ARDS: Adult Respiratory Distress Syndrome

Author: Kristi Hudson RN MSN CCRN 

Definition:

Adult (acute) Respiratory Distress Syndrome (ARDS) is the rapid onset of progressive malfunction of the lungs, usually associated with the malfunction of other organs due to the inability to take up oxygen. The condition is associated with extensive lung inflammation and small blood vessel injury in all affected organs. 

Statistics:

ARDS has a fatality rate of approximately 40 percent despite supportive therapy, including mechanical ventilators and supplement oxygen. The incidence of ARDS has been difficult to determine partly due to the variety of causes but it is a common problem in hospital Intensive Care Units. Various published estimates have ranged from 1.5 to 7.5 cases per 100,000 populations. Earlier estimates suggested that approximately 150,000 Americans are affected each year.

Pathophysiology of ARDS:

Inflammatory damage to alveolar epithelium decreases surfactant, which causes atelectasis and hyaline membrane formation. Inflammatory damage to capillary endothelium platelets attracts neutrophils, which begin to secrete destructive molecules that increase capillary permeability, widespread pulmonary edema, cellular necrosis, and hemorrhage. 

In ARDS, the injured lung is divided into three phases: exudative, proliferative, and fibrotic, but the course of each phase and the overall disease progression is variable. In the exudative phase, damage to the alveolar epithelium and vascular endothelium produces leakage of water, protein and red blood cells into the interstitial space and alveolar lumen. These changes are induced by a complex interplay of pro-inflammatory and anti-inflammatory mediators. Type I alveolar cells are irreversibly damaged and their space is replaced by the deposition of proteins, fibrin, and cellular debris, producing hyaline membranes, while injury to the surfactant-producing type II cells contributes to alveolar collapse. In the proliferative phase, type II cells proliferate with some epithelial cell regeneration, fibroblastic reaction, and remodeling. In some patients, this progresses to an irreversible tissue fibrosis that is fatal. 

Cause of ARDS:

ARDS is commonly precipitated by trauma, sepsis (systemic infection), diffuse pneumonia and shock. It may be associated with extensive surgery, and certain blood abnormalities. Less common causes include drowning and inhalation of toxic gases. In half the cases, onset occurs within 24 hours of the original illness or injury; in nearly all cases it occurs within three days. The following are known to be specific causes of ARDS:

• Breathing in (aspiration) of the stomach contents when regurgitated, or salt water or fresh water from nearly drowning.

• Inhaling smoke, as in a fire; toxic materials in the air, such as ammonia or hydrocarbons; or too much oxygen, which itself can injure the lungs.

• Infection by a virus or bacterium, or sepsis.

• Massive trauma, with severe injury to any part of the body.

• Shock with persistently low blood pressure may not in itself cause ARDS, but it can be an important factor.

• Disseminated intravascular coagulation (DIC), in which blood clots form in vessels throughout the body, including the lungs.

• Fat Emboli that lodges in small blood vessels, injuring the cells lining the vessel walls.

• Drug Overdose

• Pancreatitis causing blood proteins and enzymes, to pass to the lungs and injure lung cells.

• Severe burn injury.

• Injury of the brain, or bleeding into the brain, from any cause may be a factor in ARDS for reasons that are not clear. Convulsions also may cause some cases. 

Symptoms of ARDS:

• Dyspnea

• Profound hypoxemia

• Decreased lung compliance

• Diffuse bilateral infiltrates on chest radiography. 

Specific Criteria for Diagnosis of ARDS:

• Acute in onset of symptoms

• Oxygenation: A partial pressure of arterial oxygen to fractional inspired oxygen concentration ratio < 200 mm per Hg (regardless of PEEP)

• Bilateral pulmonary infiltrates on chest X-ray

• Pulmonary artery wedge pressure < 18 mm per Hg or no clinical evidence of Left Atrial Hypertension 

There are Three Main Goals in Treating Patients with ARDS:

1. Goal Number One - To treat whatever injury or disease has caused ARDS. Examples are: to treat septic infection with the proper antibiotics, and to reduce the level of oxygen therapy if ARDS has resulted from a toxic level of oxygen.

2. Goal Number Two - To control the process in the lungs that allows fluid to leak out of the blood vessels. At present there is no certain way to achieve this. Certain steroid hormones have been tried because they can combat inflammation, but the actual results have been disappointing.

3. Goal Number Three - To make sure the patient gets enough oxygen until the lung injury has had time to heal. There are several mechanical ventilation modes that can be used depending on the severity of this syndrome.

Treatment Options:

Pharmacological Therapy - As of yet, no medication has been shown to affect the pulmonary inflammatory process of ARDS directly. Late cases with a persistent fibro-proliferative phase may respond to steroids. Administration of antibiotics following appropriate cultures in cases of pulmonary or extra-pulmonary infection leading to ARDS may also help. The mainstays of therapy are cardiopulmonary support and treatment/eradication of the underlying or predisposing conditions. Cardiovascular instability despite fluid administration is managed with Dopamine and/or Dobutamine.

