Abbreviation: ARDS.
Respiratory insufficiency marked by progressive hypoxemia due to severe inflammatory damage causing abnormal permeability of the alveolocapillary membrane. The alveoli fill with fluid, which interferes with gas exchange.
See: disseminated intravascular coagulation; sepsis; systemic inflammatory response syndromeNursing Diagnoses Appendix

ETIOLOGY
Acute respiratory distress syndrome may result from direct trauma to the lungs (e.g., near drowning, aspiration of gastric acids, severe lung infection) or systemic disorders, (e.g., shock, septicemia, disseminated intravascular coagulation [DIC], cardiopulmonary bypass, or reaction to multiple blood transfusions). Widespread damage to the alveolocapillary membranes is initiated through the aggregation and activity of neutrophils and macrophages and the activation of complement. Cytokines, oxygen-free radicals, and other inflammatory mediators damage the walls of capillaries and alveoli, producing diffuse inflammatory interstitial and alveolar edema, fibrin exudates, and hyaline membranes that block oxygen delivery to the blood.

DIAGNOSIS
Diagnosis is based on a history of a recent event associated with the onset of ARDS, the presence of noncardiogenic pulmonary edema on the chest radiograph, and persistent hypoxemia and a PaO₂/FIO₂ ratio of < 200.

SYMPTOMS
Dyspnea and tachypnea are followed by a progressive hypoxemia that, despite oxygen therapy, is the hallmark of ARDS. Diffuse, fluffy infiltrates can be seen on chest radiographs, as inflammation increases alveolar permeability, causing visible alveolar flooding and collapse.

TREATMENT
Endotracheal intubation, mechanical ventilation with positive end-expiratory pressure (PEEP), supplemental oxygen, and tidal volumes of 4 to 8 ml/kg optimize respiratory outcomes. PEEP increases intrathoracic pressure, keeping alveoli open during exhalation. This reduces the pressure required to open alveoli during inhalation, improves gas exchange, and reduces oxygen need. The patient should be monitored and treated for acidosis, cardiac arrhythmias, DIC, oxygen toxicity, renal failure, and sepsis.

PROGNOSIS
Mortality is high, approx. 50% to 60%, depending on the amount of lung tissue affected and the ability to maintain adequate oxygen flow to vital organs. After resolution of the inflammation, the damaged lung tissue becomes fibrotic and can cause chronic restrictive lung disease. Prolonged use of more than 50% oxygen increases the risk of residual lung damage.

PATIENT CARE
To avert ARDS, respiratory status must be monitored in at-risk patients. Recognizing and treating early signs and symptoms can be crucial to a patient's survival. Ventilatory rate, depth, and rhythm must be monitored, and subtle changes noted. The onset of ARDS is marked by the onset of a rapid, shallow breathing pattern, and pulse oximetry must be monitored continuously for subtle changes. If shock ensues and blood is shunted away from body surfaces, resulting in cool skin, O₂ readings may become inaccurate, necessitating use of arterial blood gas monitoring for respiratory alkalosis (early) and mixed metabolic and respiratory acidosis (later). Serial chest x-rays should be obtained to assess for bilateral consolidation progressing to lung “whiteout.” The patient must also be observed for chest wall retractions on inspiration, use of accessory breathing muscles, and level of dyspnea. The patient's consciousness level, cardiac rate and rhythm, blood pressure, arterial blood gas (ABG) values, serum electrolyte levels, and chest radiograph results must be monitored. Fluid balance must be closely watched by 1) measuring intravenous (IV) fluid intake, urinary output, and central venous pressure; 2) weighing the patient daily; and 3) assessing for peripheral edema. A patent airway must be maintained, and oxygen therapy with continuous positive airway pressure or mechanical ventilation with positive end-expiratory pressure (PEEP) must be provided by the respiratory therapist as prescribed by the attending physician. Routine management of a mechanically ventilated patient includes 1) monitoring breath sounds, chest wall movement, vital signs and comfort, and ventilator settings and function; 2) suctioning the endotracheal tube and oropharynx; and 3) assessing changes in pulse oximetry and ABG values.

