Shasta Critical Care Specialists



Chronic obstructive pulmonary disease, or COPD, is characterized by abnormalities in the lungs that make it difficult to exhale normally. Generally, two distinct diseases are involved: emphysema and chronic bronchitis. According to the World Health Organization (WHO), the majority of deaths from COPD that occur in developed countries are directly related to smoking tobacco.

Emphysema and chronic bronchitis cause excessive inflammatory processes that eventually lead to abnormalities in lung structure that permanently obstruct airflow (hence the term "chronic obstructive").

The American Lung Association and the World Health Organization track respiratory disease and mortality rates related to tobacco use. Approximately 16.4 million people suffer from this disease. According to the American Lung Association, approximately 14 million people suffer from chronic bronchitis, the seventh leading chronic condition in the United States. There are an estimated 1.9 million people suffering with emphysema. Of these, 55.5% are men and 44.5% are women. Between 1982 and 1995 emphysema increased in women by 14.8%, probably due to the increased rate of smoking among women. An estimated 50,000 to 100,000 people, primarily of northern European descent, have AAT deficiency emphysema. COPD is the fourth leading cause of death in the United States. In 1996, approximately 100,360 people died as a result of COPD.

According to the World Health Organization, the prevalence of COPD has increased in many countries. For instance in Russian Federation the use of tobacco caused approximately one-third of all male deaths in 1995. Three–fourths of those men were under 70 years of age In the United Kingdom and Northern Ireland the death rate attributable to COPD and tobacco use has been reported as high as 63 per 100,000 men and 25.1 per 100,000 women in the mid 1990’s.

In China the Use of tobacco consumption doubles between 1965 and 1980. In the mid 1990’s, smoking caused far more deaths from COPD than from cardiovascular disease. China has the worlds’ highest rate of mortality due to tobacco use.

Tobacco use is the number one risk factor for COPD and heavy smokers are at greatest risk. Cigarette smokers are at greater risk than cigar and pipe smokers. All smokers are at greater risk than lifelong nonsmokers.

Having alpha1-antitrypsin (AAT) deficiency, also called familial emphysema, is another risk factor. People with familial emphysema have a hereditary deficiency of alpha– 1 – protease inhibitor. When there is a deficiency of AAT, the activity of elastase—an enzyme that breaks down elastin—is not inhibited and elastin degradation occurs unchecked. Individuals with a severe genetic deficiency of AAT usually have symptoms by the time they reach early middle age. It is critical that people with this deficiency never smoke. Approximately 1% to 3% of all cases of emphysema are due to AAT deficiency.

Asthma also increases the risk for developing COPD later in life especially if you smoke.

In the lung there are millions of tiny, thin-walled, elastic air sacs called alveoli. These tiny sacs perform the crucial task of replenishing the blood with oxygen (via inhalation) and ridding the body of carbon dioxide (CO2) in exhalation. Emphysema is the enlargement of the alveoli accompanied by destruction of their walls. In "smokers emphysema" an agent in cigarette smoke sets off a self-perpetuating, low-grade inflammation that causes the release of enzymes (elastase) from inflammatory cells that break down collagen and elastin — substances that maintain the structure and elasticity of alveoli — in the alveolar walls. The NHLBI (National Heart, Lung and Blood Institute) reports that this creates an imbalance between the elastin-degrading enzymes and their inhibitors. They also found that oxidants in cigarette smoke inactivate a significant number of elastase inhibitors, thereby decreasing the amount of active antielastase available to protect the lung and further upsetting the elastase-antielastase balance.

This disruption of the alveolar walls and elastin leads to a decrease in the elastic recoil of the lungs, limiting the ability of the alveoli to passively shrink and to exhale. This accounts for the main limitation to exhalation seen in severe COPD. The disruption of the alveolar walls also leads to their increase in size, making the lungs larger and placing the chest at a mechanical disadvantage. Disruption of the alveolar walls also makes exchange of oxygen from the alveoli to the capillaries and carbon dioxide from the capillaries to the alveoli more difficult. Collapse of the bronchial walls occurs when the cartilage in the bronchial walls has been weakened.

Familial emphysema
People with familial emphysema have a hereditary deficiency of alpha-1-protease inhibitor, also called alpha1-antitrypsin (AAT). When there is a genetic deficiency of AAT, the activity of elastase—an enzyme that breaks down elastin—is not inhibited and elastin degradation occurs unchecked. Individuals with a severe genetic deficiency of AAT usually have symptoms by the time they reach early middle age. It is critical that people with this deficiency never smoke.

Destruction of alveolar walls, capillaries, and attachments between alveoli and bronchioles causes (1) susceptibility of airways to compression and collapse, impeding airflow out of the lungs; (2) entrapment of air in the alveoli; (3) poor air-gas exchange, that is, reduced ability to inhale oxygen and exhale carbon dioxide (CO2), resulting in increased levels of CO2 in the blood; (4) the development of bullae (areas of lung extensively destroyed so that they become large dilated air sacs); and (5) enlarged lungs.

Chronic Bronchitis
Chronic bronchitis is the presence of cough productive of sputum for 3 months per year, in 2 consecutive years. In chronic bronchitis, tobacco smoke causes inflammatory cells (neutrophils and leukocytes) to arrive in the bronchi. These cells worsen airway obstruction by causing inflammation and thickening of the airways. Also, mucus-producing glands deep within the lining of the airways become enlarged (hypertrophy) and increase in number (hyperplasia), and the number of surface cells that produce mucus (goblet cells) increases, resulting in excessive secretion of mucus in the lungs. The resulting chronic cough and expectoration affects the central conducting.

The function of mucus in the lungs is to trap and clear particles, to dilute harmful substances, to lubricate the airways, and to humidify inspired air. In chronic bronchitis, (1) the hyperplasia and hypertrophy of the sub mucosal glands (mucus-producing glands deep within bronchial walls) thicken the airway walls; (2) the resulting increased volume of mucus that occurs plugs the airways; (3) columnar cells (cells that line the surface of the airways) undergo changes that result in the destruction of cilia — delicate hair like structures on columnar cells lining the airways that sweep mucus with offending agents up and out of the lungs. The loss of cilia and the inability to clear bacteria predispose the patient to lung infections.

Dyspnea, the most common symptom of COPD, comes on gradually and is first noticed during physical exertion or during acute exacerbations. Upon further development of COPD the body undergoes several changes including, progressive dyspnea, increase time of exhalation, barrel chest due to enlarment of the lungs and flattening of the diaphragms, chronic bronchitis and recurrent respiratory of infections.

Medical Therapies
The mainstream therapy for COPD encompasses the use of Brondilators and anti-inflammatory medications, steroids, antibiotics, oxygen, pulmonary rehabilitation, Oxygen, smoking cessation, Immunizations (flu shot and pneumonia vaccine).

Complications of COPD
Patients with COPD can developed several complications including pulmonary hypertension with right sided failure, lose of weight, acute exacerbations, recurrent pulmonary infections, polycythemia, and pneumothorax.

The overall prognosis for a patient with COPD depends on the severity of lung disease and whether the patient continues to smoke.