Lung Changes Associated With COPD

Lung Changes In COPD Responsible for Varying Degress of Symptoms

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COPD is an obstructive lung disease characterized by airflow limitation that is not fully reversible. Caused primarily by long-term exposure to airway irritants, the disease process causes a number of very distinct, physiologic and structural lung changes that are responsible for the varying degree of COPD symptoms. Let's take a closer look at four of those lung changes.

Airflow Limitation

Long-term exposure to airway irritants, such as tobacco smoke and air pollution, causes the airways to become swollen and inflamed, obstructing airflow to and from the lungs.

This process, referred to as airflow limitation, gets progressively worse over time, especially if exposure to noxious stimuli continues.

Airflow limitation directly correlates with the decline in lung function seen in COPD as measured by spirometry. The greater the airflow limitation, the lower the FEV1 and FEV1/FVC, two values critical in the diagnosis of restrictive and obstructive lung diseases.

Air Trapping

Airway obstruction causes more and more air to become trapped inside the lungs during exhalation. Like an over-inflated balloon, air trapping causes hyperinflation of the lungs, which in turn limits the amount of air that a person is able to inhale. As air trapping continues, the volume of air left in the lungs after a normal exhalation (functional residual capacity) increases, especially during exercise. This is the main reason that people with COPD become more short of breath during exercise and have a reduced ability to tolerate strenuous activity.

Abnormalities in Gas Exchange

Deep within the lungs lie the alveoli, tiny grape-like clusters where gas exchange takes place. Inhaled air contains oxygen; Exhaled air contains carbon dioxide, the waste product of respiration. Under normal circumstances, oxygen is inhaled and travels down the respiratory tract to the lungs until it reaches the alveoli.

Once in the alveoli, it diffuses into the bloodstream where it flows through the body to nourish all the vital organs. In turn, carbon dioxide that has been picked up by the blood exchanges with oxygen, diffusing back through the alveoli, into the lungs and out the respiratory tract where it is finally exhaled as waste. In the healthy lung, the exchange of oxygen and carbon dioxide is balanced; In COPD, it is not. Repeated exposure to noxious stimuli destroys the alveoli, impairing the process of gas exchange. This often leads to hypoxemia and hypercapnia, both very common in COPD. As the disease progresses, the impairment of gas exchange generally worsens, leading to worsening symptoms, disability, and severe illness.

Excess Mucus Production

Overproduction of mucus contributes to airway narrowing, airway obstruction, productive cough and shortness of breath that is characteristic of COPD. It also plays a major role in the frequency and duration of bacterial lung infections.

Mucus is a sticky substance produced by goblet cells and mucous cells of the submucosal glands. In healthy lungs, goblet cells are more abundant in the large bronchi, decreasing in number as they reach the smaller bronchioles.

Submucosal glands are restricted to the larger airways, yet become increasingly sparse as the airways narrow, disappearing completely in the bronchioles. Normally, mucus functions in a protective way to help lubricate the lungs and rid the airways of foreign debris. In COPD, mucus production, more-or-less, turns on itself.

When the lungs are continuously subjected to airway irritants, goblet cells increase in number and submucosal glands increase in size. Consequentially, they become denser in the smaller airways, outnumbering the broom-like cilia cells that help clear mucus out of the lungs. When mucus production goes into overdrive and airway clearance is impaired, mucus begins to pool in the airways, creating an obstruction and a perfect breeding ground for bacteria to multiply.

As bacteria grow in number, bacterial lung infection occurs often followed by COPD exacerbation.

What Can You Do?

The most important aspect of COPD treatment is smoking cessation. Quitting smoking can dramatically slow the lung function decline that will only worsen if smoking continues.

If you are a never-smoker, be sure to avoid, or at least limit, exposure to all airway irritants. This includes secondhand smoke, air pollution, and harsh workplace chemicals.

Prevention of COPD exacerbation is also important in the daily management of COPD. Most patients underestimate their role in this, but when taken, preventative steps help lower the risk of exacerbation and keep patients from being hospitalized.

If you have not yet been diagnosed with COPD and are experiencing symptoms, see your doctor for a spirometry test. Early diagnosis of COPD leads to earlier treatment and far better outcomes for those who develop the disease.


Global Strategies for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease. The Global Initiative for Obstructive Lung Disease. Revised 2011.

Toward, Toby J., and Broadley, Kenneth J. Goblet Cell Hyperplasia, Airway Function, and Leukocyte Infiltration after Chronic Lipopolysaccharide Exposure in Conscious Guinea Pigs: Effects of Rolipram and Dexamethasone. JPET 302:814–821, 2002.

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