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Guarding your patient against ARDS



A response to lung injury, this syndrome poses a deadly threat to your patient. Learn why and what you can do to help.

Learn to guard against and reverse alveolar collapse and other consequences of acute respiratory distress syndrome.

Medical/Surgical Clinical Nurse, Specialist, VA Pittsburgh Healthcare, System, Pittsburgh, Pa.

WHEN YOU CARE FOR a patient with acute respiratory distress syndrome (ARDS), you're caring for someone who's critically ill. His complex problems developed in response to acute lung injury caused by such life-threatening conditions as sepsis, trauma, or an adverse drug reaction.

First described in 1967, ARDS affects 8 in 100,000 people, and up to 80% of those affected die. In this article, I'll describe how ARDS develops and review the treatment options that give your patient the best chance of survival.

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Where trouble starts

The process that launches ARDS begins with either direct or indirect lung injury (see What Causes ARDS). The injury triggers an immune response that, if severe, can lead to systemic inflammatory response syndrome (SIRS). Mediators activated during SIRS injure tissues throughout the body, causing the patient to develop multiple organ dysfunction syndrome. Because the lungs are easily injured, respiratory trouble is often the first manifestation.

The pulmonary cells that are subject to damage consist of approximately 700 million alveolar/capillary (A/C) units. The function of an A/C unit is to exchange oxygen and carbon dioxide (CO2) between an alveolus and its dense capillary network. (For a closer look, see First Lung Injury, Then ARDS.)

The gas exchange in A/C units is gauged by the ventilation/perfusion (/) ratio, which measures ventilation in the alveolus versus perfusion in the capillaries. Normally, the alveoli ventilate 4 liters/minute and the capillaries perfuse 5 liters/minute.

Variations in / are normal in different areas of the lungs. For example, when the patient is in an upright position, alveolar ventilation is greater than perfusion in the apexes, but at the bases perfusion is greater than ventilation because gravity enhances blood flow there. A normal / of 0.8 reflects overall ventilation and perfusion.

When the ratio of ventilation to perfusion is mismatched, the patient develops hypoxemia, which begins the process of acute respiratory failure, a precursor of ARDS. In ARDS, ventilation is the problem: The pulmonary capillaries are adequately perfused, but the blood isn't oxygenated because collapsed or fluid-filled alveoli can't exchange oxygen and CO2. The blood returns unoxygenated to the left side of the heart and hypoxemia worsens.

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Assess early and often

After your patient sustains a lung injury or major systemic insult, his alveoli may undergo pathologic changes for days before he develops signs and symptoms of ARDS. (To learn how problems progress, see Is the Stage Set for ARDS?) Severe refractory hypoxemia is the key manifestation, so closely monitor for early signs of respiratory distress to pinpoint the need for early treatment and minimize his risk of permanent lung damage and death. Here's how:

  • Frequently monitor him for signs of respiratory distress, including increased respiratory rate, diminished breath sounds, use of accessory breathing muscles, and tachycardia.
  • Perform a neurologic assessment at the beginning of each shift and any time your patient's mental status changes. The brain needs 20% of the heart's cardiac output for adequate oxygenation, so distractibility, restlessness, anxiety, or confusion may signal hypoxia.
  • Follow trends in vital signs for early signs of decompensation. Explore the cause of any increases in heart rate, respiratory rate, and blood pressure.
  • Monitor continuous pulse oximetry, keeping in mind that readings may be inaccurate when blood is shunted away from the body surface as shock ensues. If your patient's pulse oximetry readings are inconsistent, assess him for cool skin as a sign of shock and obtain arterial blood gases (ABGs) for accurate oxygenation readings.
  • Frequently assess all his body systems for subtle changes, such as decreased bowel sounds and urine output.
  • Monitor ABGs. In early respiratory distress, the results show respiratory alkalosis; later readings show a mixed metabolic and respiratory acidosis.
  • Obtain serial chest X-rays as ordered. Abnormal findings include bilateral consolidation that often progresses to a “whiteout” image of the lungs.
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Finding the key to therapy

Years ago, scientists thought that ARDS was due strictly to atelectasis—collapsed alveoli. Treatment consisted of mechanical ventilation to keep the alveoli open until they healed. But when scientists gained a better understanding of the complex nature of the pulmonary inflammatory response, the treatment regimen changed.

Although we still lack a gold-standard treatment regimen, therapy for ARDS now includes ventilator support, drug therapy, nutritional support, and even positioning changes to promote ventilation and perfusion.

