ARDS - Acute Respiratory Distress Syndrome PDF

2/22/24, 2:06 PM Realizeit for Student Introduction Acute respiratory distress syndrome (ARDS) can be thought of as a spectrum of disease, progressing from mild to moderate to its most severe, fulminant form. Acute lung injury is a term commonly used to describe mild ARDS. ARDS is a clinical syndrom...

2/22/24, 2:06 PM Realizeit for Student Introduction Acute respiratory distress syndrome (ARDS) can be thought of as a spectrum of disease, progressing from mild to moderate to its most severe, fulminant form. Acute lung injury is a term commonly used to describe mild ARDS. ARDS is a clinical syndrome characterized by a severe inflammatory process causing diffuse alveolar damage that results in sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia unresponsive to oxygen supplementation regardless of the amount of PEEP, and the absence of an elevated left atrial pressure (Siegel, 2019a). Patients often demonstrate reduced lung compliance. A wide range of factors are associated with the development of ARDS, including direct injury to the lungs (e.g., smoke inhalation) or indirect insult to the lungs (e.g., shock). ARDS has been associated with a mortality rate ranging from 27% to 50%. Patients who survive the initial cause of ARDS may die later, commonly from HCAP or sepsis (Anesi, 2020; Siegel, 2019a). Pathophysiology Inflammatory triggers initiate the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane in addition to other structural damage to the lungs. Severe V./Q. mismatching occurs. Alveoli collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitial fluid and bronchial obstruction. Lung compliance may markedly decrease, resulting in decreased functional residual capacity and severe hypoxemia. The blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing shunting. This means that blood is interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe, refractory hypoxemia. Clinical Manifestations Initially, ARDS closely resembles severe pulmonary edema. The acute phase of ARDS is marked by a rapid onset of severe dyspnea that usually occurs less than 72 hours after the precipitating event. Arterial hypoxemia that does not respond to supplemental oxygen is characteristic. ARDS is classified according to the severity https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zSNYYvz6N%2bxRwegtqPK%2fJ7UsPJxuq7nE1D4sTAvq22Nk5Sl… 1/3 2/22/24, 2:06 PM Realizeit for Student of hypoxemia experienced by the patient as (Siegel, 2019a): mild ARDS, with arterial oxygen tension (PaO2)/fraction of inspired oxygen (FIO2) > 200 mm Hg but ≤300 mm Hg, moderate ARDS, with PaO2/FIO2 > 100 mm Hg but ≤200 mm Hg, or severe ARDS, with PaO2/FIO2 ≤ 100 mm Hg. Findings on chest x-ray are similar to those seen with cardiogenic pulmonary edema and are visible as bilateral infiltrates that quickly worsen. Mild ARDS progresses to fibrosing alveolitis with persistent, severe hypoxemia. The patient also has increased alveolar dead space (ventilation to alveoli but poor perfusion) and typically has decreased pulmonary compliance (“stiff lungs,” which are difficult to ventilate). Clinically, the patient is thought to be in the recovery phase if the hypoxemia gradually resolves, the chest x-ray improves, and the lungs become more compliant. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zSNYYvz6N%2bxRwegtqPK%2fJ7UsPJxuq7nE1D4sTAvq22Nk5Sl… 2/3 2/22/24, 2:06 PM Realizeit for Student Assessment and Diagnostic Findings On physical examination, intercostal retractions and crackles may be present as the fluid begins to leak into the alveolar interstitial space. Common diagnostic tests performed in patients with potential ARDS include plasma brain natriuretic peptide (BNP) levels, echocardiography, and pulmonary artery catheterization. The BNP level is helpful in distinguishing ARDS from cardiogenic pulmonary edema. Transthoracic echocardiography may be used if the BNP is not conclusive. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zSNYYvz6N%2bxRwegtqPK%2fJ7UsPJxuq7nE1D4sTAvq22Nk5Sl… 3/3