Lecture 13 & 14 Cardiac

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shannonm2003
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186826
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Lecture 13 & 14 Cardiac
Updated:
2012-12-03 15:19:17
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Cardiovascular
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Lecture 13 & 14 Cardiac
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  1. What is endocarditis
    infection of endocardium or valves of heart
  2. When does rheumatic heart disease occur?
    • occurs after strep infection
    • carditis can cause permanent valve damage, CHF
  3. What is one of the main causes of death in the first year of life?
    congenital heart disease
  4. What are the risk factors for congenital heart disease
    • genetic disorders (down's, trisomys, etc)
    • maternal diabetes
    • alcohol consumption
    • exposure to environmental toxins
    • family hx
  5. What happens in acyanotic?
    • increased pulmonary flow
    • obstruction of flow to heart
    • blood to body is oxygenated
  6. what happens in cyanotic
    • decreased pulmonary flow
    • mixed blood flow
    • blood going to body has venous (deoxygenated) component
  7. what do you see with CHD/CHF
    • the tachys
    • decreased cap refill
    • weak peripheral pusles
    • pallor
    • decreased urine output
    • weakness
    • restlessness (hard to breathe)
    • edema (peripheral, periorbital, ascites)
    • neck vein distention
  8. How do we care for CHD/CHF
    • improve cardiac function
    • remove fluid and sodium buildup
    • decrease cardiac demnad
    • improve O2
  9. How do we improve cardiac function
    administer meds (digoxin most common, also ACE inhibitors)
  10. How do we remove fluid and sodium buildup
    • med therapy (diuretics, potassium supplement depending on diuretic choice)
    • possibly fluid and sodium restriction
  11. how do we decrease cardiac demand
    bed rest, positioning, treat infection, may have anti-anxiety meds ordered
  12. How do you treat endocarditis?
    with high dose antibiotic therapy for 2-8 weeks
  13. what do we see with rheumatic fever
    • chest pain
    • joint pain
    • new murmurs
    • muscle weakness
    • nontender swelling over bony prominences
    • erythema to trunk and extremities
    • positive throat culture
  14. What are we going to do with rheumatic fever
    • med therapy (penicillin the drug of choice, anti-inflammatory meds)
    • family support
    • education (likelihood of relapse)
  15. how is kawasaki disease caused?
    etiology is unknown
  16. how do we dx kawasaki disease
    by clinical findings and lab results, not by diagnostic tests
  17. what do we see with kawasaki disease
    • high, persistent fever
    • edema, erythema or peeling of skin on palms and soles
    • bilateral conjunctival inflammation w/o exudate
    • erythema of lips
    • oropharyngeal reddening
    • strawberry tongue
    • cervical lymphadenopathy
    • polymorphous rash
  18. What are the 3 phase of kawasaki disease
    acute phase, subacute phase and convalescent phase
  19. What do we see with the acute phase of kawasaki disease
    • abrupt onset of high fever
    • fever unresponsive to antibiotics and antipyretics
    • very irritable
  20. what do we see with the subacute phase of kawasaki disease
    • resolution of the fever
    • lasts until all clinical signs disappear
    • child at greatest risk for coronary artery aneurysms in this phase
  21. what do we see with the convalescent phase of kawasaki disease
    • all clinical signs resolved
    • lab values have not returned to normal
    • phase complete when lab values return to normal (usually 6-8 weeks after onset)
  22. what are the long term complications of kawasaki disease
    • coronary artery aneurysms
    • myocardial infarction
    • myocardial ischemia
  23. what is the therapeutic management of kawasaki disease
    • gamma globulin infusion
    • high-dose aspirin therapy
  24. what is the prognosis of kawasaki disease
    • with early dx and treatment, full recovery anticipated
    • death primarily associated with cardaic damage (primarily thrombosis)
  25. What are we going to do for kawasaki disease
    • monitor cardiac status carefully
    • strict I/O
    • daily weights
    • assess for CHF
    • monitor during gamma-globulin infusion
    • treatment of symptoms
    • family support/education
  26. what is sickle cell anemia?
    • hemoglobin disorder
    • autosomal recessive disorder
  27. what do we see with sickle cell anemia
    • swelling of hands and feet
    • pain (can be generalized, specific, often in joints)
    • can have chest pain
    • pallor
    • can have respiratory difficulty, high levels of anxiety
  28. what are we going to do for sickle cell anemia?
    • pain management (PCA, steriod therapy)
    • possible O2 therapy
    • adequate hydration
    • blood tranfusion
  29. what are we looking at in a cardiac-focused physical assessment
    • skin color
    • hair distribution
    • cap refill
    • edema
    • temp
    • pulses
    • BP
  30. Who has the highest rates of HTN
    • older adults
    • african-americans
    • lower socioeconomic classes
    • lower education levels
  31. what are some risk factors for atherosclerosis
    • diabetes
    • smoking
    • HTN
    • obesity
    • hyperlipidemia
    • phlebitis
    • surgery
    • autoimmune diseases
  32. What are we going to see with arterial disorders
    • intermittent claudation
    • several different kinds of pain
    • localized skin temp changes
    • different skin colors in certain regions
    • edema?
    • wound healing issues
    • diminished pulses distal to the occlusion
  33. what is virchow's triad
    • venous stasis - blood not moving
    • hypercoagulability - blood clots alot
    • injury to venous walls
    • (at least 2 of 3 need to be present for thrombus formation)
  34. what are we going to see with superficial venous disorders
    • redness
    • warmth
    • tenderness
    • induration
  35. what are we going to see with deeper thrombophlebitis
    • may be asymptomatic
    • unilateral leg swelling
    • pain
    • rednesss/warmth of leg
    • dilated veins
    • low-grade fever
  36. what is the key nursing goal with thrombophlebitis
    • prevention
    • other goals include early detection, prevention of extension or spread, and prevention of further formation
  37. what are we going to do for venous disorders
    • assess and document
    • encourage ambulation
    • active ROM
    • SCDs or ted hose
    • anticoagulant therapy
    • monitor for PE
  38. what are common anticoagulants
    • heparin
    • lovenox
    • coumadin
  39. what lab tests are performed to determine need or efficacy of anticoagulant therapy
    • PT
    • PTT
    • aPTT
    • INR
  40. what is the antagonist for coumadin
    vitamin K
  41. what is the antagonist for heparin
    protamine sulfate

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