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NURS 425 > Exam #2: Respiratory Failure And ARDS > Flashcards

Exam #2: Respiratory Failure And ARDS Flashcards

1
Q

Acute Respiratory Failure results from

A
  1. Insufficiency O2 transferred to blood: Hypoxia

2. Inadequate CO2 removal: Hypercapnia

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2
Q

Classification of Respiratory Failure:

A
  1. Hypoxemic aka Oxygenation Failure (Pao2 <60 mm Hg on inspired O2 concentration >60%)
  2. Hypercapnic aka Ventilatory Failure (PaCO2 above normal (>48 mm Hg) and Acidemia (pH <7.35))
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3
Q

Hypoxemic Respiratory Failure can be caused by

A
  • Mismatch between ventilation (V) and perfusion (Q) - (V/Q mismatch) should be 1:1 (1 mL of air for each 1 mL of blood flow to lungs)
  • Shunt
  • Diffusion limitation
  • Alveolar hypoventilation
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4
Q

Hypoxemic Respiratory Failure: V/Q mismatch can be caused by

A
  • COPD
  • Pneumonia
  • Asthma
  • Atelectasis
  • Result of pain
  • Pulmonary embolus
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5
Q

Range of V/Q Relationships

A

Look at slide 7!

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6
Q

Hypoxemic Respiratory Failure: Shunt

A
  • Anatomic shunt
  • Intrapulmonary shunt

*Read notes

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7
Q

Hypoxemic Respiratory Failure: Fluid in the alveoli

A

ARDS, pneumonia

*Read notes

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8
Q

Causes of Hypoxemic Respiratory Failure: Diffuse limitations include

A
  1. R/t alveoli being scarred:
    - Severe COPD
    - Recurrent pulmonary emboli
    - Pulmonary fibrosis
    - ARDS
    - Interstitial lung disease
  2. Hypoxemia present during exercise

*Read notes

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9
Q

Diffuse limitation occurs when

A

gas exchange across the alveolar-capillary membrane is compromised by a process that thickens, damages, or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries (Fig. 67-5).

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10
Q

Causes of Hypoxemic Respiratory Failure: Alveolar Hypoventalation

A
  • Restrictive lung disease
  • CNS disease (stroke, brain infarct)
  • Chest wall dysfunction
  • Neuromuscular disease
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11
Q

Hypoxemic Respiratory Failure: Interrelationship of mechanisms

A

Combination of two or more physiologic mechanisms:

  • V/Q mismatch
  • Shunt
  • Diffusion limitation
  • Alveolar hypoventilation

*Read notes!!

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12
Q

Hypercapnia Respiratory Failure

A
  • CO2 levels cannot be maintained within normal limits due to:
    • An increase in CO2 production or
    • A decrease in alveolar ventilation
  • Acute or chronic

*Read notes

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13
Q

What can cause hypercapnic respiratory failure?

A
  1. Airway and alveoli abnormalities
  2. Central nervous system abnormalities
  3. Chest wall abnormalities
  4. Neuromuscular conditions
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14
Q

Causes of Hypercapnic Respiratory Failure: Airways and alveoli abnormalities

A
  • Asthma
  • COPD
  • Cystic fibrosis
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15
Q

Causes of Hypercapnic Respiratory Failure: Central Nervous System Abnormalities

A
  • Drug overdose
  • Brainstem infarction
  • Spinal cord injuries

*Read notes

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16
Q

Causes of Hypercapnic Respiratory Failure: Chest wall abnormalities

A
  • Flail chest (fractures prevent the rib cage from expanding normally because of pain, mechanical restriction and muscle spasm)
  • Kyphoscoliosis (compresses the lungs and prevents normal expansion of the chest wall)
  • Severe obesity
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17
Q

Causes of Hypercapnic Respiratory Failure: Neuromuscular conditions

A
  • Muscular dystrophy
  • Guillain-Barré syndrome
  • Multiple sclerosis
  • Exposure to toxins
  • Muscle wasting

