Chronic Obstructive Pulmonary Disease Process

It is not fully understood how tobacco smoke and other inhaled particles damage the lungs to cause COPD. The most important processes causing lung damage are:

Oxidative stress produced by the high concentrations of free radicals in tobacco smoke.
Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway.
Tobacco smoke and free radicals impair the activity of antiprotease enzymes such as alpha 1-antitrypsin, allowing protease enzymes to damage the lung.

Pathology

Chronic bronchitis

Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. In the airways of the lung,

the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.

Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "blue bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called "Blue Bloaters."

Emphysema

Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.

If the rate of airflow is too low, a person with COPD may not be able to completely finish breathing out (expiration) before he or she needs to take another breath. This is particularly common during exercise when breathing has to be faster. A little of the air of the previous breath remains within the lungs when the next breath is started. When this happens, there is an increase in the volume of air in the lungs, a process called dynamic hyperinflation. It is less comfortable to breathe with hyperinflation because it takes more effort to move the lungs and chest wall when they are already stretched by hyperinflation.

Another factor contributing to shortness of breath in COPD is the loss of the surface area available for the exchange of oxygen and carbon dioxide with emphysema. This reduces the rate of transfer of these gasses between the body and the atmosphere and can lead to low oxygen and high carbon dioxide levels in the body. A person with emphysema may have to breathe faster or more deeply to compensate, which can be difficult to do if there is also flow limitation or hyperinflation.

Some people with advanced COPD do manage to breathe fast to compensate, but usually have dyspnea as a result. Others, who may be less short of breath, tolerate low oxygen and high carbon dioxide levels in their bodies but this can eventually lead to headaches, drowsiness and heart failure.

Advanced COPD can lead to complications beyond the lungs such as weight loss (cachexia), pulmonary hypertension and right-sided heart failure (cor pulmonale). Osteoporosis, heart disease, muscle wasting and depression are all more common in people with COPD. No single symptom or sign can adequately confirm or exclude the diagnosis of COPD although COPD is uncommon under the age of 40 years.

Spirometry

The diagnosis of COPD is confirmed by spirometry,

Other tests

An x-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases. Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases.

A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.