Chronic obstructive pulmonary disease (COPD) is our nation’s
most rapidly growing health problem. It is now the fourth most common
cause of death and the only disease in the top 10 that continues
to rise in prevalence and mortality. Approximately 16 million adult
Americans now have symptomatic stages of COPD. It is estimated that
an equal number may have undiagnosed disease. Recent calculations
indicate that COPD results in $30.4 billion in direct and
indirect costs, presenting a huge economic impact on our society.
The purpose of this chapter is to characterize COPD as a major healthcare
problem in the United States and present a systematic approach to diagnosis
and treatment of various stages of disease, using a case-based approach.
COPD is an all-inclusive and relatively nonspecific term that
is applied to a spectrum of disease that includes chronic bronchitis,
emphysema, and asthmatic bronchitis. Cardinal symptoms are chronic
cough, mucus hypersecretion, dyspnea on exertion, and occasional
wheeze. Characteristically, there is progressive reduction in expiratory
airflow. Lung hyperinflation occurs in the majority of patients.
Laennec, who invented the stethoscope in 1819, was the first
to characterize emphysema. His Treatise
of Diseases of the Chest contains the following profound statement, “In
emphysema the air makes its escape from the air cells much slower
than in the healthy state of the organ. This seems to indicate either
more difficult communication between air contained in the air cells
or that of the bronchi, or else diminished elasticity of the air
cells themselves. Perhaps both of these causes conspire to produce
the effect in question.” Other astute observers recognized
the importance of loss of elastic recoil, as COPD began to be characterized
physiologically in the early twentieth century. Elastic recoil is
a result of stretching the lungs and thorax during a full inspiration.
Both lungs and thorax contain elastic fibers. Expiratory airflow
is due to the deflation of the system, very much like an inflated balloon
empties when released.
The first clear definitions of COPD were developed by the American
Thoracic Society and published in 1962. Concepts about COPD have
since evolved based on improved understandings of the pathogenesis
and the course and prognosis of disease.
COPD is a product of inflammatory damage to the conducting airways,
both small and large, and loss of elastic recoil due to damage of
alveolar structures. Loss of elasticity and premature loss of alveolar
walls are parallel processes, but are not related by cause and effect.
Together loss of elastic recoil and increased airways resistance
reduce expiratory airflow, which is the major indicator of disease
severity and prognosis.
The inflammatory mechanisms resulting in COPD are different from
asthma. In COPD the CD8 T-lymphocyte is involved, along with macrophages
that produce chemotactic factors that stimulate neutrophils to release
elastases and toxic oxygen species. Interleukin 8 and tumor necrosis factor α also
appear to be involved. In contrast, with asthma the CD4 T-lymphocyte,