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CAD

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cdunbar4's version from 2016-12-04 19:47

Section 1

Question Answer
Disorders atherosclerosis is associated withDM, RF, CHF, HTN, Acute MI (to name a few...)
Collaborative Mgmt Goalstreat early, modify risk factors, TREAT UNDERLYING DISEASE, control progress via meds/exercise/diet, prevent complications (prevent target organ complications)
atherosclerosisprogressive narrowing or obstruction of major arteries→fatty plaque deposits along walls = ↓ tissue perfusion
What are hopefully formed in lieu of arterial opening?collateral circulation pathways
atherosclerosis is major contributing factor to development of HTN, Angina, MI, CHF, death
Non-modifiable risk factorsage 65+, gender M>F, ethnicity (A.A. at higher risk), family hx,
modifiable MAJOR risk factors -TEACH elevated serum lipids, HTN, tobacco use, physical inactivity, obesity
Modifiable CONTRIBUTING risk factorsDM (even if well-controlled); metabolic syndrome (r/t insulin resistance); psychologic states (type-A, depression, anxiety); homocysteine (byprod. of a.a. breakdown)
Total cholesterol levels<200mg/dL
LDL <100mg/dL
HDL>60 is desirable
Triglycerides<150mg/dL
Gerontologic considerations↑RF CAD for older adults or are physically inactive, have one or more chronic diseases and/or have lifestyles (smoking & diet) habits that contribute to atherosclerosis.
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Section 2

Question Answer
statins MOA blocks synthesis of cholesterol and ↑ LDL receptors in the liver: ↓LDL/triglycerides and ↑HDL
statins SErash, GI disturbances, ↑liver enzymes, myopathy & rhabdomyolysis
statins nursing considerationsmonitor liver enzymes & CK levels (if muscle weakness or pain occurs)
Bile acid sequestrants (cholestyramine, colesevelam, colestipol) MOAprevents reabsorption of cholesterol from SI
Bile Acid SE, nursing considerationsGI abd pain, blaoting...use in caution with GI conditions!; ↑ fluids and maintain high fiber to prevent constipation
Fibric Acid Agents (fenofibrate, gemfibrozil) MOAmost effective for lowering TG levels & increasing HDL levels
Fibric acid SErashes, mild Gi, may increase effects of warfarin and some antihyperglycemic drugs
Niacin nicotonic acid MOAB complex vitamin that can lower lipid levels
Niacin AElimit use to combo therapy with statins or bile acids; flushing and GI disturbances
Patient and Caregiver teaching guide to ↓ RF for CAD **WILL BE A ? on test***
drugs that restrict lipoprotein productionnicotonic acid-interferes with production
drugs that increase lipoprotein removalEx. cholestyramine (Questran)-conversion to bile acids in liver
drugs that decrease cholesterol absorptionEx. Zetia-selectively interferes with absorption along the intestinal wall
anti-platelet therapyASA, works for men better than women
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Section 3

Question Answer
Angina extra cardiac factorsphysical exertion, temp. extremes, strong emotions, heavy metal, tobacco use, stroke, sex, stimulants
Chronic stable angina manifestationO2 demand exceeds supply (either ↑demand or ↓supply); primary reason is coronary artery narrowing (>75%) mostly atherosclerosis, but can also be thrombus or spasm
chronic stable angina at cellular levelcellular level→myocardium cyanotic (w/in 10 sec)→anaerobic respiration →lactic acid→irritates nerves (thus referred pain)
Angina vs. infarctionangina-from ischemia caused by reversible cell injury (no damage) vs. infarction from sustained ischemia=cell death (damage)
PQRST?Precipitating event (exertion of exercise causes ↑pain?); Quality of pain; Radiation (yes or no?); Severity (0-10) get a # to compare for next time); Timing (when, changed, ever had it before?)
silent ischemiaabsence of objective symptoms (esp. DM neuropathies)
nocturnal anginaonly at night, but not necessarily asleep
angina decubitusonly when lying down & relieved by getting up
Prinzmetal's anginaat rest, usually a spasm, associated with migraines & raynauds; associated with ↑Ca++; CCB and/or nitrates
Is chronic stable angina an ER?No, rest, nitro x3, usually ST depression
Drug therapy focuses on vasodilationshort-acting nitrates (nitroglycerin); long-acting nitrates (isordil, nitro ointment, transdermal controlled release nitrates)
SE of vasodilators?H/A, maybe give Tylenol, ortho hypoTN, change position slowly, flex, ease self to floor if going to fall; try to have 8 hrs. of day w/o nitrates
Other drugs for management of chronic stable anginaBB's (propranolol to ↓ sympathetic activity); CCB's (Norvasc works in heart for less contraction and in vessels to reduce afterload); ACE inhibitors to ↓vascular resistance/↓afterload; Ranolazine (do not use in conjunction with others)
Two main things to accomplish for patients having cardiac events like unstable angina or MI?REDUCE WORKLOAD OF THE HEART: ↑O2 to cells and ↓O2 demand of the heart muscle (demand less oxygen)
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Section 4

