COPD Definitions and Pathogenesis

The Early Recognition and
Management of Chronic Obstructive Pulmonary Disease



COPD Definitions
and Pathogenesis

National Lung Health Education Program

of Smoking Cessation

Management of Symptomatic COPD

of Advanced Disease

New Era




COPD Definitions and Pathogenesis

We are all aware of the high cost of smoking; however, approximately 45
million teenagers and adults continue to smoke.  Fortunately,
teenagers are smoking less, and adults are quitting more.  The
anti-smoking programs directed at elementary school-aged children need to
continue.  We have not found an effective way to greatly reduce the
initiation of smoking by pre-teens and teenagers.  Accordingly, more
emphasis needs to be placed on smoking cessation programs in early

COPD is characterized by premature losses of ventilatory function as
judged by spirometry (FEV1).  Whereas, the normal decline
in FEV1of a six-foot man averages about 25 ccs per year, the
accelerated decline of FEV1 on the pathway to symptomatic
COPD averages 80-100 ccs per year.  COPD is a result of host risk
factors and environmental exposures.  Of course, host risk factors
cannot be changed, but the control of smoking, air pollution and
occupational exposures can make a major difference in the course and
prognosis of COPD.  COPD is not only a smokers’ disease that clusters
in families, but one that worsens with age.  As we face an aging
population, we will have more and more patients with COPD.

COPD shares common factors with asthma.  Both diseases have a
familial component; both are caused by inflammation that results in
bronchospasm; both are potentially reversible or progressive.
Sometimes it is difficult to separate asthma from COPD and, indeed,
the diseases may coexist.  However, the pathogenesis of COPD is quite
different from asthma and involves macrophages, neutrophils, elastases,
oxidants and CD8 lymphocytes.

The natural history of COPD covers 30-40 years.  It begins with
biochemical and cellular events occurring at the tissue level, which
quickly attack small airways and surrounding alveoli.  By the time
clinical and x-ray signs of COPD are present, the disease is far advanced.
The original attack is on the alveolar attachments of small airways
that serve to tether airways and maintain their patency.  Alveolar
lesions are probably due, at least in part, to accelerated apoptosis of
alveolar capillaries caused by cigarette smoking.  Thus the airways
lesions are inflammatory and bronchospastic, but alveolar lesions are

Airflow abnormalities are measured by a spirometer and are key to
the assessment of all chronic pulmonary diseases, including COPD.
Expiratory airflow is a function of pressure against resistance.
Thus, in COPD, airflow is limited or reduced by loss of elastic
recoil, airway narrowing, or both.  Simple office spirometers have
been introduced in response to the NLHEP and must be used for assessment
and responses to therapy.

The Clinical Spectrum of COPD

COPD has had many definitions in the past.  The clinical labels of
chronic bronchitis, asthmatic bronchitis and emphysema, and overlaps of
these individual components, are commonly used.  COPD is an all
inclusive, non-specific term with chronic symptoms of cough, excess mucus
and exercise-related dyspnea.  COPD is characterized by a progressive
reduction in airflow that is not fully reversible with broncho-active
drugs.  Hyperinflation is common.

Signs and symptoms in the early stages of COPD are often absent or
ignored by both the patient and the healthcare workers   Chest x-ray
or EKG abnormalities are also not seen during the early stages of


Spirometry should be looked upon as a simple expression of a complex
process just as with blood pressure.  All primary care physicians
need to understand the essence of spirometry, and this can be easily
taught.  The lungs are filled by muscular effort, and in the normal
state, there is a uniform distribution of ventilation.  Expiratory
airflow is a function of muscular force, elastic recoil, large airways
function, small airways function and interdependence.  Conventional
spirometry measures volume over time.  A second convention measures
flow over volume.  Both expressions measure exactly the same thing
but express it in a different way.  NLHEP recommends only two
parameter spirometry, (i.e., FEV1, FVC and the ratio between
the two).  The normal ratio is greater than 70%.  Since normal
lungs empty in six seconds or less, the FEV6 has become
the surrogate for FVC.

FEF 25-75% and other “nonsense numbers” should be eliminated.
These tests do not measure small airways disease and are often

Whereas, no reasonable doctor would prescribe insulin without measuring
blood sugar, use antihypertensives without measuring blood pressure, treat
cardiac arrhythmias without EKG evidence, or use Coumadin without
measuring international neutralization ratio (INR), many physicians still
continue to use powerful bronchoactive drugs, including corticosteroids,
without spirometric documentation.  In fact, this sometimes leads to
lawsuits when steroid complications occur.

The concept of lung age can be understood by patients.  Normal
lung age is that age for which a patient’s lung function is normal.
Thus, a patient may have a reasonable pulmonary function at age 45,
(say an FEV1 of 2.5 liters), but this is actually the
normal lung function for a patient 70 years old!  This means that
this 45 year-old has a ‘lung age’ of 70.  This fact may gain a
patient’s attention and help to motivate him/her to initiate a smoking
cessation attempt.