Acute Respiratory
 Distress Syndrome

         (ARDS)

Presented by Melinda C. Jordan
Acute Respiratory
       Distress Syndrome
Sudden, progressive form of acute
respiratory failure
Characterised by:
  Sever...
Clinical Conditions Associated with
     the development of ARDS
Sepsis
Severe Trauma
Pulmonary contusion
Pneumonia
Near d...
Aetiology and Pathophysiology

 Develop from a variety of direct or
 indirect lung injuries
 Exact cause for damage to alv...
Pathophysiology of ARDS




                          Fig. 66-9
Aetiology and Pathophysiology

Phases:
 Exudative
 Proliferative
 Fibrotic
Aetiology and Pathophysiology
  Exudative phase
    1-7 days after direct lung injury or host
    1-7
    insult
    Neutr...
Oedema Formation in Acute
Respiratory Distress Syndrome
             A, Normal alveolus and
             pulmonary capilla...
Aetiology and Pathophysiology
 Alveolar cells type 1 and 2 are damaged
   Surfactant dysfunction → atelectasis
 Hyaline me...
Aetiology and Pathophysiology

   ↑ WOB
   ↑ RR
   ↓ Tidal volume
     Produces respiratory alkalosis from increase in
   ...
Aetiology and Pathophysiology

  Proliferative phase
    1-2 weeks after initial lung injury
    1-2
    Influx of neutrop...
Aetiology and Pathophysiology

    Hypoxaemia worsens
      Thickened alveolar membrane
         Causes diffusion limitati...
Aetiology and Pathophysiology
  Fibrotic phase
    2-3 weeks after initial lung injury
    2-3
    Lung is completely remo...
Clinical Progression

Some persons survive acute phase of
lung injury
  Pulmonary oedema resolves
  Complete recovery
Clinical Progression


Survival chances are poor for those who
enter fibrotic phase
  Requires long-term mechanical ventil...
Clinical Manifestations
Initial presentation often insidious
  May only exhibit dyspnea, tachypnea,
  cough, and restlessn...
Clinical Manifestations

Symptoms worsen with progression of
fluid accumulation and decreased lung
compliance
Evident disc...
Clinical Manifestations
As ARDS progresses
   Increasing Tachypnea
  Diaphoresis
  Cyanosis
  Pallor
  Decreases in sensor...
Clinical Manifestations

If prompt therapy not initiated, severe
hypoxaemia, hypercapnea, and
hypoxaemia,
metabolic acidos...
Complications

Nosocomial pneumonia
 Strategies for prevention
   Infection control measures
   Elevating HOB 45 degrees o...
Complications

Barotrauma
 Rupture of overdistended alveoli during
 mechanical ventilation
 To avoid, ventilate with small...
Complications
Volu-pressure trauma
Volu-pressure
  Occurs when large tidal volumes used to
  ventilate noncompliant lungs
...
Complications

Stress ulcers
  Bleeding from stress ulcer occurs in 30%
  of patients with ARDS on PPV
  Management strate...
Complications

Renal failure
  Occurs from decreased renal tissue
  oxygenation from hypotension, hypoxemia,
  or hypercap...
Nursing Assessment
History of lung disease, Smoking
Restlessness
Agitation
Pale, cool, clammy or warm, flushed
skin
Shallo...
Nursing Assessment

Tachycardia progressing to bradycardia
Extra heart sounds
Abnormal breath sounds
Hypertension progress...
Nursing Assessment

Somnolence, confusion, delirium
Changes in pH, PaCO2, PaO2, SaO2
Decreased tidal volume, FVC
Abnormal ...
Planning

Patient with at least 60 mmHg and
adequate lung ventilation to maintain
normal pH following recovery will have
 ...
Treatment

Oxygen
 High flow systems used to maximize O2   2
 delivery
 SaO2 continuously monitored
      2
 Give lowest c...
Treatment

