muscle
2. elevate w/in 2-3 hrs and returns to norm within 24h |
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in what order does acute MI affect heart tissue
diff b/w UA, nonstemi, stemi |
1. from inside to outside:
subendocardium->myocardium->epicardium 2. UA-no dead areas in heart nstemi-areas of necrosis limited to subendocardium stemi-transverse dmg |
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acute MI:
def, usually caused by, time to perm damage? |
def: death/irreversible dmg of myocardial cells
cause: usually a rupture of atherosclerotic plaque & thrombus formation time: 20-40 min to perm myocardial dmg |
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steps of platelet functions in arterial thrombosis (3)
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1. adhere-stick
2. activate-spread the word. platelets dump out cell contents, which initiates cascade of coagulation 3. aggregate-clump together |
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immediate goals for acute MI (3)
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1. relieve chest pain
2. maintain cardio stability 3. decrease cardiac workload |
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acute MI drugs (3)
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1. antiplatelet drugs
2. fibrinolytics/thrombolytics 3. morphine sulfate |
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antiplatelet drugs-names and used for
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used in tx for ACS (UA, NSTEMI, STEMI) and other cardio events.
1. aspirin 2. Plavix 3. effient 4. brilinta *1-3 affects lifespan of platelets |
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how does aspirin work for MI pt?
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inside platelet, TXA2 usually triggers rxn that leads to platelet activation and aggregation
ASA decreases TXA2 production which inhibits platelet activation and aggregation |
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action of fibrinolytics
goal of fibrinolytic therapy name of 2 fibrinolytics |
1. dissolve clots blocking coronary arteries
2. goals: dissolve clots obstructing coronary arteries & restore circulation to myocardium 3. streptase and activase (TPA) |
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mech of action of morphine sulfate
goal |
goal: eliminate pain
mech of action: dilates both venous and arterial beds resulting in decreased preload/afterload. also binds w/ opiod receptor sites in brain resulting in diminished transmission of pain impulses |