*Read notes

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18
Q

Respiratory Failure: The major threat is inability of the lungs to meet the O2 needs of tissues:

A
  • Inadequate O2 delivery to tissues or
  • Tissues cannot use O2 delivered to them:
    • Septic shock
    • Acid-base alterations

*Read notes

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19
Q

Respiratory Failure Characteristics of Clinical Manifestations

A
  • Sudden or gradual onset
  • A sudden decrease in PaO2 or rapid rise in PaCO2 implies a serious condition
  • When compensatory mechanisms fail, respiratory failure occurs
  • Signs may be specific or nonspecific
  • Mental status changes often occur early

*Read notes!!

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20
Q

Respiratory Failure: Early Signs

A
  • Tachycardia
  • Tachypnea
  • Mild HTN

*read notes

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21
Q

Respiratory Failure: Late sign

A

Cyanosis

*read notes

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22
Q

Consequences of Hypoxemia and hypoxia

A
  • Cells shift from aerobic to anaerobic metabolism (Metabolic acidosis and cell death)
  • Decreased cardiac output
  • Impaired renal function
  • GI tissue ischemia

*Read notes

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23
Q

Specific Clinical Manifestations of Respiratory Failure

A
  • Rapid, shallow breathing pattern
  • Tripod position
  • Pursed-lip breathing
  • Dyspnea
  • Retractions
  • Paradoxic breathing
  • Diaphoresis

*Read notes!

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24
Q

Clinical Manifestations of Respiratory Failure:: Abnormal breath sounds

A
  • Crackles
  • Loud crackles
  • Absent or diminished
  • Bronchial
  • Pleural friction rub

*read notes

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25
Q

Respiratory Failure: Diagnostic Studies

A
  • Physical assessment
  • Chest x-ray
  • ABG analysis**
  • Pulse oximetry
  • CBC (look at hgb and hct), serum electrolytes, urinalysis (baseline)
  • ECG
  • Sputum/blood cultures (pneumonia?)
  • CT scan (tells you what’s in those lungs, structural problems, etc)
  • V/Q lung scan
  • End-tidal CO2 (ETCO2) (how much CO2 you’re retaining)
  • Pulmonary artery catheter (severe cases): CVP, PA pressures, CO, SV, Scvo2/Svo2

*read notes on slides 25 and 26

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26
Q

Acute Respiratory Failure Nursing Assessment: Health information includes

A
  • Health history
  • Medications
  • Surgery
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27
Q

Acute Respiratory Failure Nursing Assessment: Functional health patterns

A
  • Health perception–health management
  • Nutritional-metabolic
  • Activity-exercise
  • Sleep-rest
  • Cognitive-perceptual
  • Coping–stress tolerance
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28
Q

Acute Respiratory Failure Nursing Assessment: Physical assessment includes

A
  • General
  • Integumentary (dusky colored)
  • Respiratory
  • Cardiovascular (increased HR, Dysrhythmias)
  • Gastrointestinal (delayed emptying)
  • Neurologic

+ lab findings (ABGs!! pH, PO2, PCO2)

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29
Q

Acute Respiratory Failure: Nursing Diagnosis

A
  • Impaired gas exchange related to alveolar hypoventilation, intrapulmonary shunting, V/Q mismatch, and diffusion impairment
  • Ineffective airway clearance related to excessive secretions, decreased level of consciousness, presence of an artificial airway, neuromuscular dysfunction, and pain
  • Ineffective breathing pattern related to neuromuscular impairment of respirations, pain, anxiety, decreased level of consciousness, respiratory muscle fatigue, and bronchospasm
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30
Q

Acute Respiratory Failure Planning: Overall goals

A
  • Independent maintenance of airway
  • Effective cough and ability to clear secretions
  • Normal ABG values or values within patient’s baseline
  • Absence of dyspnea or recovery to baseline breathing patterns for patient
  • Breath sounds within patient’s baseline
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31
Q