Mechanical ventilation
  May still be necessary to maintain FIO2 at
                                        2
 ...
Treatment

Positioning strategies
  Turn from prone to supine position
    May be sufficient to reduce inspired O2 or PEEP...
Medical Supportive Therapy

Maintenance of cardiac output and
tissue perfusion
  Continuous hemodynamic monitoring
  Arter...
Medical Supportive Therapy

Use of inotropic drugs may be
necessary
Hemoglobin usually kept at levels >9 or
10 with SaO2 >...
Evaluation
No abnormal breath sounds
Effective cough and expectoration
Normal respiratory rate, rhythm, and
depth
Synchron...
Evaluation

PaO2 and PaCO2 within normal ranges
Maintenance of weight or weight gain
Serum albumin and protein within
norm...
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ARDS Overview

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ARDS Overview

  1. 1. Acute Respiratory Distress Syndrome (ARDS) Presented by Melinda C. Jordan
  2. 2. Acute Respiratory Distress Syndrome Sudden, progressive form of acute respiratory failure Characterised by: Severe dyspnea Hypoxaemia ↓ Lung compliance Diffuse pulmonary infiltrates
  3. 3. Clinical Conditions Associated with the development of ARDS Sepsis Severe Trauma Pulmonary contusion Pneumonia Near drowning Massive transfusion Fat embolism
  4. 4. Aetiology and Pathophysiology Develop from a variety of direct or indirect lung injuries Exact cause for damage to alveolar- alveolar- capillary membrane not known Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems
  5. 5. Pathophysiology of ARDS Fig. 66-9
  6. 6. Aetiology and Pathophysiology Phases: Exudative Proliferative Fibrotic
  7. 7. Aetiology and Pathophysiology Exudative phase 1-7 days after direct lung injury or host 1-7 insult Neutrophils adhere to pulmonary microcirculation Damage to vascular endothelium Increased capillary permeability Results in leakage of H2O Protein Inflammatory chemical
  8. 8. Oedema Formation in Acute Respiratory Distress Syndrome A, Normal alveolus and pulmonary capillary B, Interstitial oedema occurs with increased flow of fluid into the interstitial space C, Alveolar oedema occurs when the fluid crosses the blood-gas barrier Fig. 66-8
  9. 9. Aetiology and Pathophysiology Alveolar cells type 1 and 2 are damaged Surfactant dysfunction → atelectasis Hyaline membranes line alveoli Contribute to atelectasis and fibrosis Lungs become less compliant
  10. 10. Aetiology and Pathophysiology ↑ WOB ↑ RR ↓ Tidal volume Produces respiratory alkalosis from increase in CO2 removal 2 ↓ CO and tissue perfusion
  11. 11. Aetiology and Pathophysiology Proliferative phase 1-2 weeks after initial lung injury 1-2 Influx of neutrophils, monocytes, and lymphocytes Fibroblast proliferation Lung becomes dense and fibrous Lung compliance continues to decrease
  12. 12. Aetiology and Pathophysiology Hypoxaemia worsens Thickened alveolar membrane Causes diffusion limitation and shunting If reparative phase persists, widespread fibrosis results If phase is arrested, fibrosis resolves
  13. 13. Aetiology and Pathophysiology Fibrotic phase 2-3 weeks after initial lung injury 2-3 Lung is completely remodeled by sparsely collagenous and fibrous tissues ↓ Lung compliance Reduced area for gas exchange Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis
  14. 14. Clinical Progression Some persons survive acute phase of lung injury Pulmonary oedema resolves Complete recovery
  15. 15. Clinical Progression Survival chances are poor for those who enter fibrotic phase Requires long-term mechanical ventilation long-term
  16. 16. Clinical Manifestations Initial presentation often insidious May only exhibit dyspnea, tachypnea, cough, and restlessness Auscultation may be normal or have fine, scattered crackles Mild hypoxaemia Chest x-ray may be normal x-ray Oedema may not show until 30% increase in lung fluid content
