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Braddk1
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what is the pathophys leading to ashd (atherosclerotic heart disease)
- fatty streaks--fibrofatty lesions--
- fibrous plaques
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deterioration of a once stable plaque is accomplished by
- rupture--platlet aggregation--thrombus
- partial or total coronary artery occlusion
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prolonged ischemia leads to acs, acs encompasses
- unstable angina (UA)
- NSTEMI
- STEMI
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Define unstable angina
- occuring at rest usually lasting >20mins
- severe frank new onset<1month
- crescendo(more sever or frequent)
- unpredictable
- medical emergency
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what is the difference between ua and nstemi vs stemi
total occlusion as opposed to partial occlusion
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Define MI
- ischemia>20mins
- irreversible necrosis
necrosis covering entire thickness of myocardium takes 4-6hours
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what part of the heart is affected when the lad is occluded
anterior septal
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what resulting problems come from an lad occlusion
- contratile or pump
- ventricular dysrhythmias
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what part of the heart is affected when the rca is occluded
inferior
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when the rca is occluded what are the resulting issues
- conduction
- rhythm (sa and av node)
- bradycardia av blocks
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what area of the heart is affected wht the circumflex artery is occluded
posterior and lateral
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what are the resulting problems with the occlusion of the circumflex artery?
sinus dysrhythmias
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clinical manifestations of mi as far as pain goes
- pain from lactic acid build up not relieved by rest or nitro
- heavy, tight,burning, crushing pressure
- in the substernal retrosternal, epigastric that radiates
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physical objective mi clinical manifestations
- diaphoresis
- peripheral vasoconstiction
- ashen cool clammy shin
- n/v
- fever
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cardiovascular clinical manif of mi including vs
- increased hr and bp but after decreased co the b/p goes with it
- s3 or s4 murmer
- percardial fxn rub that continues if breath is held
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description coming from client to consider mi
- indigestion
- heartburn
- dyspnea
- weakness
- anxiety
- syncope
- decreased loc
- feeling of doom
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healing process of mi
- macrophages attack within first 24 hours
- collateral circ
- 10-14 days most vulnerable to stress
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ventricular remodeling
heart will compensate by enlarging ventricles
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what drug can be used to tx ventricular remodeling
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what do ace inhibitors do
prevent the na and h2o reabsorptionstop raasdecrease svr (afterload)(force heart goes against)decrease preload(volume returning to heart
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what can be retained while taking ace inhibitors and therefore the labs must be closely monitored
- K+, normal level is 3.5-5
- creatnine normal level 0.6-1.5
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what are sighn of hyperkalemia
- malaise
- palpitations
- muscle weakness or twitching
- diarrhea
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what are signs of hypokalemia
- shallow respirations
- increased b/p
- weak pulse
- dizziness
- confusion
- irregular hb
- irritability
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what are complications of mi
- dysrhtyhmias
- hf - will see dyspnea, restlessness,agitation, tachycardia and later jbd decreased co, pulmonary congestion and s3/s4
- cardiogenic shock
- papillary muscle dysfuntion - mitral valve regurg
- ventricular aneurism
- acute pericarditis
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what is acute pericarditis
- results in cardiac compression
- decreased ventricular filling
- inflammation of visceral and parietal pleura
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what is dressler syndrome
- occurs 4-6 weeks post mi
- arthralgia, elevated wbc and esr
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what is a normal wbc
4.3-10,000
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what diagnostic studies need to be done with ua and mi
- ekg
- troponin
- ck-mb
- angiogram with poss pci
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what do inverted t waves or st depression mean on ekg
ischemia
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what does st elevation mean on ekg
injury
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what does a pathologic q wave mean on ekg
infarct
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when does troponin rise, peak and how long does it last
- rises 3-5 hours
- peaks 24 hours
- lasts 10-15 days
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when does ck-mb rise, peak and how long does it last
- rises 4-6 hours
- peaks 14-20
- lasts 2-3 days
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when does myoglobin rise, peak and how long does it last
- rises 2-4 hours
- peaks at 6-10hrs
- lasts 12-36 hours
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which of the 3 cardiac markers rises the quickest
- 1 myoglobin
- 2 troponin
- 3 ck-mb
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which of the 3 cardiac markers last longest
troponin
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which peaks the quickest
myoglobin
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what are interventions for pt with acs
- abc's
- o2
- iv
- asa, beta blockers, antiplatlets
- anticoagulants, morphine, antidysrhythmics
- dfib, cardioversion, pacing
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what is pci
- baloon angioplasty with stent placement,
- done in cath lab with versed or valium
- heparin or lmwh admin to keep vessel open
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tx of acs includes fibrinolytics which include
drugs that end in ase
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treatment of nstemi or ua with negative cardiac markers include
- asa to prevent platlet aggregation
- heparin to anticoag
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what is the antidote for heparin
protamine sulfate
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what is the therapeutic ptt with heparin
1.5-2.5 times the norm
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what is the normal ptt
30-40 secs
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drug therapy with acs --beta blockers
- olol
- decrease hr
- slow conduction
- decrease o2 demand
- decreasing contractions
- suppress renin
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drug therapy for acs -- ace inhibitors
- cause K+ retention
- watch for dry non-productive cough
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antidysrhythmics
- amiodarone
- no grapefruit juice
- do not double up if miss dose
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cholesterol lowering drugs
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what are goal cholesterol lab values
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what kind of diet should a pt with cad be on?
low salt, saturated fat, cholesterol
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when is coronary surgical revascularization indicated
when they are not a candidate for pci
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priority tx of pain with mi
- nitro
- morphine
- oxygen
- balance rest and activity
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when can pt resume sexual activity
when they can safely go up 2 flights of stairs without tiring
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what is dig and what does it do and what do you need to watch
- cardiac glycoside
- increases contractility of heart (pos ino)
- slows the hr (neg chrono)
- slows conductio (neg dromo)
- promotes diuresis
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what electrolyte imbalance can contribute to dig toxicity
hypokalemia
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what is metoprolol
- beta blocker
- negative all
- decreases hr
- decreases contractility
- decreases dromotrope
- decreases o2 demand
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what is lasix
decreases volume
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why are ace inhibitors indicated in acs
makes it easier for the heart to pump
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when and why asa
as soon as mi or acs suspected to prevent platelet aggregation
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why heparin
prevent clotting
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why plavix
alternative to asa
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what is a normal dig level
0.5-2.0
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when a patient c/o non radiating chest pain that increases while lying down what would you expect to find
pericardial fxn rub
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where should the pmi be found 5ics micclavicular line if outside those perameters consider
left ventricular hypertropy and ventricular remodeling
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