Acute Respiratory Distress Syndrome (ARDS) Flashcards

1
Q

Causes

A

Alveolar capillary interface becomes damaged and more permeable to intravascular fluid
Alveoli fill with fluid

• Sepsis*
• Pneumonia
• Aspiration
• Trauma*
• Massive transfusions
• Pancreatitis
• Shock states
                           Inflammation
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2
Q

ARDS
Failure of Oxygenation how it happens?
Ratio?

A
  • Acute onset
  • Bilateral infiltrates
• Severe, refractory hypoxemia
     – PaO2/FiO2 ratio
• 200 – 300 – mild ARDS
• 100-200 – moderate ARDS
• <100 – severe ARDS

*in the absence of isolated cardiogenic pulmonary edema

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3
Q

Severe V/Q mismatch and shunting of

pulmonary capillary blood result in ?

A

…refractory hypoxemia

  • Unresponsive to increasing O2 concentrations
  • Lungs become less compliant
  • Increased airway pressures must be generated
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4
Q

Exudative Phase Changes

A
•Inflammatory
mediators
• Disruption of alveolar
capillary membrane
• Fluid in the alveoli
• V/Q mismatch
• Loss of
surfactant=alveolar
collapse
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5
Q

Exudative Phase Manifestations

A

• Tachypnea and
tachycardia

• Mild hypoxemia and
respiratory alkalosis
caused by
hyperventilation

• Dyspnea, tachypnea,
cough, restlessness

• Chest auscultation may
be normal or may reveal
fine, scattered crackles

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6
Q

Proliferative Phase Changes:

A
• Inflammatory
mediators cross ACM =
damaged alveolar and
capillary epithelium =
diffusion defects

• V/Q worsens

• Pulmonary HTN due to
hypoxemic
vasoconstriction=R HF

• Fibrotic changes

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7
Q

Proliferative Phase Manifestations:

A

• Decreased lung
compliance=increased
work of
breathing=tachypnea

• Hypercarbia and
worsening refractory
hypoxemia

• Diaphoresis, decreased
LOC, cyanosis, and pallor

• Increased peak
inspiratory pressures

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8
Q

Fibrotic Phase Changes:

A
• Diffuse scarring
• Worsening pulmonary
HTN
• Worsening V/Q
mismatch, diffusion
defects and shunting
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9
Q

Fibrotic Phase Manifestations :

A
• R sided HF
• Decreased BP, CO
• Refractory hypoxemia
• Tissue hypoxia/lactic
acidosis (increased lactate)
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10
Q

Diagnosis

A

• CXR – bilateral infiltrates
– Ground glass appearance

• Laboratory testing
– ABGs
– CBC with differential
– Cultures
– CMP
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11
Q

Treatment

A
• Treat the Cause!
• Mechanical Ventilation with PEEP
• Diuresis
• Antibiotics
• Steroids - improve oxygenation, not survival
    – use is controversial
• Hydration – maintain circulatory volume, decrease
viscosity of secretions
• Nutrition
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12
Q

Respiratory Therapy

A
• Mechanical ventilation
– Low Tidal Volumes to reduce barotrauma
– High PEEP to aid in recruitment
– No mode proven to improve outcomes
– Requires advanced airway*
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13
Q

Positive End Expiratory Pressure

PEEP

A

• Increase FRC and open up collapsed alveoli
• Higher levels of PEEP are often needed to maintain
PaO2 at 60 mm Hg or greater
• High levels of PEEP can compromise venous return
• ↓ Preload, CO, and BP

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14
Q

Nursing Interventions

A

• Optimize O2 delivery
– Frequent assessment – hemodynamic and ventilatory
– Keep the airways clear

• Minimize O2 demand - Decrease O2 consumption
– Comfort
– Sedation
– Pain relief
– Neuromuscular blockade

• Positioning
– Prone positioning
– Elevate HOB
– Frequent changes

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