respiratory - impaired gas exchange

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Author:
giep
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80237
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respiratory - impaired gas exchange
Updated:
2011-04-17 20:22:29
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nurse
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  1. process w/c supplies cells w/ o2 and removes co2
    respiration
  2. pulmonary system fails in one or both functions; o2 or CO2 elimination
    acute respiratory failure
  3. acute respiratory failure is a syndrome or a disease?
    syndrome

    • can be acute or chronic
    • can be hypoxemia or hypercapnic
  4. how is acute resp failure defined?
    Pao2?
    sao2?
    paco2?
    ph?
    • pao2 <60
    • sao2 <90%
    • paco2 >50
    • ph <7.35
  5. mechanism of malfunction. name 3
    • 1. impaired ventilation
    • 2. impaired perfusion
    • 3. impaired ventilation & perfusion
  6. give examples of what would cause IMPAIRED VENTILATION
    • obstruction
    • copd
    • injury
  7. give examples of what would cause IMPAIRED PERFUSION
    • pulmonary edema
    • pneumonia
    • ARDs
  8. give examples of what would cause IMPAIRED PERFUSION AND VENTILATION
    • COPD
    • acute asthma attack
  9. what is TYPE I RESP FAILURE
    hypoxemia
  10. what is the issue between ventilation and perfusion in type 1 resp failure?
    normal ventilation vs abnormal perfusion
  11. type 1 resp failure (hypoxemia)
    alveoli?
    oxygenation?
    commonly involve fluid or collapse of alveoli (CHF, pneumonia)

    • pao2 <60
    • paco2 =<35
  12. the following conditions can cause which type of respiratory failure:
    COPD, obesity, ARDs, pulm edema, pneumothorax, asthma, PE
    • type I respiratory failure
    • *this is the most common form of respiratory failure
  13. normal ventilation vs abnormal perfusion
    type I respiratory failure
  14. hypercapnic? w/c type of respiratory failure
    type II respiratory failure
  15. what is the issue of perfusion and ventilation in type II resp failure?
    normal perfusion vs. abnormal ventilation
  16. in type II respiratory failure, there is an issue with ventilation. t or f?
    true

    insufficient ventilation - pt isn't breathing, not blowing off co2 (hypercapnic)

    • paco2 >50
    • ph <7.35
  17. this following conditions may cause w/c type of respiratory failure:
    COPD, poisoning, myasthenia gravis, pulmonary edema, obesity, drug overdose, ARDS
    type II respiratory failure
  18. normal perfusion vs. abnormal ventilation
    type II respiratory failure
  19. s/s on the CNS during assessment for acute respiratory failure
    • RESTLESS
    • confusion
    • irritability
    • IMPENDING DOOM
    • somnulence
    • *co2 accumulates
  20. s/s on the respiratory system in acute resp failure
    • dyspnea - sob, difficulty
    • increased depth = hypoxemia
    • decreased depth = hypercapnia
  21. s/s on cardiovascular system in acute resp failure
    • tachycardia - early
    • HTN - early
    • bradycardia - late
    • hypotension - late
    • arrhythmias
  22. dx tests for acute respiratory failure
    • abgs - ph < 7.35; po2 <60; pco2 >50
    • chest xray
    • sputum culture, cbc, electrolytes
    • ecg
  23. nursing care for acute respiratory failure
    • PREVENTION:
    • treat cause
    • airway - clearance
    • breathing patterns

    • IMPROVE OXYGENATION:
    • o2
    • airway adjuncts - endotracheal tube and ventilation

