Chapter 28: ACUTE RESPIRATORY DISTRESS SYNDROME
Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute
respiratory failure in which the alveolar capillary membrane becomes damaged and more
permeable to intravascular fluid.
o Alveoli fill with fluid, resulting in severe dyspnea, hypoxemia refractory to
supplemental O ,2reduced lung compliance, and diffuse pulmonary infiltrates.
o The most common cause of ARDS is sepsis.
o Direct lung injury may cause ARDS, or ARDS may develop as a consequence of
the systemic inflammatory response syndrome, or multiple organ dysfunction
The pathophysiologic changes of ARDS are thought to be due to stimulation of the
inflammatory and immune systems, which causes an attraction of neutrophils to the
pulmonary interstitium. The neutrophils cause a release of biochemical, humoral, and
cellular mediators that produce changes in the lung.
The injury or exudative phase of ARDS occurs approximately 1 to 7 days (usually 24 to
48 hours) after the initial direct lung injury or host insult.
o The primary pathophysiologic changes that characterize this phase are interstitial
and alveolar edema (noncardiogenic pulmonary edema) and atelectasis resulting
in V/Q mismatch, shunting of pulmonary capillary blood, and hypoxemia
unresponsive to increasing concentrations of O 2termed refractory hypoxemia).
o Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung
parenchyma (J reflex) initially cause an increase in respiratory rate, decrease in
tidal volume, respiratory alkalosis, and an increase in cardiac output.
The reparative or proliferative phase of ARDS begins 1 to 2 weeks after the initial lung
o During this phase, there is an influx of neutrophils, monocytes, and lymphocytes
and fibroblast proliferation as part of the inflammatory response.
o Lung compliance continues to decrease as a result of interstitial fibrosis and
o If the reparative phase persists, widespread fibrosis results. If the reparative phase
is arrested, the lesions resolve.
The fibrotic or chronic phase of ARDS occurs approximately 2 to 3 weeks after the
initial lung injury.
o The lung is completely remodeled by sparsely collagenous and fibrous tissues and
there is diffuse scarring and fibrosis, resulting in decreased lung compliance.
o Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.
Progression of ARDS varies among patients and several factors determine the course of
ARDS, including the nature of the initial injury, extent and severity of coexisting
diseases, and pulmonary complications. Clinical Manifestations
ARDS is considered to be present if the patient has (1) refractory hypoxemia, (2) a chest
x-ray with new bilateral interstitial or alveolar infiltrates, (3) a pulmonary artery wedge
pressure of 18 mm Hg or less and no evidence of heart failure, and (4) a predisposing
condition for ARDS within 48 hours of clinical manifestations.
Initially the patient may exhibit only dyspnea, tachypnea, cough, and restlessness and
chest auscultation may be normal or reveal fine, scattered crackles.
ABGs usually indicate mild hypoxemia and respiratory alkalosis caused by
Chest x-ray may be normal, exhibit evidence of minimal scattered interstitial infiltrates,
or demonstrate diffuse and extensive bilateral infiltrates (termed whiteout or white lung).
As ARDS progresses, tachypnea and intercostal and suprasternal retractions may be
present and pulmonary function tests reveal decreased compliance and decreased lung
Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and
pallor may develop.
Pulmonary artery wedge pressure does not increase in ARDS because the cause of
pulmonary edema is noncardiogenic.
Hypoxemia and a PaO /F2O rat2o below 200 (e.g., 80/0.8 = 100) despite increased FIO 2
are the hallmarks of ARDS.
Complications may develop as a result of ARDS itself or its treatment.
o A frequent complication of ARDS is hospital-acquired pneumonia.
Strategies to prevent hospital-acquired pneumonia include infection
control measures (e.g., strict hand washing and sterile technique during
endotracheal suctioning) and elevating the head of the bed 30 to 45
degrees to prevent aspiration.
o Barotrauma may result from rupture of overdistended alveoli