An acute lung condition evidenced by bilateral pulmonary infiltrates and refractory hypoxemia. The definition of refractory hypoxemia is hypoxemia that is unresponsive to treatment and a PaO2 level that remains low despite increasing FiO2. This is measured with the PaO2/FiO2 ratio of <300 (mild), <200 (moderate), or <100 (severe).
The diffuse damage and fluid filling the alveoli can be caused by anything that initiates an inflammatory or immune response or causes damage to the capillaries around the alveoli. Some examples are sepsis/bacteremia, pulmonary contusions, fat embolus, burns, massive transfusion or fluid resuscitation, or near-drowning.
To optimize oxygenation and ventilation while preventing complications like oxygen toxicity and ventilator acquired pneumonia. We need to treat the underlying cause so that the body’s immune and inflammatory responses can decrease and stop causing reactions within the lungs.
Evaluate P/F ratio by dividing PaO2 by FiO2:
PaO2 92, FiO2 60%
92 / 0.6 = 153.3
You can’t determine if the hypoxemia is refractory (nonresponsive to treatment) without verifying the P/F ratio.
The normal PaO2 is 60-100 mmHg on Room Air (21% FiO2). Having a PaO2 in normal range may NOT be adequate if their FiO2 is actually high.
Enables quicker interventions and may change them (for example, wheezing noted on auscultation would potentially indicate steroids and a breathing treatment, while crackles could require suctioning, repositioning, and potential fluid restriction). The sooner we can intervene for whatever the underlying cause is, the less likely the patient is to develop ARDS.
Supplemental oxygen will ideally increase their oxygen levels. The earlier we can intervene, the better for the patient. If you notice you are requiring more oxygen and not seeing results, notify the provider.
Patients who begin to show signs of ARDS should be in an Intensive Care Unit – if you are not in one of those units, notify the provider or call a Rapid Response to begin the transfer process as soon as possible.
Sitting up in bed to enable appropriate lung expansion allows for adequate inspiration and expiration, which facilitates better gas exchange (if clinically appropriate to be sitting up). Deep breathing and coughing might be able to get secretions out of the lungs and prevent damage to alveoli and improve gas exchange.
For the love of the airway, tell your Respiratory Therapist if your patient is struggling to maintain their airway.
Helpful to be prepared, as this can progress quickly. Know where the necessary meds and equipment are and how to get ahold of assistive personnel.
Once ventilated, these patients are at risk for VAP. This is especially dangerous once ARDS has developed as it furthers the inflammatory and immune response in the lungs, which can make the damage worse.
Most facilities have a “VAP Bundle” of interventions that should be implemented for all patients to prevent VAP, including oral care and GI prophylaxis (prevent reflux).
The underlying cause must be treated and routinely reevaluated for the patient to progress.
Because of the damage and decreased compliance in the lungs, the pressure in the lungs builds up. This can cause pressure on the major vessels leading to decreased cardiac output. Hypoxia could also cause ischemia to the heart muscle and ultimately lead to cardiogenic shock.
Many providers use lung-protective vent settings as last-resort strategies even though the evidence shows that early intervention makes the biggest difference.
Part of the patho of ARDS is excessive fluid buildup in the alveoli – we need to ensure the patient gets appropriate coughing or suctioning as needed to clear these secretions so that gas exchange can occur appropriately.
For more information, visit www.nrsng.com/cornell
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