Acute Respiratory Failure: Prevention

A
  • Thorough history and physical assessment to identify at-risk patients
  • Early recognition of respiratory distress
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32
Q

Acute Respiratory Failure: Respiratory Therapy includes

A
  • Oxygen therapy

- Mobilization of secretions

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33
Q

Acute Respiratory Failure Treatment: Oxygen Therapy

A

Delivery system should:

  • Be tolerated by the patient
  • Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible ***

*Read notes

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34
Q

Acute Respiratory Failure Treatment: Mobilization of secretions can be done through

A
  • Effective coughing
  • Adequate hydration and humidification
  • Chest physiotherapy
  • Airway suctioning
  • Patient positioning
  • Ambulation
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35
Q

Tripod position

A

Increases chest and lung expansion

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36
Q

How is an augmented cough done?

A
  • Perform augmented coughing by placing one or both hands on the anterolateral base of the lungs (Fig. 67-7).
  • As the patient ends a deep inspiration and begins the expiration, move your hands forcefully upward, increasing abdominal pressure and facilitating the cough.
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37
Q

Huff cough

A
  • Serious of coughs performed while saying “huff”

- Effective in clearing central airways

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38
Q

Staged cough

A
  • Sit leaning forward

- Take three deep breaths through mouth and cough

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39
Q

Acute Respiratory Failure Treatment: Hydration and Humidification includes what methods

A
  • Adequate fluid intake (2-3L/day)
  • IV hydration
  • Humidification devices
  • O2 via aerosol mask
  • Mucolytic drugs (i.e mucomyst to thin secretions)
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40
Q

Acute Respiratory Failure Treatment: Chest Physiotherapy

A
  • Postural drainage
  • Percussion
  • Vibration
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41
Q

What does FiO2 measure?

A

Measured from ventilator.

What does it measure though?

42
Q

Acute Respiratory Failure Treatment: Airway Suctioning

A
  • Nasopharyngeal
  • Oropharyngeal
  • Nasotracheal
43
Q

Respiratory Therapy includes

A
  • Positive pressure ventilation (PPV)
  • Noninvasive PPV
    • BiPAP
    • CPAP

*Read notes

44
Q

Bilevel positive airway pressure(BiPAP)

A

is a form of NIPPV in which different positive pressure levels are set for inspiration and expiration (Fig. 67-8).

45
Q

Continuous positive airway pressure (CPAP)

A

Continuous positive airway pressure (CPAP) is another form of NIPPV in which a constant positive pressure is delivered to the airway during inspiration and expiration.

46
Q

Non-invasive PPV is not appropriate for what patients?

A

Not appropriate for patients who have excessive secretions, decreased level of consciousness, high O2 requirements, facial trauma, or hemodynamic instability.

47
Q

Acute Respiratory Failure Drug Therapy

A
  1. Relief of bronchospasm = Bronchodilators
  2. Reduction of airway inflammation = Corticosteroids
  3. Reduction of pulmonary congestion = Diuretics, nitrates if heart failure present
  4. Treatment of pulmonary infections = IV antibiotics
  5. Reduction of severe anxiety, pain, and agitation = Benzodiazepines and Opioids
48
Q

Acute Respiratory Failure: Medical Supportive Therapy includes

A
  • Treat the underlying cause
  • Maintain adequate cardiac output and hemoglobin concentration

*Read notes

49
Q

Acute Respiratory Failure: Nutritional Therapy

A
  • Maintain protein and energy stores
  • Enteral or parenteral nutrition
  • Nutritional supplements

*Read notes!