    • NUTRITION:
    • increased need

    MAINTAIN OPTIMAL CARDIAC OUTPUT
  24. other nursing interventions for acute resp failure
    • SCD
    • IS 10x/hr
    • deep breathe, cough
    • ambulation
    • control pain = ^ breathing
  25. syndrome of lung inflammation and injury, potentially fatal non-cardiac pulmonary edema
    acute respiratory distress syndrome (ARDS)
  26. characteristics of ARDS
    hypoxemia?
    rr?
    alveoli?
    xray?
    PCWP?
    • acute and refractory hypoxemia (despite 100% FIO2)
    • tachypnea
    • decreased lung compliance
    • alveolar collapse
    • bilateral infiltrates on xray "white out"
    • PCWP <18 mmhg
  27. pathophysiology of ARDS
    activation of systemic inflammatory response syndrome (SIRS) in response to direct or indirect lung injury
  28. phases of ARDS
    • 1. acute exudative phase
    • 2. proliferative phase
    • 3. fibrotic phase
  29. ARDS: this phase there is damage to alveolar epithelial cells. fluid accumulates in alveoli
    acute exudative phase
  30. ARDS: this phase the damage spreads from base to upper lobes
    proliferative phase
  31. ARDS: this phase damage to the alveoli; scarring; alveoli can no longer open and close
    fibrotic phase
  32. name some direct causes that can lead to alveolar injury and inflammation
    • aspiration
    • inhalation injury
    • contusion
    • embolism
    • radiation
    • reperfusion injury
    • o2 toxicity
  33. name some indirect causes of ARDS: activation of SIRS outside the lung; tissue destructive cytokines travel to the lungs
    • shock
    • sepsis
    • trauma
    • pancreatitis
    • drug OD
    • massive blood transfusion
    • disseminated intravascular coagulopathy
  34. dx of ARDS:
    ABNORMAL CHEST XRAY

    • ABNORMAL ABGS
    • early resp alkalosis
    • later resp acidosis
    • eventually metabolic acidosis

    • REFRACTORY HYPOXEMIA
    • despite supplemental o2

    • ABNORMAL PUMONARY FUNCTION TEST
    • decrease compliance
    • decrease FRC (functional residual capacity

    *might hear crackles or NOTHING
  35. early ABGs in ARDS?
    respiratory alkalosis
  36. later ABGs in ARDS?
    • respiratory acidosis
    • eventually leads to METABOLIC ACIDOSIS
  37. nursing care for ARDS
    1. collaborative management

    • 2. support and improve oxygenation
    • -mechanical ventilation
    • -medications
    • -positioning

    3. nutritional support BIG NEED

    • 4. prevention of complications
    • -multi-organ system dysfunction/failure
    • -ventilatore acquired pneumonia
  38. a collection of particulate matter that enters the venous system and lodges in the pulmonary vessels
    pulmonary embolism

    • can be:
    • fat
    • amniotic fluid embolism
    • blood clot
  39. pathophysiology of PE
    • thrombus formation
    • portion of clot dislodges
  40. name some causes of clot formation and dislodge
    • vena caba
    • R side of heart
    • occlusion of pulm vessel
    • ventilation (V/Q) mismatch
    • pulmonary vessel constriction
    • pulmonary hypertension
    • decreased surfactant
    • atelectasis
    • pulmonary infarction
  41. what is VIRCHOW'S triad
    • 1. venous stasis
    • 2. endothelial damage
    • 3. hypercoagulability
  42. some factors that may cause VENOUS STASIS
    • immobility
    • obesity
    • advanced age
    • varicose veins
    • blockage/compression of femoral or iliac vein
  43. some factors that may cause ENDOTHELIAL DAMAGE
    • CENTRAL VENOUS CATHETERS
    • HX OF dvt
    • trauma
    • surgery
  44. what may cause HYPERCOAGULABILITY
    • pregnancy
    • estrogen tx
    • CVA
    • fam hx
  45. turner's syndrome?
    hint: dvt
    femoral artery easily compresses = clot formation
  46. s/s of PE
    • restless
    • apprehension
    • impending doom
    • cough
    • hemptysis
    • tachypnea
    • fever
    • diaphoresis
    • pleural friction rub
    • petechiae
    • s3 or s4
    • decrease sao2
    • dyspnea, abrupt onsent
    • pleuritic chest pain
    • tachycardia
  47. DX of PE
    abnormal ABGs (same as ARDS)