  • Ventilator support improves oxygenation and helps prevent further lung damage. The current trend in treating someone with ARDS is to deliver tidal volumes of less than 5 ml/kg or only as high as necessary to maintain peak airway pressures at about 25 cm H2O. These lower volumes prevent the alveoli from overdistending and minimize damaging shearing forces to them. (See Why High Ventilator Settings Are Out to learn how higher volumes can make matters worse.)
  • The downside of receiving lower tidal volumes is that the patient tends to retain CO2. Nevertheless, permissive hypercapnia (CO2 of 50 to 70 mEq/liter) is considered an acceptable risk in ARDS if you can control his CO2 level and prevent associated adverse responses. To keep CO2 levels within an acceptable range, administer intravenous (I.V.) sodium bicarbonate and increase the ventilator respiratory rate.
  • Ventilator support typically includes positive end-expiratory pressure (PEEP) to maintain some alveolar inflation to the end of exhalation, which in turn increases the alveolar surface area available for gas exchange. The amount of PEEP, typically 10 to 15 cm H2O, is balanced with the lowest possible oxygen concentration to maintain the optimal blood oxygen level. Keep in mind that adverse responses to PEEP can be serious, including barotrauma and decreased cardiac output. The higher the PEEP level, the more likely these risks.
  • Another support strategy for someone with ARDS is inverseratio ventilation. Normally, inhalation time is half that of expiration, so the inhalation/exhalation ratio is 1:2. In healthy lungs, longer exhalation prevents air from being trapped in the alveolus. But in ARDS, exhalation time is intentionally decreased to trap air. Setting the ventilator to deliver an equal (1:1) or inverse (2:1) ratio keeps the alveoli continually inflated and increases the surface area available for gas exchange. As a result, oxygenation improves.
  • A drawback of inverse-ratio ventilation is that the unnatural breathing rhythm generally causes discomfort, so the patient may become restless and agitated. For this reason, he'll probably receive sedation or neuromuscular blockade and sedation to decrease oxygen consumption caused by agitation and to keep him comfortable.
  • Drug therapy for ARDS can help decrease the cellular inflammatory response, replace surfactant, and increase pulmonary perfusion. Research is currently under way to determine when in the process various drugs are most effective and whether prophylaxis can help prevent ARDS in high-risk patients.
  • The antifungal agent ketoconazole can be beneficial at inhibiting inflammation and the pulmonary hypoxic vasoconstrictive response. It's most appropriate for patients who are at high risk for ARDS. In research studies, ketoconazole was given in a liquid form through an enteral tube.
  • Using steroids to reduce inflammation in ARDS is controversial. Doses as high as 15 mg/kg/day used early in the process have been ineffective, but lower doses (2 to 8 mg/kg/day) administered in stage IV, when fibroproliferation occurs, may help. The downside of using steroids is that they can mask infection, which is a concern in critically ill patients who have multiple invasive devices.
  • Inhaled nitric oxide (NO) is used as a rescue therapy for refractory hypoxemia in ARDS. It works by limiting the lungs' vasoconstrictive response to hypoxia. Delivered through the ventilator in doses of 5 to 80 parts per million, NO relaxes the vascular endothelium and dilates the pulmonary vessels. Although pulmonary perfusion increases and oxygenation improves, the benefits generally don't last more than 24 hours. Inhaled NO doesn't affect systemic circulation, but it oxidizes iron and can cause methemoglobinemia, which inhibits the blood's oxygen-carrying capacity.
  • Surfactant replacement therapy has been used successfully in premature neonates suffering from respiratory distress syndrome. Delivered via ventilator, aerosol phospholipid provides the surfactant layer that the alveoli lack. However, the effectiveness of this therapy in adults with ARDS is unclear. Effective doses and delivery methods for adults are currently under study, with tracheal and bronchoalveolar lavage delivery among the options.
  • Prone positioning, although not universally practiced because it could trigger complications, will increase oxygenation and improve secretion clearance. Prone positioning increases blood flow via gravity to the anterior lung areas. Your patient's / ratio may improve and his blood oxygen levels increase for 4 to 6 hours after he's placed prone. This position also improves drainage of secretions and allows maximal expansion of his diaphragm.
  • However, turning the patient is labor intensive and poses risks. He could be accidentally extubated or develop hemodynamic instability, facial edema or pressure ulcers, corneal ulceration, increased intracranial pressure, or cardiac arrhythmias. Seven staff members should be on hand to place him prone: three on each side of the bed to turn him and one at the head to protect his I.V. lines and endotracheal tube. Some facilities use pronator devices that strap onto the patient to make turning easier.
  • While your patient is prone, monitor him for changes in blood pressure, heart rate, and respiratory rate, which could indicate intolerance to the position. Reposition his head hourly to prevent facial skin necrosis, provide oral care, and suction his airway as needed. Continue enteral tube feedings as ordered and return him to the supine position within 6 hours.
  • Nutritional support for the ARDS patient can be provided by either enteral or total parenteral means. Enteral nutrition is preferred to reduce the risk of infection. Nutritional support should be started early to promote regeneration of pulmonary cells and pave the way for successful weaning from the ventilator. If your patient is retaining CO2, an enteral formula lower in carbohydrate than a standard formula will decrease CO2 formation during metabolism.