Mechanical Ventilation – The mainstay of supportive care of ARDS is mechanical ventilation.  By stabilizing respirations, mechanical ventilation allows time for administration of treatment for the underlying cause of ARDS and for the evolution of natural healing processes. Because one of the clinical hallmarks of ARDS is decreased respiratory system compliance caused by atelectasis, lung-protective ventilation with small tidal volumes (less then 10 to 15 ml/kg) can be used to decrease:

• Over Distention of Less Affected Lung Regions

• Acute Inflammation

• Alveolar Hemorrhage

• Intra-pulmonary Shunting

• Diffuse Radiographic Infiltrates 

Note: Pressure Control Ventilation (PCV) – If small tidal volumes are ineffective in assuring adequate oxygenation during the healing process. 

Considerations for Patients on Pressure Control Ventilation:

Arterial Blood Gases – Measurement of arterial blood gases should always be considered when indicated while optimizing mechanical ventilation. The desired gas exchange results should be monitored to assure optimal lung opening. The use of peripheral monitoring devices (SpO2) will enhance one's ability to optimize ventilator settings to achieve appropriate gas exchange during the initial setup of Pressure Control Ventilation. 

Capnography – Measuring ETCO2 can be used to optimize the ventilation to perfusion ratio. As dead space is decreased, CO2 will also decrease demonstrating an improvement in lung function. 

Hemodynamic Monitoring - Hemodynamic monitoring is a very important aspect of Pressure Control Ventilation. Optimizing right heart filling pressures can minimize the sometimes-negative effects of positive pressure. Mean pulmonary artery pressure should always slightly exceed the mean airway pressure to ensure adequate pulmonary blood flow. Appropriate urine output is essential to minimize lung water and optimize static lung compliance. Well functioning kidneys (or adequate dialysis will lead to dry lungs). 

Weaning Settings - Once optimal ventilator settings have been found it is important to choose a weaning strategy to prevent lung closure at all costs (when lung closure occurs very high pressures are needed to re-expand the lung). Peak inspiratory pressures should be decreased very cautiously to prevent the peripheral lung units from closing. Peak pressures should be weaned one cm H2O at each interval, and lung mechanics should be assessed for stability. The ventilator rate should be kept at basal levels until PIP has been decreased to 35 cm H2O. PEEP levels should always be kept at 10 cm H2O. The Fi02 should be kept at levels that prevent tissue hypoxia and arterial desaturation. 

Note: Peak inspiratory pressures from 50 to 55 cm are usually required to open lungs with ARDS (Keep a Chest Tube Handy). 

Prognosis:

If the patient's lung injury does not soon begin to heal, the lack of sufficient oxygen can injure other organs, such as the kidneys. There always is a risk that bacterial pneumonia will develop at some point. Without prompt treatment, as many as 90% of patients with ARDS can be expected to die. With modern treatment, however, about half of all patients will survive. Those who do live usually recover completely, with little or no long-term breathing difficulty. Lung scarring is a risk after a long period on a ventilator, but it may improve in the months after the patient is taken off ventilation. Whether a particular patient will recover depends to a great extent on whether the primary disease that caused ARDS to develop in the first place can be effectively treated. 

References 

Allen, J. M.D. (2006). Weaning from mechanical ventilation. Retrieved on December 26, 2006 at:http://home.columbus.rr.com/allen/ventilator_weaning.htm  

Broccard, A., F. (May 2003). Prone position in ARDS: are we looking at a half-empty or half-full glass? Retrieved on December 24, 2003 at:http://www.findarticles.com/p/articles/mi_m0984/is_5_123/ai_102519817  

Byrd, R., P. (2006). Ventilation, mechanical. Retrieved on December 26, 2006 at:http://www.emedicine.com/med/topic3370.htm

Critical Care Medicine Tutorials. (2003). Key points of acute lung injury. Retrieved on December 25, 2003 at:www.ccmtutorials.com/rs/ali/09_alikp.htm 

Goodrich, C., (2002). Principles of oxygen delivery and consumption. Edwards Lifesciences. Irvine California. 

Marino, W., D., & O’Connell-Szaniszlo, M. (2005). Short term analysis of pulmonary mechanics during mechanical ventilation for ARDS. Retrieved on December 26, 2006 at:http://www.findarticles.com/p/articles/mi_m0984/is_4_128/ai_n15789839  

Raksha, J., M.D., & Dalnorgare, A., M.D. (2006). Pharmacological therapy for acute respiratory distress syndrome.  Mayo Clin Proc. February 2006; 81(2): 205-212. Retrieved on December 26, 2006 from CINAHL Plus with Full Text Database.