  17. 17. Clinical Manifestations Symptoms worsen with progression of fluid accumulation and decreased lung compliance Evident discomfort and WOB Pulmonary function tests reveal decreased compliance and lung volume
  18. 18. Clinical Manifestations As ARDS progresses Increasing Tachypnea Diaphoresis Cyanosis Pallor Decreases in sensorium Chest x-ray termed whiteout or white lung x-ray due to consolidation
  19. 19. Clinical Manifestations If prompt therapy not initiated, severe hypoxaemia, hypercapnea, and hypoxaemia, metabolic acidosis may ensue Mechanical Ventilation may be required to prevent profound hypoxaemia
  20. 20. Complications Nosocomial pneumonia Strategies for prevention Infection control measures Elevating HOB 45 degrees or more to prevent aspiration
  21. 21. Complications Barotrauma Rupture of overdistended alveoli during mechanical ventilation To avoid, ventilate with smaller tidal volumes Results in higher PaCO2 2 “Permissive hypercapnia” “Permissive hypercapnia”
  22. 22. Complications Volu-pressure trauma Volu-pressure Occurs when large tidal volumes used to ventilate noncompliant lungs Alveolar fractures and movement of fluids and proteins into alveolar spaces Avoid by using smaller tidal volumes or pressure ventilation
  23. 23. Complications Stress ulcers Bleeding from stress ulcer occurs in 30% of patients with ARDS on PPV Management strategies include correction of predisposing conditions, prophylactic antiulcer agents, and early initiation of enteral nutrition
  24. 24. Complications Renal failure Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia May also be caused by nephrotoxic drugs used for infections associated with ARDS
  25. 25. Nursing Assessment History of lung disease, Smoking Restlessness Agitation Pale, cool, clammy or warm, flushed skin Shallow breathing with increased respiratory rate Use of accessory muscles
  26. 26. Nursing Assessment Tachycardia progressing to bradycardia Extra heart sounds Abnormal breath sounds Hypertension progressing to hypotension
  27. 27. Nursing Assessment Somnolence, confusion, delirium Changes in pH, PaCO2, PaO2, SaO2 Decreased tidal volume, FVC Abnormal x-ray x-ray
  28. 28. Planning Patient with at least 60 mmHg and adequate lung ventilation to maintain normal pH following recovery will have PaO2 within normal limits 2 SaO2 >90% 2 Patent airway Clear lungs on auscultation
  29. 29. Treatment Oxygen High flow systems used to maximize O2 2 delivery SaO2 continuously monitored 2 Give lowest concentration that results in PaO2 60 mmHg or greater 2 Risk for O2 toxicity increases when FIO2 2 2 exceeds 60% for more than 48 hours
  30. 30. Treatment Mechanical ventilation May still be necessary to maintain FIO2 at 2 60% or greater to maintain PaO2 at 60 2 mmHg or greater PEEP at 5 cm H2O2 Opens collapsed alveoli
  31. 31. Treatment Positioning strategies Turn from prone to supine position May be sufficient to reduce inspired O2 or PEEP 2 Fluid pools in dependent regions of lung Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone position
  32. 32. Medical Supportive Therapy Maintenance of cardiac output and tissue perfusion Continuous hemodynamic monitoring Arterial catheter
  33. 33. Medical Supportive Therapy Use of inotropic drugs may be necessary Hemoglobin usually kept at levels >9 or 10 with SaO2 >90% >90% Packed RBCs Maintenance of fluid balance
  34. 34. Evaluation No abnormal breath sounds Effective cough and expectoration Normal respiratory rate, rhythm, and depth Synchronous thoracoabdominal movement Appropriate use of accessory muscles
  35. 35. Evaluation PaO2 and PaCO2 within normal ranges Maintenance of weight or weight gain Serum albumin and protein within normal ranges

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