Research is currently under way on gamma-linolenic acid and eicosapentaenoic acid. These nutritional products contain antioxidants that promote cell regeneration and may decrease production of inflammatory mediators.

Fluid replacement for patients with ARDS is directed at maintaining adequate circulating volume without overhydrating the patient. Generally, a pulmonary artery catheter is needed to carefully monitor cardiac and pulmonary artery pressures and help determine the proper I.V. fluid infusion rates.

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Improved chance for recovery

No one can predict which patients will recover from ARDS or which survivors will develop chronic lung problems. What we do know is that the patient's best hope lies with detecting trouble early and quickly restoring the balance in lung function. By frequently assessing him and detecting hypoxemia, you set the stage for early treatment and improve his chance for survival and recovery.

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What causes ARDS

Direct lung injury

  • Pneumonia*
  • Aspiration of gastric contents*
  • Pulmonary contusion
  • Near drowning
  • Inhalation injury

Indirect lung injury

  • Sepsis*
  • Severe trauma with shock state that requires multiple blood transfusions*
  • Drug overdose
  • Acute pancreatitis
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Why high ventilator settings are out

Historically, ventilator therapy for ARDS consisted of high tidal volumes (10 to 12 ml/kg) with high positive end-expiratory pressure (PEEP, 20 to 25 cm H2O) to improve oxygen delivery. But high airway pressures and decreased cardiac output related to decreased venous return commonly caused patients to develop pneumothorax (barotrauma).

Research has shown that high tidal volumes and PEEP levels significantly overdistend the alveoli (volutrauma), which triggers release of inflammatory cytokines and decreases surfactant production. In ARDS, these effects exacerbate the underlying disease process.

The current ventilation strategy is to deliver moderate amounts of tidal volume and PEEP to keep the alveoli open and diminish the negative effects of high-pressure settings.

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First lung injury, then ARDS



The alveolar/capillary (A/C) unit, the basic pulmonary structure of gas exchange, is where oxygen enters the blood and carbon dioxide leaves it. Each A/C unit has two alveolar layers (epithelium and basement membrane) and two capillary layers (basement membrane and endothelium) with an interstitial space between them.

Surfactant, a phospholipid, lines the alveolar epithelium and decreases surface tension during inspiration and expiration. It's necessary to maintain an intact surface area to keep the alveolus “open” for gas exchange. If the amount of surfactant decreases or it functions ineffectively, the alveolus collapses, oxygenation is impaired, and the work of breathing increases.

The pathologic changes of ARDS occur when a lung injury triggers cellular damage to the alveolar epithelium and capillary endothelium. Inflammatory mediators start destroying the cells, the A/C membrane becomes permeable, and fluid moves into the alveoli, causing noncardiogenic pulmonary edema. Cells in the epithelium are damaged and surfactant production greatly decreases.

The surfactant that remains becomes dysfunctional and loses its ability to maintain alveolar expansion. Because of inflammation and decreased surfactant, the alveoli continue to flood with protein-rich fluid and eventually become atelectatic, causing hypoxemia and hypoxia.

Table. I

Table. I

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ARDS Support Center

Last accessed on February 4, 2002.

