Acute Respiratory Distress Syndrome

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Acute Respiratory Distress Syndrome

Chapter Objectives

After reading this chapter, you will be able to:

• List the anatomic alterations of the lungs associated with acute respiratory distress syndrome.

• Describe the causes of acute respiratory distress syndrome.

• List the cardiopulmonary clinical manifestations associated with acute respiratory distress syndrome.

• Describe the general management of acute respiratory distress syndrome.

• Describe the clinical strategies and rationales of the SOAPs presented in the case study.

• Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

Key Terms

Anatomic Alterations of the Lungs

The lungs of patients affected by acute respiratory distress syndrome (ARDS) undergo similar anatomic changes, regardless of the cause of the disease. In response to injury the pulmonary capillaries become engorged, and the permeability of the alveolar-capillary membrane increases. Interstitial and intraalveolar edema and hemorrhage ensue, as well as scattered areas of hemorrhagic alveolar consolidation. These processes result in a decrease in alveolar surfactant and in alveolar collapse, or atelectasis.

As the disease progresses, the intraalveolar walls become lined with a thick, rippled hyaline membrane identical to the hyaline membrane seen in newborns with infant respiratory distress syndrome (hyaline membrane disease). The membrane contains fibrin and cellular debris. In prolonged cases there is hyperplasia and swelling of the type II cells. Fibrin and exudate develop and lead to intraalveolar fibrosis.

In gross appearance the lungs of patients with ARDS are heavy and “red,” “beefy,” or “liver-like.” The anatomic alterations that develop in ARDS create a restrictive lung disorder (see Figure 27-1).

image
FIGURE 27-1 Cross-sectional view of alveoli in acute respiratory distress syndrome. AC, Alveolar consolidation; AT, atelectasis; HM, hyaline membrane; M, macrophage.

The major pathologic or structural changes associated with ARDS are as follows:

Historically, ARDS was first referred to as the “shock lung syndrome” when the disease was first identified in combat casualties during World War II. Since that time, the disease has appeared in the medical literature under many different names, all based on the conditions believed to be responsible for the disease. In 1967 the disease was first described as a specific entity, and the term acute respiratory distress syndrome was suggested. This term is predominantly used today. Box 27-1 provides some of the other names that have appeared in the medical journals to identify ARDS.

Box 27-1   Other Names Used in the Past to Identify Acute Respiratory Distress Syndrome (ARDS)

Etiology and Epidemiology

A multitude of causative factors may produce ARDS. Box 27-2 provides some of the better-known causes.

Box 27-2   Common Causes of Acute Respiratory Distress Syndrome

• Aspiration (e.g., of gastric contents, or water in near-drowning episodes)

• Central nervous system (CNS) disease (particularly when complicated by increased intracranial pressure)

• Cardiopulmonary bypass (especially when the bypass is prolonged)

• Disseminated intravascular coagulation (seen in patients with shock; it is a condition of paradoxic simultaneous clotting and bleeding that produces microthrombi in the lungs)

• Drug overdose (e.g., heroin, barbiturates, morphine, methadone)

• Fat or air emboli (the fat emboli act as a source of harmful vasoactive material, including fatty acids and serotonin)

• Infections (bacterial, viral, fungal, parasitic, mycoplasma)

• Inhalation of toxins and irritants (e.g., chlorine gas, nitrogen dioxide, smoke, ozone; oxygen also may be included in this category of irritants)

• Immunologic reaction (e.g., allergic alveolar reaction to inhaled material or Goodpasture’s syndrome)

• Massive blood transfusion (in stored blood the quantity of aggregated white blood cells [WBCs], red blood cells [RBCs], platelets, and fibrin increases; these blood components may in turn occlude or damage small blood vessels)

• Nonthoracic trauma

• Oxygen toxicity (e.g., when patients are treated with an excessive oxygen concentration—usually greater than 60%—for a prolonged period)

• Pulmonary ischemia (resulting from shock and hypoperfusion; may cause tissue necrosis, vascular damage, and capillary leakage)

• Radiation-induced lung injury

• Shock (e.g., hypovolemia)

• Systemic reactions to processes initiated outside the lungs (e.g., reactions caused by hemorrhagic pancreatitis, burns, complicated abdominal surgery, septicemia)

• Thoracic trauma (direct contusion to the lungs)

image OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Acute Respiratory Distress Syndrome

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-9), Alveolar Consolidation (see Figure 9-9), and Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10)—the major anatomic alterations of the lungs associated with ARDS (see Figure 27-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Restrictive Lung Pathophysiology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC FEVT FEV1/FVC ratio FEF25%-75%
↓ N or ↓ N or ↑ N or ↓
FEF50% FEF200-1200 PEFR MVV
N or ↓ N or ↓ N or ↓ N or ↓

image

LUNG VOLUME AND CAPACITY FINDINGS

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