Acute respiratory distress syndrome (ARDS), also called shock lung or adult respiratory distress syndrome, results from increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood. Severe ARDS can cause intractable and fatal hypoxemia. However, patients who recover may have little or no permanent lung damage.

ARDS results from a variety of respiratory and nonrespiratory insults, such as:

Asthma is a reversible lung disease characterized by obstruction or narrowing of the airways, which are typically inflamed and hyperresponsive to a variety of stimuli. It may resolve spontaneously or with treatment. Its symptoms range from mild wheezing and dyspnea to life-threatening respiratory failure. Symptoms of bronchial airway obstruction may persist between acute episodes.

Cystic fibrosis is a generalized dysfunction of the exocrine glands that affects multiple organ systems. Transmitted as an autosomal recessive trait, it’s the most common fatal genetic disease in white children. Affecting about 30,000 U.S. children and adults, cystic fibrosis is most common in Whites (1 in 3,300 births) and less common in Blacks (1 in 15,300 births), Native Americans, and Asians. It occurs equally in both sexes.

Most cases of cystic fibrosis arise from a mutation that affects the genetic coding for a single amino acid, resulting in a protein that doesn’t function properly. The abnormal protein resembles other transmembrane transport proteins. It lacks phenylalanine (an essential amino acid) that’s usually produced by normal genes. This abnormal protein may interfere with chloride transport by preventing adenosine triphosphate from binding to the protein and interfering with activation by protein kinase. The lack of essential amino acids leads to dehydration and mucosal thickening in the respiratory and intestinal tracts.

Emphysema is a form of chronic obstructive pulmonary disease characterized by the abnormal, permanent enlargement of the acini accompanied by destruction of alveolar walls without fibrosis. Obstruction results from tissue changes rather than mucus production, which occurs in asthma and chronic bronchitis. The distinguishing characteristic of emphysema is airflow limitation caused by thick elastic recoil in the lungs.

Senile emphysema results from degenerative changes that cause stretching without destruction of the smooth muscle. Connective tissue usually isn’t affected.

Even though it’s largely preventable, lung cancer has long been the most common cause of cancer death in men and is an increasing cause of cancer death in women. Lung cancer usually develops within the wall or epithelium of the bronchial tree. The most common type is non-small-cell cancer, which includes epidermoid (squamous cell) carcinoma, adenocarcinoma, and large cell (anaplastic) carcinoma. Less common is small-cell lung cancer. prognosis varies with the extent of metastasis at the time of diagnosis and the cell type growth rate.

Pneumonia is an acute infection of the lung parenchyma that commonly impairs gas exchange. The prognosis is generally good for people who have normal lungs and adequate host defenses before the onset of pneumonia; however, pneumonia is the sixth leading cause of death in the United States.

Pneumonia can be classified by microbiologic etiology, location, or type.

Predisposing factors for bacterial and viral pneumonia include:

Predisposing factors for aspiration pneumonia include:

Pulmonary edema is the accumulation of fluid in the extravascular spaces of the lung. With cardiogenic pulmonary edema, fluid accumulation results from elevations in pulmonary venous and capillary hydrostatic pressures. A common complication of cardiac disorders, pulmonary edema can occur as a chronic condition or it can develop quickly and cause death.

Pulmonary edema usually results from left-sided heart failure due to arteriosclerotic, hypertensive, cardiomyopathic, or valvular heart disease. With such disorders, the compromised left ventricle can’t maintain adequate cardiac output; increased pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed. This increased pulmonary capillary hydrostatic force promotes transudation of intravascular fluids into the pulmonary interstitium, decreasing lung compliance and interfering with gas exchange.

Pulmonary embolism is an obstruction of the pulmonary arterial bed that occurs when a mass—such as a dislodged thrombus—lodges in a pulmonary artery branch, partially or completely obstructing it. This causes a ventilation-perfusion mismatch, resulting in hypoxemia, as well as intrapulmonary shunting.

The prognosis varies. Although the pulmonary infarction that results from embolism may be so mild that the patient is asymptomatic, massive embolism (more than 50% obstruction of pulmonary arterial circulation) and infarction can cause rapid death.

In most patients, pulmonary embolism results from a dislodged thrombus (blood clot) that originates in the leg veins. More than one-half of such thrombi arise in the deep veins of the legs; usually multiple thrombi arise. Other, less common sources of thrombi include the pelvic, renal, and hepatic veins, the right side of the heart, and the upper extremities.