50
Q

Acute Respiratory Failure: Expected Outcomes

A
  • Maintain a patent airway with effective removal of secretions
  • Achieve normal or baseline respiratory rate and rhythm, and breath sounds
  • Maintain adequate oxygenation as indicated by normal or baseline ABGs
  • Experience normal hemodynamic status
51
Q

Acute Respiratory Distress Syndrome

A
  • Sudden progressive form of acute respiratory failure

- Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid -> Alveoli fill with fluid

52
Q

Stages of Edema Formation in ARDS

A

Slide48

53
Q

ARDS results in

A
  • Severe dyspnea
  • Hypoxia
  • Decreased lung compliance
  • Diffuse pulmonary infiltrates
54
Q

ARDS Etiology and Pathophysiology: Lung Injury

A
  • Develops from a variety of direct or indirect lung injuries
  • Most common cause is sepsis
  • Exact cause for damage to alveolar-capillary membrane not known
  • Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems

Slide 51 has diagram and Read through slides

55
Q

ARDs Etiology and Pathophysiology: Immune response

A
  • Neutrophils are attracted and release mediators, producing changes in lungs including:
    • ↑ Pulmonary capillary membrane permeability
    • Destruction of elastin and collagen
    • Formation of pulmonary microemboli
    • Pulmonary artery vasoconstriction
56
Q

The physiologic changes in ARDS are divided into three phases

A
  1. Injury or educative phase
  2. Reparative or proliferative phase
  3. Fibrotic phase
57
Q

ARDs Etiology and Pathophysiology: What happens during the Injury or Exudative Phase?

A
  • 1–7 days after initial lung injury or host insult
  • Neutrophils adhere to pulmonary microcirculation leading to:
    • Damage to vascular endothelium
    • ↑ Capillary permeability
58
Q

ARDS Etiology and Pathophysiology: What is the result of injury or exudative phase?

A
  • Engorgement of peribronchial and perivascular interstitial space
  • Fluid crosses into alveolar space
  • Intrapulmonary shunt develops as alveoli fill with fluid, and blood passing through cannot be oxygenated
  • Alveolar cells type 1 and 2 are damaged
  • Hyaline membranes line alveoli
  • Interstitial and alveolar edema and atelectasis
  • Severe V/Q mismatch and shunting of pulmonary capillary blood result in refractory hypoxemia (unresponsive to increasing O2 concentrations)
  • Lungs become less compliant (higher airway pressures must be generated)
59
Q

Injury/Exudative Phase: Alveolar cells type 1 and 2 are damaged

A

Surfactant dysfunction -> atelectasis

60
Q

Injury/Exudative Phase: Hyaline membranes line alveoli

A
  • Contribute to fibrosis and atelectasis

- Leads to decreased gas exchange capability and lung compliance

61
Q

Injury/Exudative Phase can lead to what findings?

A
  • ↑ Work of breathing (WOB)
  • ↑ Respiratory rate
  • ↓ Tidal volume:
    • Produces respiratory alkalosis from increase in CO2 removal
    • ↓ CO2 and tissue perfusion

*Read notes

62
Q

Reparative Proliferative Phase: What happens during this phase?

A
  • 1–2 weeks after initial lung injury
  • Influx of neutrophils, monocytes, and lymphocytes
  • Fibroblast proliferation
  • Lung becomes dense and fibrous
  • Lung compliance continues to ↓
  • Worsening hypoxemia
63
Q

Reparative or Proliferative Phase: Worsening hypoxemia

A

Thickened alveolar membrane -> diffuse limitation and shunting

64
Q

What happens if the reparative phase persists?

A

Widespread fibrosis results

65
Q

If reparative phase is stopped,

A

Lesions will resolve

66
Q

Fibrotic or Chronic/Late Phase

A
  • 2–3 weeks after initial lung injury

- Lung is completely remodeled by collagenous and fibrous tissues

67
Q

What findings can be seen in a patient in the fibrotic or chronic/late phase of ARDs?