Cardiac output may be decreased because PEEP increases intrathoracic pressure and reduces venous return. For this reason, health care professionals must monitor blood pressure, urine output, mental status, peripheral pulses, and pulmonary capillary wedge pressure to determine the effects of positive-pressure ventilation on hemodynamics. Inotropic drugs must be administered as prescribed if cardiac output falls. Hemoglobin levels and oxygen saturation values must also be monitored closely because packed red blood cell transfusion may be required if hemoglobin is inadequate for oxygen delivery. The nurse and respiratory therapist must observe for signs and symptoms of barotrauma, e.g., subcutaneous emphysema, pneumothorax, and pneumomediastinum. If mechanical ventilation is used, sedation may help calm the patient and reduce the incidence of poor synchronization between the patient and the ventilator. Nutritional support should begin early to promote pulmonary cell regeneration and to provide proteins needed for successful weaning from a ventilator. Enteral nutrition is preferred over parenteral means because it reduces the risk of infection. A formula that is lower in carbohydrates helps decrease CO₂ formation during metabolism in ARDS patients retaining CO₂. Fluid replacement should maintain sufficient circulating volume without causing overhydration as determined by central venous pressure readings. Nursing measures must be used to prevent problems of immobility. Prone positioning may be prescribed to improve oxygenation while lessening the risk of barotrauma, but it complicates some elements of nursing care. Prone positioning, if prescribed (usually for 4 to 6 hours daily), is often labor-intensive and requires several staff members to position the patient and therefore is best accomplished on day shift when more staff are available in an emergency. To limit the patient's fear and isolation, the procedure should be explained to the patient, assuring him or her of its safety. Sedation or analgesia are prescribed 30 to 60 minutes before turning the patient on his or her abdomen. To reduce compression of the lungs by the heart and mediastinum, a specialty bed may be used, or a pronator device (a padded metal frame that is placed against the patient's chest and abdomen, with belt buckles that secure and protect the head, chest, and abdomen during the procedure) is strapped to the patient. To use this device, the side rails on the patient's bed are lowered, and the patient is pulled close to the edge of the bed farthest from the ventilator. The patient's face is turned away from the ventilator, his/her arm tucked under the body, and the leg farthest from the ventilator crossed over the other leg at the ankle to aid in turning the patient. The patient can then be turned by one staff member on each side of the bed and one (usually a respiratory therapist [RT]) at the head, who protects the endotracheal tube, IV lines, and other attachments. The prone patient's blood pressure and heart and respiratory rates must be closely monitored for evidence of position tolerance, and the RT may confirm correct endotracheal tube position by capnography. Vital signs should return to baseline within 5 min after prone positioning, repositioning the patient in the supine position if there is any drop in O₂ saturation, deterioration in ABG results, or uncontrollable patient anxiety. Once in the prone position, the patient's feet and elbows should be padded to prevent pressure injuries. The patient's head should be repositioned every hour to prevent necrosis of facial skin and to provide oral care and airway suctioning. Range of motion exercises should be performed at least every 2 hr. The patient should be repositioned to the supine position after 4 or 6 hr, as prescribed. Strict asepsis must be observed in dressing changes, suctioning, hand hygiene, and oral care. The patient must be routinely assessed for fever, changes in sputum color, and elevated WBC count. Response to therapy must be evaluated and adverse reactions noted. The family must be encouraged to talk to the patient even though he or she may not be able to respond verbally.

Respiratory therapists play a key role in the care of patients with ARDS. They initiate mechanical ventilation as prescribed by the attending physician and monitor arterial blood gases and pulse oximetry to ensure adequate oxygenation. They adjust the tidal volume, respiratory rate, and PEEP levels to optimize tissue oxygenation. They also help determine when the patient may be ready for weaning from mechanical ventilation by periodic assessment of the patient's cardiopulmonary status.

Subentries:
primary acute respiratory distress syndrome
secondary acute respiratory distress syndrome