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8 Cards in this Set

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Coronary atherosclerosis assessment
manifestations:
chest pain
15% of men and women have no symptoms
elderly or hx of diabetes and HF may report SOB
women may have dyspnea, nausea, weakness
prodromal symptoms i.e. angina hours to days before episode
major cardiac event may be first indication of coronary atherosclerosis
Coronary atherosclorosis risk factors
nonmodifiable:
family hx, age, gender, race
modifiable:
hyperlipedemia, smoking, htn, DM, metabolic syndrome: three of the following: insulin resistance, central obesity, dyslipedemia, BP>130/85 persistently, proinflammatory state (high C reactive protien), prothrombotic state
obesity, physical inactivity
coronary atherosclorosis tx/management
diet, exercise, quit smoking, controlling cholesterol, managing HTN, controlling DM
angina pectoris
pain or pressure in the anterior chest caused by insufficient blood flow resulting in decreased oxygen supply when there is increased demand for oxygen - exercise or emotional stress
types of angina (5)
stable: predictable, consistent and relieved by rest/nitroglycerin
unstable: symptoms increase and may not be relieved by meds or rest
intractable or refractory: severe incapacitating pain
variant:pain at rest with reversible ST segment elevation, thought to be caused by coronary artery vasospasm
silent ischemia: ECG changes but no symptoms
pharmacologic therapy for angina pectoris
(8)
nigroglycerin (short acting)- vasoactive agent that reduces myocardial oxygen consumption which relieves pain. can be given sublingual, orally, patches, IV for recurring s/s of ischemia - not for systolic of <90
beta-adrenergic blocking agents - metoprolol (Lopressor, Toprol) and atenolol (Tenormin) reduce myocardial O2 consumption by blocking beta-adrenergic sympathetic stimulation to the heart - side effects and possible contraindications hypotension, bradycardia, advanced atrioventricular block and acute HF/other side effects: deptession, fatigue, decreased libido, masking hypoglycemia
Calcium channel blocking agents: amlodipine (Norvasc) and diltiazem (Cardizem, Tiazac) these decrease SA node automaticity and AV node conduction resulting in slower heart rate
Aspirin prevents platelet aggregation and reduces indcidence of MI and death in patients with CAD - may need H2 blockers when taking aspirin to avoid stomach upset
Clopidogrel (Plavix) given for high risk patients
Heparin - IV unfractionated heparin prevents the formation of blood clots and reduces occurence of MI
LMWH (low-molecular-weight heparin) subq can be given treat unstable or non ST segment elevated MIs *follow bleeding precautions: apply pressure for longer than usual, avoid IMs, avoid constrictive devices and tissue injury or bruising*
glycoprotein IIb/IIIa agents prevent platelet aggregation by blocking GP IIb/IIIa receptors.
Oxygen: administered to increase oxygen delivered to the myocardium and to decrease pain
Coronary syndrome/MI assessment (s/s of ACS or MI)
cardiovascular: chest pain not relieved by rest/nitroglycerin, S3, S4 heart sounds, increased jugular venous distention, increased BP, irregular pulse (atrial fib), ECG changes (tachy, brady, dys, STsegment and T wave changes)
respiratory:
sob, dyspnea, tachypnea, crackles, pulmonary edema
gastro:
nausea and vomiting
genitourinary:
decreased urinary output
skin:
cool, clammy, diaphoretic, paleness
neurologic:
anxiety, restlessness, lightheadedness
psychological:
fear with feeling of impending doom
coronary syndrome/MI lab tests/
creatine kinase (CK-MB) heart muscle - elevates when damage occurs to the cells - increases within a few hours and peaks within 24
myoglobin - protein that helps transport O2 and increases within 1-3 hours and peaks within 12 hours - increase not very specific of MI, but negative results great for ruling out MI
troponin - regulates myocardial contractile process
troponons T and I specific for cardiac muscle and are reliable markers for MI - can be detected within a few hours and stays elevated for up to 3 weeks