ACUTE RESPIRATORY DISTRESS SYNDROME

Taufan Arif, S.Kep., Ns., M.Kep

 Description
• Acute respiratory distress syndrome (ARDS) is a
systemic process that is considered to be the
pulmonary manifestation of multiple organ
dysfunction syndrome.
• It is characterized by noncardiac pulmonary edema
and disruption of the alveolarcapillary membrane as
a result of injury to either the pulmonary vasculature
or the airways
 The Berlin Definition of ARDS is as follows
• Timing—within 1 week of known clinical insult or new or worsening respiratory
symptoms
• Chest imaging—bilateral opacities not fully explained by effusions, lobar/lung
collapse or nodules
• Origin of edema—respiratory failure not fully explained by heart failure or fluid
overload; need objective assessment to exclude hydrostatic edema if no risk
factor present
• Oxygenation—mild (200 mg Hg less than Pao2/Fio2 less than or equal to 300 mm
Hg with positive end-respiratory airway pressure [PEEP] or constant positive
airway pressure [CPAP] greater than or equal to 5 cm H2O); Moderate (100 mg
Hg less than Pao2/Fio2 less than or equal to 200 mm Hg with PEEP greater than
or equal to 5 cm H2O); or Severe (Pao2/Fio2 less than or equal to 100 mm Hg
with PEEP greater than or equal to 5 cm H2O)
 Etiology
• These are categorized as direct or indirect, depending on
the primary site of injury (Box 20-5).
• Direct injuries are those in which the lung epithelium
sustains a direct insult. Indirect injuries are those in which
the insult occurs elsewhere in the body and mediators are
transmitted via the bloodstream to the lungs.
• Sepsis, aspiration of gastric contents, diffuse pneumonia,
and trauma were found to be major risk factors for the
development of ARDS
 Pathophysiology
• Activation of inflammatory mediators and cellular
components resulting in damage to capillary endothelial
and alveolar epithelial cells
• Increased permeability of alveolar capillary membrane
• Influx of protein rich edema fluid,blood cells, inflammatory
cells into alveoli
• Dysfunction of surfactant
• Alveoli collapse(atelektasis) fibrotic
• Lungs become stiff, less compliant, very hard to inspire
• Decrease in gas exchange /shunted Hypoxia
 STAGES
1. Exudative (acute) phase - 0- 4 days
2. Proliferative phase - 4- 8 days
3. Fibrotic phase - >8 days
4. Recovery
 Clinical Manifestation
• Rapid onset of severe dyspnea • ABG’s
• with in 12-48 hours PaO2 < 70mmHg
• Intercostal and suprasternal PaCO2 > 45
retractions HCO3
• Increased resp rate • Normal
• Hypoxemia that does not respond to • < 22
O2 pH
• Confusion anxiety • low
• Restlessness Analysis
• Cyanosis • Resp. and met. Acidosis
• Fever
 Complication
• Lung damage (such as pneumothorax) due to
use of high settings on the breathing machine
needed to treat the disease
• Multiple organ system failure
• Pulmonary fibrosis
• Ventilator-associated pneumonia
 Diagnostic Test
• Arterial blood gas analysis reveals hypoxemia (reduced
levels of oxygen in the blood)
• A complete blood count may be taken. The number of
white blood cells is increased in sepsis
• Chest x-ray will show the presence of fluid in the lungs
• CT scan of the chest may be required only in some
situations (routine chest x-ray is sufficient in most cases)
• Echocardiogram (an ultrasound of the heart) may help
exclude any heart problems that can cause fluid build-up in
the lung
 Diagnostic Test
• Monitoring with a pulmonary artery catheter may be
done to exclude a cardiac cause for the difficulty in
breathing.
• Bronchoscopy (a procedure used to look large airways
of the lung) may be considered to evaluate the
possibility of lung infection
• Sputum cultures and analysis
 MANAGEMENT
INTENSIVE CARE UNIT
• O2 Intubation and mechanical vent
• Give lowest possible level of O2 to prevent toxicity
• Higher airway pressures usually necessary
• PEEP may be indicated
• Maintain PaO2 at > 60mm Hg
• Potitioning and chest fisioterapi
• Increase cardiac output and maintain blood pressure
• Fluid therapy
• Dobutrex, dobutamine
• Maintenance of fluid balance
• Diuretics may be indicated Diuretics may be indicated
 MANAGEMENT
• Surfactant replacement
• Corticosteroids
• Antibiotis
• Sedatives
• Diuretics
 SELECT PEEP
• PEEP/FiO2 relationship to maintain adequate
PaO2/SpO2
• PaO2 goal: 55-80mmHg or SpO2 88-95% use
FiO2/PEEP combination to achieve oxygenation goal

Fio2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0

PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 20-24