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The ARDS Network: “Ketoconazole for Early Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome: A Randomized Controlled Trial,” JAMA. 283(15):1995–2002, April 19, 2000.
Bulger, E., et al.: “Current Clinical Options for the Treatment and Management of Acute Respiratory Distress Syndrome,” The Journal of Trauma. 48(3):562–572, March 2000.
Hart, M.: “Nitric Oxide in Adult Lung Disease,” Chest. 115(5):1407–1417, May 1999.
Lynn-McHale, D. (editor): “Manual Pronation Therapy” in AACN Procedure Manual for Critical Care, 4th edition. Philadelphia, Pa.: W.B. Saunders Co., 2001.
    Thies, R., and Hotter, A.: “Preventing Complications of ARDS Therapy,” American Journal of Nursing. Suppl. 99(5), May 1999.
      Van Soeren, M., et al.: “Pathophysiology and Implications for Treatment of Acute Respiratory Syndrome,” AACN Clinical Issues. 11(2):179–197, May 2000.
      Vollman, K.: “Prone Positioning for the ARDS Patient,” Dimensions in Critical Care Nursing. 16(4):184–193, July-August 1997.
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      PURPOSE To improve nursing practice and the quality of care by providing a learning opportunity that enhances a participant's understanding of acute respiratory distress syndrome (ARDS). OBJECTIVES After reading the preceding article and taking this test, you should be able to:

      1. Indicate understanding of alveolar physiology and the pathophysiology of ARDS. 2. Identify the clinical manifestations and diagnostic monitoring tools related to ARDS. 3. Identify the treatment options for ARDS.

      1. What's the function of an A/C unit?

      1. to exchange oxygen and CO2

      2. to promote ventilation in the alveolus

      3. to promote perfusion in the capillaries

      4. to move fluid into the alveoli

      2. What can occur when the ratio of ventilation to perfusion is mismatched?

      1. ARDS

      2. increased use of accessory breathing muscles

      3. hypoxemia

      4. tachycardia

      3. What's the key manifestation of ARDS?

      1. increased respiratory rate

      3. refractory hypoxemia

      2. diminished breath sounds

      4. restlessness

      4. Which statement is correct regarding the neurologic assessment of a patient at risk for ARDS?

      1. It's necessary because the brain needs 40% of cardiac output for adequate oxygenation.

      2. Do it only on patients with mental status changes.

      3. It'll reveal neurologic changes in the late stages of ARDS.

      4. Do it at the beginning of each shift and any time the patient's mental status changes.

      5. Which of the following is a sign of decompensation in someone at risk for ARDS?

      1. decreased heart rate

      2. decreased blood pressure

      3. warm skin

      4. increased respiratory rate

      6. In early respiratory distress, ABGs can detect

      1. metabolic alkalosis.

      3. metabolic acidosis.

      2. respiratory alkalosis.

      4. respiratory acidosis.

      7. What's the goal of ventilator support in treating ARDS?

      1. to retain CO2

      2. to prevent the alveoli from overdistending

      3. to minimize shearing forces to the alveoli

      4. to improve oxygenation

      8. What tidal volumes are currently used to treat ARDS?

      1. 10 to 15 cm H2O

      2. less than 5 ml/kg

      3. 10 to 12 ml/kg

      4. 20 to 25 cm H2O

      9. Which of the following is an adverse response to PEEP?

      1. methemoglobinemia

      2. tachycardia

      3. decreased cardiac output

      4. increased cardiac output

      10. How does inverse-ratio ventilation improve oxygenation?

      1. It delivers a longer exhalation time.

      2. It prevents air trapping.

      3. It prevents overinflation of the alveoli.

      4. It increases the alveolar surface area available for gas exchange.

      11. What treatment modality limits the lungs' vasoconstrictive response to hypoxia?

      1. inhaled NO

      2. administration of steroids

      3. surfactant replacement

      4. prone positioning

      12. Which of the following allows maximum expansion of the patient's diaphragm?

      1. PEEP ventilation

      2. prone positioning

      3. surfactant replacement

      4. inhaled NO

      13. Which type of nutritional support decreases CO2 formation during metabolism?

      1. parenteral support

      2. enteral support with increased carbohydrates

      3. enteral support with standard formula

      4. enteral support with decreased carbohydrates

      14. Which of the following is considered a direct cause of ARDS?

      1. near drowning

      2. sepsis

      3. drug overdose

      4. acute pancreatitis

      15. How soon after the initial injury can ARDS-associated physiologic changes begin?

      1. within 24 hours

      2. within 48 hours

      3. within 2 to 10 days

      4. after 10 days



      Ware, L., and Matthay, M.: “The Acute Respiratory Distress Syndrome,” The New England Journal of Medicine. 342(18):1334–1349, May 4, 2000.
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