Nurses Notes on Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS) also known as Shock lung, Wet lung, Vietnam lung, and Adult Hyaline Membrane Disease

ARDS is a form of acute respiratory failure that occurs as a complication of some other condition, is caused by a diffuse lung injury and leads to extravacular lung fluid.

- it is characterized by noncardiac pulmonary edema and progressive refractory hypoxemia.

- characterized by sudden and progressive edema, increasing bilateral infiltrates and reduced lung compliance

Signs and Symptoms

Initial manifestations of ARDS typically develop 24 to 48 hours after the initial insult.

a. Dyspnea, Tachypnea, and anxiety are early manifestations

b. Progressive respiratory distress develops, with increasing respiratory rate, intercostals retractions, and use of accessory muscles of respiration.

c. Cyanosis develops that may not improve with oxygen administration

d. Breath sounds are initially clear, but crackles (rales) and rhonchi develop later.

e. As respiratory failure progresses, mental status changes such as agitation, confusion, and lethargy occur.

Risk Factors

a. Chronic Alcoholism

b. Sepsis. The most common cause of ARDS is sepsis, a serious and widespread infection of the bloodstream.

c. Inhalation of harmful substances. Breathing high concentrations of smoke or chemical fumes can result in ARDS, as can inhaling (aspirating) vomit.

d. Severe pneumonia. Severe cases of pneumonia usually affect all five lobes of the lungs.

e. Head or chest injury. Accidents, such as falls or car crashes, can directly damage the lungs or the portion of the brain that controls breathing.

Nursing Diagnoses

a. Decreased Cardiac Output

            With positive pressure, increased intrathoracic pressure decreases cardiac output. Manifestations of decreased cardiac output include hypotension and compensatory tachycardia as the heart attempts to maintain cardiac output despite decreased stroke volume. In the client who is already hypoxic because of ARDS, this drop in cardiac output can increase tissue damage. Urine output falls, and dysrhytmias may develop.

b. Ineffective Airway Clearance

c. Impaired Gas Exchange

Nursing Interventions

1. Identify the treat cause of the acute respiratory distress syndrome

2. Administer oxygen as prescribed. Maintain normal/ stable arterial blood gas.

3. Position client in high Fowler’s position (independent nursing intervention)

4. Restrict fluid intake as prescribed

5. Provide respiratory treatments as prescribed

6. Administer diuretics, anticoagulants, or corticosteroids as prescribed

7. Prepare the client for intubation and mechanical ventilation using PEEP

Diagnostic Tests

Refractory Hypoxemia (hypoxemia that does not improve with oxygen administration) is a hallmark of ARDS.

·         Arterial Blood Gases initially show hypoxemia with a PO2 of less than 60 mmHg and respiratory alkalosis due to tachypnea

·         Chest X- ray changes may not be evident for as long as 24 hours after the onset of ARDS. Diffuse infiltrates are seen initially, progressing to a “white out” pattern

·         Pulmonary function testing shows decreased lung compliance with reduced vital capacity,  minute volume, and functional vital capacity

·         Pulmonary artery pressure monitoring shows normal pressures in ARDS, helping distinguish ARDS from cardiogenic pulmonary edema.

Note: Endotracheal Suctioning

1. When suctioning, the nurse should use a sterile catheter each time the client is suction

2. Hyperoxygenate patient before and after suctioning

3. When suctioning, the nurse must limit suctioning to a maximum of 10 seconds.

4. During suctioning, the nurse must monitor for the vital signs of the patient.  A decrease in heart rate and blood pressure may indicate vagal stimulation. Stimulation of the vagus nerve may stimulate the function of the parasympathetic nervous system causing vasodilation, decrease in heart rate, and decrease in blood pressure. The nurse then should stop the procedure and hyperoxygenate the patient.

Medications

Inhaled Nitric Acid reduces intrapulmonary shunting and improves oxygenation by dilating blood vessels in better- ventilated areas of the lungs.

Surfactant Therapy may be prescribed. Surfactant is a complex mixture of phospholipids, neutral lipids, and proteins that forms a thin layer of water on the inner surface of the alveolus, reducing the surface tension within the alveoli. Surface tension tends to pull the walls of the alveoli together, increasing the likelihood of collapse during exhalation. Surfactant, by reducing surface tension, helps maintain open alveoli, decreasing the work of breathing, improving compliance and gas exchange, and preventing atelectasis.

NSAIDs and corticosteroids may be used late in the course of ARDS  to improve oxygenation and lung mechanics when fibrotic changes occur.

NOTE: Steroids must be taken with food or immediately after a meal to prevent stomach upset.