Acute Respiratory Distress Syndrome (ARDS) is a sudden, progressive form of respiratory failure characterized by severe dyspnea, hypoxemia, and decreased lung compliance. It develops from direct or indirect lung injuries and is thought to be caused by stimulation of the inflammatory and immune systems, resulting in leakage of fluid into the lungs. The clinical progression of ARDS involves exudative, proliferative, and fibrotic phases that can lead to respiratory failure if not promptly treated with oxygen supplementation, mechanical ventilation, and other supportive therapies.

1. Acute Respiratory
Distress Syndrome
(ARDS)
Presented by Melinda C. Jordan

2. Acute Respiratory
Distress Syndrome
Sudden, progressive form of acute
respiratory failure
Characterised by:
Severe dyspnea
Hypoxaemia
↓ Lung compliance
Diffuse pulmonary infiltrates

3. Clinical Conditions Associated with
the development of ARDS
Sepsis
Severe Trauma
Pulmonary contusion
Pneumonia
Near drowning
Massive transfusion
Fat embolism

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. Pathophysiology of ARDS
Fig. 66-9

6. Aetiology and Pathophysiology
Phases:
Exudative
Proliferative
Fibrotic

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. 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. 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. Aetiology and Pathophysiology
↑ WOB
↑ RR
↓ Tidal volume
Produces respiratory alkalosis from increase in
CO2 removal
2
↓ CO and tissue perfusion

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

15. Clinical Progression
Survival chances are poor for those who
enter fibrotic phase
Requires long-term mechanical ventilation
long-term

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. 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. 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. 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. Complications
Nosocomial pneumonia
Strategies for prevention
Infection control measures
Elevating HOB 45 degrees or more to prevent
aspiration

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

27. Nursing Assessment
Somnolence, confusion, delirium
Changes in pH, PaCO2, PaO2, SaO2
Decreased tidal volume, FVC
Abnormal x-ray
x-ray

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

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. Evaluation
No abnormal breath sounds
Effective cough and expectoration
Normal respiratory rate, rhythm, and
depth
Synchronous thoracoabdominal
movement
Appropriate use of accessory muscles

35. Evaluation
PaO2 and PaCO2 within normal ranges
Maintenance of weight or weight gain
Serum albumin and protein within
normal ranges