Acute Respiratory Distress Syndrome (ARDS)

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1.0 Introduction

Acute respiratory distress syndrome also called adult respiratory distress syndrome. Acute respiratory distress syndrome (ARDS) was originally defined by Ashbaugh et al in 1967 as a condition identify by rapid onset tachypnoea and hypoxaemia with loss of lung compliance and bilateral infiltrates on chest radiograph. ARDS happen both adult and children. ARDS may happen in people of any age. Its rate increases with advancing age, ranging from 16 cases per 100,000 person-years in those aged 15-19 years to 306 cases per 100,000 person-years in those between the ages of 75 and 84 years. The age reflects the incidence of the causes. Thousands and thousands of Americans pain from ARDS each year. Many more suffer all around the world.
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Neutrophils release of biochemical, humoral and cellular mediators that produce changes in the lung. Pulmonary capillary membrane permeability increased, destruction of elastin and collagen, formation of pulmonary microemboli, and pulmonary artery vasoconstriction. Pathophysiologic changes in ARDS are described in three phases.These three phases unfold sequentially over a period of several weeks to several months.First is exudative level. The exudative phase unfolds over the first 1 to 7 days after attack of lung injury. Accumulation in the alveoli of excessive fluid, protein and inflammatory cells that have move into the air spaces from the alveolar capillaries. Intrapulmonary shunt develop and blood passing cannot be oxygenated. Alveolar type I and type II cells are spoiled causing surfactant dysfunction. Alveoli become unstable and collapse and fibrotic changes take place. Hyaline membranes help to the development of fibrosis and atelectasis (collapse) essential to decrease in gas exchange capability and lung dysfunction. These changes cause the lungs to become stiff, patient work hard to inspire. Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma leading to increase respiratory rate and decrease in tidal volume. Breathing irregular increase carbon dioxide removal,…show more content…
The diagnosis is based on the physical exam, chest X-ray and oxygen levels and by ruling out other diseases and conditions.
4.3.1 Imaging. A chest X-ray can reveal which parts of lungs and how much of the lungs have fluid in them and whether heart is enlarged. In addition chest x-ray demonstrate diffuse and extensive bilateral interstitial and alveolar infiltrates. Computerized tomography (CT) scan combines X-ray images taken from many different directions into cross-sectional views of internal organs. CT scans can provide detailed information about the structures within the heart and lungs.
4.3.2 Lab tests.
A test using blood from an artery in your wrist can measure oxygen level. ABGs showed a normal or decreased PaCo2 despite severe dyspnea and hypoxemia. Other types of blood tests can check for signs of infection or anemia. If Doctor suspects that patient have a lung infection, secretions from airway may be tested to determine the cause of the infection.
4.3.3 Heart

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