Emphysema (cont.)
Benjamin Wedro, MD, FACEP, FAAEM
Dr. Ben Wedro practices emergency medicine at Gundersen Clinic, a regional trauma center in La Crosse, Wisconsin. His background includes undergraduate and medical studies at the University of Alberta, a Family Practice internship at Queen's University in Kingston, Ontario and residency training in Emergency Medicine at the University of Oklahoma Health Sciences Center.
George Schiffman, MD, FCCP
Dr. Schiffman received his B.S. degree with High Honors in biology from Hobart College in 1976. He then moved to Chicago where he studied biochemistry at the University of Illinois, Chicago Circle. He attended Rush Medical College where he received his M.D. degree in 1982 and was elected to the Alpha Omega Alpha Medical Honor Society. He completed his Internal Medicine internship and residency at the University of California, Irvine.
In this Article
- Emphysema facts
- Introduction to emphysema
- What is emphysema?
- What are the causes or risk factors for emphysema?
- What are symptoms of emphysema?
- How is emphysema diagnosed?
- Physical examination
- Exams and tests
- What are the stages of emphysema?
- What is the treatment for emphysema?
- Smoking cessation
- Medications for emphysema
- Pulmonary rehabilitation for emphysema
- Surgery
- What is the prognosis and life-expectancy of a person with emphysema?
- COPD (Chronic Obstructive Pulmonary Disease) FAQs
- Find a local Pulmonologist in your town
What is emphysema?
Emphysema is a long-term, progressive disease of the lung(s) and occurs when the alveolar walls are destroyed along with the capillary blood vessels that run within them. This lessens the total area within the lung where blood and air can come together, limiting the potential for oxygen and carbon dioxide transfer.
In early emphysema, there is associated inflammation of the small airways or bronchioles that limits the amount of air that can flow to the alveoli. In more severe emphysema, there is also loss of elasticity in the alveolar walls that have not been destroyed. When the person breathes out, the alveoli and small airways collapse. The loss of elasticity of the lung tissue makes it harder for air to get to the periphery or furthest part of the lung during inhalation, and also harder for air to exit the damaged part of the lung during exhalation. As emphysema progresses and more and more alveoli are destroyed, bullae can be formed. Bullae are air filled sacs of lung that do not function. They can become extremely large and often are located in the upper parts of the lung. A bulla (plural=bullae) are at risk for rupturing and causing a pneumothorax, or collapse of the lung.
As more of the lung is destroyed and the lung cannot maintain oxygen concentrations in the bloodstream, the body compensates by gradually increasing the breathing rate. After a while, even hyperventilation (hyper=more + ventilation=breathing) cannot maintain adequate oxygen levels, and the arteries in the lung begin to constrict or narrow. The heart has to work harder to push blood into these narrower blood vessels, causing the blood pressure in the lung arteries to increase (pulmonary hypertension). Over time, the extra work requirement causes the heart muscle to enlarge (hypertrophy) and can cause heart failure.
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