Test your lungs know your numbers
  National Lung Health Education Program   Home | Return to Resources page

The Early Recognition and Management of Chronic Obstructive Pulmonary Disease

Index:

 Introduction

COPD Definitions and Pathogenesis

The National Lung Health Education Program

Methods of Smoking Cessation

Maintenance Management of Symptomatic COPD

Treatment of Advanced Disease

The 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 adulthood.

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 ischemic.

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 COPD.

Spirometry

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 misleading.

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.

BACK TO TOP