Emphysema

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• What Is Emphysema?
• What Causes Emphysema?
• What Are Emphysema Symptoms and Signs?
• When to Seek Medical Care and Who to See
• How to Test for Emphysema
• What Is Emphysema Medical Treatment?
• What Is Emphysema Surgery?
• Important of Pulmonary Rehabilitation
• Emphysema Follow-up
• Emphysema Prevention
• Emphysema Prognosis
• Read more on Emphysema from Healthwise

Emphysema is a long-term, progressive disease of the lungs that primarily causes shortness of breath due to over-inflation of the alveoli (air sacs in the lung). In people with emphysema, the lung tissue involved in exchange of gases (oxygen and carbon dioxide) is impaired or destroyed. Emphysema is included in a group of diseases called chronic obstructive pulmonary disease or COPD (pulmonary refers to the lungs). Emphysema is called an obstructive lung disease because airflow on exhalation is slowed or stopped because over-inflated alveoli do not exchange gases when a person breaths due to little or no movement of gases out of the alveoli.

Emphysema changes the anatomy of the lung in several important ways. This is due to in part to the destruction of lung tissue around smaller airways. This tissue normally holds these small airways, called bronchioles, open, allowing air to leave the lungs on exhalation. When this tissue is damaged, these airways collapse, making it difficult for the lungs to empty and the air (gases) becomes trapped in the alveoli.

Normal lung tissue looks like a new sponge. Emphysematous lung looks like an old used sponge, with large holes and a dramatic loss of “springy-ness” or elasticity. When the lung is stretched during inflation (inhalation), the nature of the stretched tissue wants to relax to its resting state. In emphysema, this elastic function is impaired, resulting in air trapping in the lungs. Emphysema destroys this spongy tissue of the lung and also severely affects the small blood vessels (capillaries of the lung) and airways that run throughout the lung. Thus, not only is airflow affected but so is blood flow. This has dramatic impact on the ability for the lung not only to empty its air sacs called alveoli (pleural for alveolus) but also for blood to flow through the lungs to receive oxygen.

COPD as a group of diseases is one of the leading causes of death in the United States. Unlike heart disease and other more common causes of death, the death rate for COPD appears to be rising.

Cigarette smoking is by far the most dangerous behavior that causes people to develop emphysema, and it is also the most preventable cause. Other risk factors include a deficiency of an enzyme called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.

The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized. Cigarette smoke contributes to this disease process in two ways. It destroys lung tissue, which results in the obstruction of air flow, and it causes inflammation and irritation of airways that can add to air flow obstruction.

• Destruction of lung tissue occurs in several ways. First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions. Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long-term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased at the same time that the ability to clear the secretions is decreased. The resulting mucous buildup can provide bacteria and other organisms with a rich source of food and lead to infection.
• The immune cells in the lung, whose job it is to prevent and fight infection, are also affected by cigarette smoke. They cannot fight bacteria as effectively or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.
• Over time, enzymes released during this persistent inflammation lead to the loss of proteins responsible for keeping the lungs elastic. In addition, the tissue separating the air cells (alveoli) from one another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.
• Alpha-1-antitrypsin (also known as alpha-1-antiprotease) is a substance that fights a destructive enzyme in the lungs called trypsin (or protease). Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food. It is also released by immune cells in their attempt to destroy bacteria and other material. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung. The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking. The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately. The imbalance that develops between trypsin and antitrypsin results in an “innocent bystander” effect. Foreign objects (e.g. bacteria) are trying to be destroyed but this enzyme destroys normal tissue since the second enzyme (antiprotease) responsible for controlling the first enzyme (protease) is not available or is poorly functioning. This is referred to as the “Dutch” hypothesis of emphysema formation.
• Air pollution acts in a similar manner to cigarette smoke. The pollutants cause inflammation in the airways, leading to lung tissue destruction.
• Close relatives of people with emphysema are more likely to develop the disease themselves. This is probably because the tissue sensitivity or response to smoke and other irritants may be inherited. The role of genetics in the development of emphysema, however, remains unclear.
• Abnormal airway reactivity, such as bronchial asthma, has been shown to be a risk factor for the development of emphysema.
• Men are more likely to develop emphysema than women. The exact reason for this is unknown, but differences between male and female hormones are suspected.
• Older age is a risk factor for emphysema. Lung function normally declines with age. Therefore, it stands to reason that the older the person, the more likely they will have enough lung tissue destruction to produce emphysema.

It is important to emphasize that COPD is often not purely emphysema or bronchitis, but varying combinations of both.

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