exam 3

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Braddk1
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145256
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exam 3
Updated:
2012-04-02 13:36:47
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mi/acs
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  1. what is the pathophys leading to ashd (atherosclerotic heart disease)
    • fatty streaks--fibrofatty lesions--
    • fibrous plaques
  2. deterioration of a once stable plaque is accomplished by
    • rupture--platlet aggregation--thrombus
    • partial or total coronary artery occlusion
  3. prolonged ischemia leads to acs, acs encompasses
    • unstable angina (UA)
    • NSTEMI
    • STEMI
  4. Define unstable angina
    • occuring at rest usually lasting >20mins
    • severe frank new onset<1month
    • crescendo(more sever or frequent)
    • unpredictable
    • medical emergency
  5. what is the difference between ua and nstemi vs stemi
    total occlusion as opposed to partial occlusion
  6. Define MI
    • ischemia>20mins
    • irreversible necrosis

    necrosis covering entire thickness of myocardium takes 4-6hours
  7. what part of the heart is affected when the lad is occluded
    anterior septal
  8. what resulting problems come from an lad occlusion
    • contratile or pump
    • ventricular dysrhythmias
  9. what part of the heart is affected when the rca is occluded
    inferior
  10. when the rca is occluded what are the resulting issues
    • conduction
    • rhythm (sa and av node)
    • bradycardia av blocks
  11. what area of the heart is affected wht the circumflex artery is occluded
    posterior and lateral
  12. what are the resulting problems with the occlusion of the circumflex artery?
    sinus dysrhythmias
  13. 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
  14. physical objective mi clinical manifestations
    • diaphoresis
    • peripheral vasoconstiction
    • ashen cool clammy shin
    • n/v
    • fever
  15. 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
  16. description coming from client to consider mi
    • indigestion
    • heartburn
    • dyspnea
    • weakness
    • anxiety
    • syncope
    • decreased loc
    • feeling of doom
  17. healing process of mi
    • macrophages attack within first 24 hours
    • collateral circ
    • 10-14 days most vulnerable to stress
  18. ventricular remodeling
    heart will compensate by enlarging ventricles
  19. what drug can be used to tx ventricular remodeling
    • ace inhibitors
    • prils
  20. what do ace inhibitors do
    prevent the na and h2o reabsorptionstop raasdecrease svr (afterload)(force heart goes against)decrease preload(volume returning to heart
  21. 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
  22. what are sighn of hyperkalemia
    • malaise
    • palpitations
    • muscle weakness or twitching
    • diarrhea
  23. what are signs of hypokalemia
    • shallow respirations
    • increased b/p
    • weak pulse
    • dizziness
    • confusion
    • irregular hb
    • irritability
  24. 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
  25. what is acute pericarditis
    • results in cardiac compression
    • decreased ventricular filling
    • inflammation of visceral and parietal pleura
  26. what is dressler syndrome
    • occurs 4-6 weeks post mi
    • arthralgia, elevated wbc and esr
  27. what is a normal wbc
    4.3-10,000
  28. what diagnostic studies need to be done with ua and mi
    • ekg
    • troponin
    • ck-mb
    • angiogram with poss pci
  29. what do inverted t waves or st depression mean on ekg
    ischemia
  30. what does st elevation mean on ekg
    injury
  31. what does a pathologic q wave mean on ekg
    infarct
  32. when does troponin rise, peak and how long does it last
    • rises 3-5 hours
    • peaks 24 hours
    • lasts 10-15 days
  33. when does ck-mb rise, peak and how long does it last
    • rises 4-6 hours
    • peaks 14-20
    • lasts 2-3 days
  34. when does myoglobin rise, peak and how long does it last
    • rises 2-4 hours
    • peaks at 6-10hrs
    • lasts 12-36 hours
  35. which of the 3 cardiac markers rises the quickest
    • 1 myoglobin
    • 2 troponin
    • 3 ck-mb
  36. which of the 3 cardiac markers last longest
    troponin
  37. which peaks the quickest
    myoglobin
  38. what are interventions for pt with acs
    • abc's
    • o2
    • iv
    • asa, beta blockers, antiplatlets
    • anticoagulants, morphine, antidysrhythmics
    • dfib, cardioversion, pacing
  39. what is pci
    • baloon angioplasty with stent placement,
    • done in cath lab with versed or valium
    • heparin or lmwh admin to keep vessel open
  40. tx of acs includes fibrinolytics which include
    drugs that end in ase
  41. treatment of nstemi or ua with negative cardiac markers include
    • asa to prevent platlet aggregation
    • heparin to anticoag
  42. what is the antidote for heparin
    protamine sulfate
  43. what is the therapeutic ptt with heparin
    1.5-2.5 times the norm
  44. what is the normal ptt
    30-40 secs
  45. drug therapy with acs --beta blockers
    • olol
    • decrease hr
    • slow conduction
    • decrease o2 demand
    • decreasing contractions
    • suppress renin
  46. drug therapy for acs -- ace inhibitors
    • cause K+ retention
    • watch for dry non-productive cough
  47. antidysrhythmics
    • amiodarone
    • no grapefruit juice
    • do not double up if miss dose
  48. cholesterol lowering drugs
    • statins
    • zetia
  49. what are goal cholesterol lab values
    • total <200
    • ldl <100
  50. what kind of diet should a pt with cad be on?
    low salt, saturated fat, cholesterol
  51. when is coronary surgical revascularization indicated
    when they are not a candidate for pci
  52. priority tx of pain with mi
    • nitro
    • morphine
    • oxygen
    • balance rest and activity
  53. when can pt resume sexual activity
    when they can safely go up 2 flights of stairs without tiring
  54. 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
  55. what electrolyte imbalance can contribute to dig toxicity
    hypokalemia
  56. what is metoprolol
    • beta blocker
    • negative all
    • decreases hr
    • decreases contractility
    • decreases dromotrope
    • decreases o2 demand
  57. what is lasix
    decreases volume
  58. why are ace inhibitors indicated in acs
    makes it easier for the heart to pump
  59. when and why asa
    as soon as mi or acs suspected to prevent platelet aggregation
  60. why heparin
    prevent clotting
  61. why plavix
    alternative to asa
  62. what is a normal dig level
    0.5-2.0
  63. when a patient c/o non radiating chest pain that increases while lying down what would you expect to find
    pericardial fxn rub
  64. where should the pmi be found 5ics micclavicular line if outside those perameters consider
    left ventricular hypertropy and ventricular remodeling

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