A
  • ↓ Lung compliance
  • ↓ Area for gas exchange: Hypoxemia continues
  • Pulmonary hypertension: Results from pulmonary vascular destruction and fibrosis
68
Q

Progression of ARDS: People who survive the acute phase of lung injury

A
  • Pulmonary edema resolves

- Makes a complete recovery

69
Q

Survival changes for those who enter the fibrotic phase

A
  • Poor

- Requires long-term mechanical ventilation

70
Q

ARDS: Early Clinical Manifestations include

A
  • Dyspnea, tachypnea, cough, restlessness
  • Chest auscultation may be normal or may reveal fine, scattered crackles
  • Edema (may not show until 30% increase in fluid content in lungs)
71
Q

ARDS: Early Clinical Lab Findings

A
  • ABGs: Mild hypoxemia and respiratory alkalosis caused by hyperventilation
  • CXR may be normal or reveal scattered interstitial infiltrates
72
Q

ARDS: Characteristics of Late Clinical Manifestations

A
  • Symptoms worsen with increased fluid accumulation and decreased lung compliance
  • Pulmonary function tests reveal decreased compliance, lung volumes, and functional residual capacity (FRC)
73
Q

Late Clinical Manifestations for ARDS include

A
  • Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor
  • Diffuse crackles and coarse crackles
  • Hypoxemia despite increased FIO2
  • Increasing WOB despite initial findings of normal PaO2 or SaO2
74
Q

Clinical Manifestations: As ARDS progresses, profound respiratory distress requires

A

Endotracheal intubation and PPV

75
Q

ARDS: Chest x-rays are termed

A
  • Whiteout or white lung because of consolidation and widespread infiltrates throughout lungs
  • Leaves few recognizable air spaces
76
Q

ARDS: Complications of Treatment include

A
  • Ventilator-associated pneumonia
  • Barotrauma
  • Volutrauma
  • High risk for stress ulcers
  • Renal failure
77
Q

ARDS Complications of Treatment: Strategies for prevention of Ventilator associated pneumonia

A
  • Strict infection control measures
  • Ventilation protocol bundle:
    • Elevate HOB 30 to 45 degrees
    • Daily “sedation holidays”
    • Venous thromboembolism prophylaxis
    • Daily oral care with chlorhexidine
78
Q

ARDS Complications of Treatment: Barotrauma

A
  • Rupture of overdistended alveoli during mechanical ventilation
  • Can lead to Interstitial emphysema, pneumothorax and subcutaneous emphysema, etc.
79
Q

XUTE Respiratory Distress Syndrome Clinical Network (ARDSNet)

A

Ventilate with smaller tidal volumes

Higher Paco2 - permissive hypercapnia

80
Q

ARS Complications of Treatment: Volutrama

A
  • Occurs when large tidal volumes are used to ventilate noncompliant lungs -> Alveolar fracture (damage or tears in the alveoli) and movement of fluids and proteins into alveolar spaces
  • Smaller tidal volumes or pressure-control ventilation is now standard in ARDS
81
Q

ARDS Complications of Treatment: Stress Ulcers

A

Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation

82
Q

PEEP and its affect on CO

A

Look it up

83
Q

How to manage stress ulcers associated with ARDS treatment?

A
  • Correction of predisposing conditions
  • Prophylactic antiulcer drugs (Proton pump inhibitors)
  • Early initiation of enteral nutrition
84
Q

ARDS Complications of Treatment: Renal Failure

A
  • Occurs from decreased renal perfusion and subsequent decreased delivery of O2 to kidneys: From hypotension, hypoxia, or hypercapnia
  • May also be caused by nephrotoxic drugs used to treat ARDS-related infections
85
Q

ARDS: Nursing Assessment includes

A
  • History of lung disease
  • Exposures to lung toxins
  • Tobacco, alcohol, or drug use
  • Related hospitalizations
  • Thoracic or spinal cord trauma
  • Severe obesity
  • Use of O2, inhalers, nebulizers, OTC drugs, immunosuppressant therapy
  • Previous intubation
  • Thoracic or abdominal surgery
  • Exercise
  • Immunizations
86
Q