Question Answer
Diagnostics of anginaH&P, CXR, 12-lead EKG, Labs (lipids), Holter monitor checks rhythms over days, Echo
If there is a known CAD, then what tests are ran?Stress test, nuclear imaging, cardiac catheterization, ballon angioplasty, maybe stents
ACS acute coronary syndromeprolonged unstable ischemia that is not immediately reversible (could be ST elevation→MI sign; non ST elevation does not R/O MI
Signs of unstable angina?new onset angina, increasing frequency, increasing duration, increasing severity, nitro doesn't help
MIsustained ischemia, less O2 than cells need, irreversible destruction and death of cardiac cells
80-90% are caused by>thrombus, usually preceded by atherosclerosis
Where is the "widow maker"Left anterior descending artery
Clinical Manis of MIPain, SNS stimulation (shunting blood to vital organs), N/V, fever
Healing Process MI-why are the first three days so important?cardiac markers are diagnostic d/t inflammation process in effect
If ER MI, what do you do 1st and 2nd?stablize/monitor; let heart rest so it can repair (as little O2 demand as possible)
Why is day 10-14 so tricky?scar tissue is still weak and vulnerable to ↑ stress. this is when pt. starts to ↑ exercise too. About six weeks is "healed"
What is ventricular remodeling?remodeling of pathways, takes a long time
Complications of MI?80% is dysrhythmias, HF, cardiogenic shock
Dysrhythmias complicationmost common -fatal, treat ASAP-the closer the infarct to AV node, the worse it is
Heart Failure is a complication"Too pooped to pump;" ↓CO, early signs include mild dyspnea, restless, agitation, tachy
Other complications of MIcardiogenic shock, less common, but deadly; papillary muscle dysfunction-mitral valve regurg; ventricular aneurysm (thrombi); pericarditis 2-3days after MI...Pain: insp>exp; Dressler syndrome
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Section 5

Question Answer
Diagnostics of MI: NSTEMInon ST segment elevation of MI (usually transient thrombus)
STEMIST segment elevation of MI; more extensive with complete occlusion
Coronary angiographypercutaneous coronary interventions (you can see pinched off artery post MI, you can see if you are perfusing)
CK-MB marker time it begins to rise, peak and return to normal post MI? rise: 3-12 peak: 24 normal: 2-3days
Troponin marker time it begins to rise, peak and return to normal post MI? 3-12; 1-2 days; 5-14days;
Myoglobin marker time it begins to rise, peak and return to normal post MI? 1-2 hours; 3-5 hours; 12-18 hours
CC: emergent PCIopen coronary arteries w/in 90 minutes of arrival; cardiac cath, maybe stent, maybe intraaortic balloon or CABG
CC: thrombolytic therapyclot busters; goal is to dissolve thrombus (best w/in 1 hours)
Drug of choice post MI for pain that is also a vasodilator?Morphine-helps to decrease stress as well
Why stool softeners?So pt. doesn't have to strain when using the pooper
Why NPO till stable post MI?You don't want all of the blood shunted to the GI system
What is transmyocardial laser revascularization?creates channels for flow in diseased heart
Coronary bypass graftcreate your own collaterol channels
Nursing Implementation: acute coronary syndromepain, o2, monitor, rest and comfort (DECREASE O2 demand); anxiety; emot'l & behavioral rxns
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Section 6

Question Answer
PE May have ECG changes, may have CPK changes, D-dimer elevated (a fibrin degradation product, small portein fragment in blood after clot is broken down by fibrinolysis
PneumothoraxNo ECG changes, no cardiac enzyme changes
PleurisyNo ECG changes, no cardiac enzyme changes,
Peptic ulcerNo ECG or cardiac enz changes, maybe be decreased H&H if bleeding
psychosomaticNo ECG or cardiac enz changes
GERDNo ECG or cardiac enz changes
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