![]() Intermediate ( 8–14 days) to late ( > 15 days) findings: a phase of stability is followed either by resolution or progressive development of fibrosis.Additional findings may include small pleural effusions, air bronchograms (see “ Chest x-ray” above).Dense consolidation in dependent regions.The lungs may appear normal in nondependent regions.Symmetrical ground-glass opacities are the most important finding.Indications: may be used if chest x-ray findings are insufficient or to further investigate for underlying causes or complications.Findings supportive of ARDS rather than CHF.Fibrotic course: Reticular opacities begin to appear and may become permanent.Typical course: Acute features remain stable, then resolve.ĪRDS diagnostic criteria include: Abnormal x-ray, Respiratory failure 15 days) findings Respiratory failure cannot be fully accounted for by heart failure or fluid overload.Moderate ARDS: PaO 2/ FiO 2 = 101–200 mm Hg.Mild ARDS: PaO 2/ FiO 2 = 201–300 mm Hg.Hypoxemia: PaO 2/ FiO 2 ≤ 300 mm Hg (measured with a minimum of 5 cm H 2O PEEP ).Not sufficiently explained by pleural effusions, lobar or lung collapse, or nodules.Bilateral opacities (on chest x-ray or CT).Acute onset : respiratory failure within one week of a known predisposing factor (e.g., sepsis, pneumonia ) or worsening respiratory symptoms.All four of the following conditions must be met: The Berlin criteria are the criteria most commonly used to define ARDS. Consider additional testing in order to:.Perform an ABG and calculate the P/F ratio (the ratio of arterial oxygen partial pressure, as measured by arterial blood gas, to fractional inspired oxygen administered to the patient).Order chest x-ray to evaluate for characteristic findings (bilateral infiltrates).Consider ARDS in patients with rapid-onset respiratory failure and a potential trigger. Organizing phase (late stage) : proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosisĪRDS is a diagnosis of exclusion (see the Berlin criteria for ARDS ).Damage to type I and type II pneumocytes → decrease in surfactant → alveolar collapse → intrapulmonary shunting.Hypoxemia → chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension and right-to-left pulmonary shunt (increased shunt fraction ).Hypoxemia → compensation through hyperventilation → respiratory alkalosis.Hyaline membrane formation : exudation of neutrophils and protein-rich fluid into the alveolar space → formation of alveolar hyaline membranes → impaired gas exchange → hypoxemia.Exudative phase : excess fluid in interstitium and on alveolar surface → pulmonary edema with normal pulmonary capillary wedge pressure ( noncardiogenic pulmonary edema ) → decreased lung compliance and respiratory distress.Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1 ) → inflammatory reaction → migration of neutrophils in to alveoli → excessive release of neutrophilic mediators (e.g., cytokines, proteases, reactive oxygen species ) → injury to alveolar capillaries and endothelial cells ( diffuse alveolar damage, DAD ) leading to:.Most patients improve significantly in the weeks following the initial presentation, but some cases progress to pulmonary fibrosis, which prolongs hospital stays and delays the resolution of symptoms. Even if adequate treatment is initiated, ARDS remains an acutely life-threatening disease with a high mortality rate. Moreover, any treatable causes of ARDS should be addressed. Management of ARDS is focused on maintaining adequate oxygenation, which often requires intubation and lung-protective mechanical ventilation. A defining laboratory feature of ARDS is a PaO 2/FiO 2 ratio ≤ 300 mm Hg. Chest x-ray typically shows diffuse bilateral infiltrates. The chief finding in ARDS is hypoxemic respiratory failure with decreased arterial oxygen pressure, which can progress to hypercapnic respiratory failure. Affected individuals initially present with acute-onset cyanosis, dyspnea, and tachypnea. ![]() While sepsis is the most common cause, a variety of systemic and pulmonary factors (e.g., pneumonia, aspiration) can lead to ARDS. Acute respiratory distress syndrome (ARDS) is a severe inflammatory reaction of the lungs to pulmonary damage.
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