ARDS Nursing Assessment of Symptoms include

A
  • Eating habits, change in appetite
  • Weight gain/loss
  • Fatigue
  • Dizziness
  • Dyspnea, wheezing, cough, sputum, palpitations, swollen feet
  • Changes in sleep pattern, use of CPAP
  • Shallow, increasing respiratory rate progressing to decreased rate
  • Use of accessory muscles
  • Asymmetric chest expansion
  • Abnormal breath sounds
  • Pleural friction rub
  • Tachycardia progressing to bradycardia
  • Hypertension progressing to hypotension
  • Pulsus paradoxus, JVD, pedal edema
  • Abdominal distention, ascites
  • Somnolence, confusion, delirium
87
Q

ARDS Nursing Assessment: Changes in labs

A
  • Decreased tidal volume, FVC
  • Abnormal x-ray
  • Abnormal central venous or pulmonary artery pressures
  • Initial increased CO: As hypoxemia, hypercapnia, and acidosis become more severe, CO will decrease
  • Changes in pH, PaCO2, PaO2, SaO2
88
Q

ARDS: Nursing Diagnoses can include

A
  • Ineffective airway clearance
  • Ineffective breathing pattern
  • Risk for imbalanced fluid volume
  • Anxiety
  • Impaired gas exchange
  • Imbalanced nutrition: less than body requirements

*Read notes for reasons

89
Q

ARDS: Following recovery, overall goals include

A
  • PaO2 within normal limits for age or at baseline on room air
  • SaO2 >90%
  • Resolution of precipitating factor(s) for ARDS
  • Clear lungs on auscultation
90
Q

Respiratory Therapy: Goals of Oxygen Administration

A

Primary goal is to correct hypoxemia:

  • Initially nasal cannula or face mask with high-flow systems used to maximize O2 delivery
  • SpO2 continuously monitored
91
Q

Respiratory Therapy for ARDs: Modest to severe ARDS and refractory hypoxemia requires what treatments?

A

Need intubation with mechanical ventilation to maintain the PaO2 at acceptable levels

92
Q

Respiratory Therapy for ARDS: Positive Pressure Ventilation

A
  • PEEP at 5 cm H2O compensates for loss of glottic function: Opens collapsed alveoli
  • Apply PEEP at 3 to 5 cm H2O increments
  • Higher levels of PEEP may be used in patients with ARDS
93
Q

Respiratory Therapy: Problems with PPV

A
  1. Can compromise venous return to right side of the heart: decreases preload, CO and BP
  2. Higher levels of PEEP can hyperinflate the alveoli = barotrauma or volutrauma.

*Read notes

94
Q

Respiratory Therapy for ARDS: Alternative modes of mechanical ventilation and respiratory therapies if hypoxemia persists

A
  • Airway pressure release ventilation
  • Pressure control inverse ratio ventilation
  • High-frequency ventilation
  • Permissive hypercapnia
95
Q

Respiratory Therapy for ARDS: Positioning Strategies

A

-Turn from supine to prone position “proning”: May be sufficient to reduce inspired O2 or PEEP

  • When in supine position mediastinal and heart contents place more pressure on lungs than when in prone
  • Predisposes patient to atelectasis
  • Fluid pools in dependent regions of lung
96
Q

Respiratory Therapy for ARDS: Other positioning Strategies include

A
  1. Continuous lateral rotation therapy

2. Kinetic Therapy

97
Q

ARDS Positioning Strategies: Continuous lateral rotation therapy

A
  • Continuous, slow side-to-side turning <40 degrees

- 18 of every 24 hours

98
Q

ARDS Positioning Strategies: Kinetic therapy

A

Patient rotated side-to-side >40 degrees

99
Q

ARDS Medical Supportive Therapy: Maintenance of CO and tissue perfusion

A
  • Hemodynamic monitoring via a central venous or pulmonary artery catheter:
    • Monitor CO and BP
    • Sample blood for ABGs
100
Q

ARDS Medical Supportive Therapy: Nutrition/fluid balance

A
  • Enteral or parenteral feedings are started
  • Monitor hemodynamic parameters
    (e. g., CVP, stroke volume variation)
  • Monitor daily weight, intake and output

*Read notes

101
Q

ARDS Evaluation:

A

Add last three slides

NURS 425 (19 decks)

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