Objective 10.txt

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  1. Pulmonary edema
    fluid in the lung, life-threatening, acute, flash pulmonary edema
  2. Key features of edema
    crackles, dyspnea, distortion, tachycardia, hyper/hypo tension, reduced urinary output, cough with frothy pink sputum, PVSc, anxiety, restlessness, lethargy
  3. How to check lungs for pulmonary edema
    start at bottom and work up
  4. Position for someone with pulmonary edema
    high fowlers unless hypotension then lay flat
  5. Oxygen for someone with pulmonary edema
    2-5L is nasal cannula, 5-6 mask, 10-15 respirator with goal to get O2 above 90%
  6. Assess early signs of pulm edema
    respiratory distress, anxiety, increased HR (weak), JVD, agitation and confusion due to not enough oxygen
  7. Origin of pulm edema
    cardiac; overload, respiratory status, left ventricular function
  8. Meds to give someone with pulm edema
    nitro (vasodilator), rapid acting diuretics, morphine 1-2 mg which reduces preload
  9. In pulmonary edema
    left ventricle fails to eject sufficient blood and pressure causes fluid to leak across the pulmonary capillaries and into the lung airways and tissues
  10. Goal with someone with pulm edema
    decrease volume overload, increase ventricular function, increase respiratory exchange
  11. Pulmonary embolism
    in Afib the loss of coordinated contractions can lead to stagnation of blood resulting in PE; clot would move from right atrium to right ventricle to lungs
  12. Clinical indicators of PE
    chest pain, SOB, tachycardia, change in LOC, symptoms of DVT
  13. Pt mgmt. of PE
    assess, keep pt calm, anticoagulant therapy
  14. What can cause PE
    c venous catheter, age, hx of clots
  15. Symptoms of PE
    dyspnea, chest pain, restlessness, impending doom, cough, hemoptysis
  16. Signs of PE
    tachypnea, crackles, pleural friction rub, tachycardia, S3 or S4, diaphoresis, fever, petechiae, decreased O2 sats
  17. Complications of PE
    rt sided HR, respiratory failure, death
  18. HR
    increases with inhalation and decreases with exhalation
  19. Tachydysrhythmias
    shorten diastolic time, increased workload of heart, can lead to HF
  20. Bradydysrhythmias
    reduced O2 demand, hypotension
  21. Premature complexes
    early rhythm dinctions, decreased cardiac output
  22. What meds increase HR
    epi and atropine
  23. Cause of sinus bradycardia
    hypoxia, MI, dig, BAB agents
  24. Treatment of bradycardia
    meds, IV fluids, atropine may be drug of choice, DON’t stimulate vagal response
  25. SVT
    if they don’t convert, give adenosine to get into sinus rhythm and then cardiovert
  26. SVT may lead to
    cardiogenic shock, angina
  27. AFib
    rapid uncontrolled twitching of atria, AV node is bombarded, high chance of clots, usually use IV meds to convert to sinus
  28. Drug for Afib
    amiodarone, also Cardizem, dig and veraprimil, anticoagulants
  29. No discerable P wave in AFib
  30. Atrial flutter
    block at AV node
  31. Signs of Aflutter
    low BP, SOB, treat like afib, sawtootk
  32. Ventricular dysrhythmias
    lost protection of AV node
  33. PVC
    impulse starts in ventricle, not atria; acidosis; drug is amiodarone or lidocaine
  34. Vtach
    3 or more PVCs in a row, cardiovert if necessary, lethal rhythm
  35. Worst thing about vtach?
    Can turn into vfib
  36. VFib
    quivering of ventricles, no atrial, absent heartbeat and palpable pulses
  37. Treatment of vfib
    immediate defib
  38. Vfib voltage
    200 joules
  39. Are asystole and v asystole shockable?
  40. AV blocks
    first-all sinus impulses reach ventricles; second-some do; third none do
  41. NSTEMI
    baseline of EKG is depressed
  42. STEMI
    baseline of EKG is elevated
  43. Acute coronary syndrome
    emergent situation, myocardial death
  44. #1 problem of acute coronary syndrome
    plaque at least 40% before it stops blood flow
  45. Patient with unstable angina
    might not have changes in troponin or CK levels
  46. Nursing process for ACS
    assess, compare to baseline, monitor EKG
  47. Nursing diagnoses for ACS
    ineffective cardiac tissue perfusion, risk for fluid imbalance, risk for ineffective peripheral tissue perfusion
  48. Problems that can add to ACS
    acute pulmonary edema, HF, cardiogenic shock, cardiac arrest, pericardial effusion, cardiac tamponade, pleural effusion
  49. Nursing goals for ACS
    relieve pain, prevent further damage, good respiratory, reduce anxiety, adhere to self care program, know early indicators
  50. Prevention of ACS
    smoking, diet, cholesterol, physical activity, diabetes, BP, obesity
  51. What culture has highest genetic risk for CAD
    AFA and Hispanic women more than white women
  52. Cholesterol levels for MI
    elevated LDL and low HDL increase risk for MI
  53. How long does angina last versus MI
    angina-less than 15 minutes, MI more than 30 minutes and relieved only by opiods
  54. Cardiac markers
    CK (CK-MB), troponin T and I, myoglobin
  55. What meds for MI
    aspirin 325 mg, nitro, morphine, beta blockers, ACE inhibitors within 24 hours, evaluate thrombolytic therapy, give bed rest
  56. Pericardial effusion can lead to
    cardiac tamponade
  57. Cardiac tamponade
    excess fluid within pericardial activity, restriction of heart function, pericardial effusion
  58. Clinical manifestations of cardiac tamponade
    chest pain, engorged neck veins, falling systolic BP, narrowing pulse pressure, muffled heart sounds, paradoxal pulse
  59. How to relieve cardiac tamponade
    pericardiocentesis to remove fluid and relieve the pressure on the heart
  60. An increase in pericardial fluid
    increases pressure within pericardial sac and compresses the heart; increases pressure in all chambers, decreases venous return due to atrial compression and ventricles cannot distend and fill adequately
  61. Cardiogenic shock causes
    MI, cardiac arrest, vfib, vetch, cardiac amyloidosis, cardiacmyopathies
  62. Early stage of shock
    H and RR increase or slight increase in diastolic BP may be only objective manifestation
  63. Definition of cardiogenic shock
    rt or left fails to pump oxygenated blood into systemic circulation; necrosis of more than 40% of left ventricle
  64. Left ventricle infarction
    necrotic area impairs contractility and cardiac output; oxygenated blood not moved forward into systemic circulation
  65. Right ventricle infarction
    ejects too little blood into left ventricle, tissues decrease O2
  66. Non progressive stage
    decreased HR and RR, vasoconstriction, increase in pulse pressure, MAP and urinary output; tissue hypoxia in nonvital organs
  67. Progressive stage
    rapid changes, BP decrease, weak pulse, MAP decrease and O2 stats, decreased ABGs, heart dysrhythmias, all organs begin to fail
  68. Respiratory rate
    increases as shock progresses
  69. ABGs in shock
    decreased tissue oxygenation (decreased PH, decreased PaO2, increased PaCO2)
  70. Diagnostic procedures for shock
    arterial line insertion to monitor continuous BP, pulmonary artery cath
  71. Vasopressors
    dobutamine-strengthens cardiac contraction and increases cardiac output
  72. Vasodilator
    nipride, reduces afterload and preload, causes vasodilation, decreases cardiac output and afterload
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Objective 10.txt
2013-09-02 18:22:47
Objective 10

Objective 10
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