Damage or injury to the alveolar-capillary membrane triggers the release of inflammatory mediators, eventually leading to increased membrane permeability. These changes in the lungs allow fluid from the interstitial space to enter and fill the alveoli. When this occurs, the alveoli can no longer function to oxygenate the blood that flows through the capillaries, causing impaired gas exchange.
Patients who are not getting enough oxygen will become restless, anxious, and diaphoretic. The body will attempt to compensate for the lack of oxygen by increasing heart rate, causing ARDS patients to become tachycardic.
Changes in the lungs that interfere with gas exchange will cause patients with ARDS to become dyspneic. Difficulty breathing and the feeling of not getting enough air will lead to tachypnea, and eventually, respiratory alkalosis.
In patients with ARDS, the lungs are being adequately perfused, but gas exchange is disrupted due to atelectasis and fluid in the alveoli. The result is a V/Q mismatch and an intrapulmonary shunt, which lead to hypoxemia. Hypoxemia in this situation is refractory to oxygen therapy.
Impaired gas exchange will cause a decrease in arterial oxygen levels in the blood, despite increasing oxygen concentrations used in oxygen therapy.
An x-ray of healthy, air-filled lungs will appear black. However with ARDS, an x-ray of the patient’s chest will reveal lungs that appear white, due to widespread infiltrates and minimal air spaces. It is often referred to as whiteout or white lung.
Damage to alveolar cells causes decreased production of surfactant, the substance that functions to help keep alveoli open. This, in addition to accumulation of fluid in the alveoli, contribute to atelectasis.
The inflammatory process involved in ARDS will eventually cause destruction of the pulmonary vasculature and decreased lung compliance. As this occurs, pulmonary vascular resistance will increase, and pulmonary hypertension may result. Pulmonary hypertension is considered a late sign of decreased lung compliance.
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