    • early resp alkalosis
    • later resp acidosis
    • eventually metabolic acidosis

    • abnormal chest xray (may see large emboli)
    • infiltrates

    abnormal angiogram

    increased wbc

    positive d-dimer
  48. goal of nursing care for PE
    improve ventialtion and perfusion, minize risk of additional clot formation, prevent complications
  49. nurse interventions for PE:
    assessments?
    clots?
    surgery?
    respiratory assessment - crackles, admin o2

    cardiac assessment - s3; s4

    anticoagulation meds - iv heparin, warfarin, thrombolytic

    surgical management - vena cava filter

    *antidote - predatine sulfate
  50. influenza:
    who's at risk?
    caused by what?
    • older adults
    • debilitated
    • immunocompromised

    caused by ABC
  51. highly contagious acute viral respiratory infection
    flu
  52. the following sx of manifestations of what:
    severe HA, muscle ache, fever, chills, fatigue, wekaness, anorexia
    flu
  53. how to prevent influenza
    vaccines

    antivirals may be effective
  54. when is someone contagious with the flu?
    from 24 hrs before sx and up to 5 day s after they begin
  55. nursing care for the flu
    • prevention
    • education
    • vaccination
    • handwashing
  56. excess fluid in the lungs resulting from an inflammatory process
    pneumonia
  57. what may be the cause of inflammation in pneumonia
    • infectious organism
    • inhalation of irritants
  58. where can one get pneumonia
    • community acquired pneumonia (CAP)
    • nosocomia or hospital acquired (HAP)
  59. what manifesations does pneumonia have
    • atelectasis
    • hypoxemia
    • dyspnea
    • cough
    • sputum
    • fever
    • pleuritic chest pain
  60. which is more common, community or hospital acquired pneumonia?
    CAP, occurs late fall and winter as complications of influenza

    *HAP has 10-50% mortality rate
  61. dx for pneumonia:
    • gram stain, culture, sensitivity testing of sputum
    • cbc
    • abgs
    • serum bun level
    • electrolytes
    • creatinine
    • imaging assessment (CXR)
    • pulse ox
  62. nurse interventions/treatment of pneumonia
    • o2
    • IS
    • meds - antiinfectives, bronchodilators
    • avoid dehydration
    • teaching, prevetnion (pt and staff)
    • vaccination
    • HANDWASHING
  63. a syndrome of acute resp failure (non cardiogenic pulmonary edema) that can be triggered by a wide variety of conditions:
    • direct pulmonary trauma
    • indirect pulmonary trauma
  64. patho of ARDS: 2 main insults to lungs
    • 1. alveolar-capillary membrane damage
    • 2. decreased surfactant production -> decreases lung compliance "stiff lungs"
  65. early clinical manifestations of ARDS
    • tachypnea
    • tachycardia
    • dyspnea
    • confusion
    • agitation
    • fine crackles
  66. later clinical manifestations of ARDS
    • diffuse crackles
    • rhonchi (gurgles)
    • cyanosis
  67. occlusion of portion of the pulmonary arterial bed by a thrombus or other foreign
    pulmonary emboli
  68. the air that reaches the lungs
    ventilation
  69. the blood that reaqches the lungs
    perfusion "Q"
  70. since it is difficults to keep SAo2 above 90% in ards. we need extra measures. what is this?
    PEEP (positive end expiratory pressure)
  71. the purpose of PEEP (positive end expiratory pressure) ?
    helps keep alveoli expanded inspite of inflammation and fluid levels
  72. what can happen if PEEP is too low?
    alveoli will collapse w/ every exhalation
  73. what can happen if PEEP IS TOO HIGH
    • trauma to alveoli
    • decreased CO (actual pressure on heart form constantly air filled bronchi and airways)
    • decrease surfactant production
    • impede capillary blood flow at alveolus
    • worse V/Q matching if not balanced well

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