What Are the Goals of COPD Care?

It is important to identify and treat COPD as early as possible in its natural history. Unfortunately, the diagnosis of COPD is frequently made when patients are in their late 50s or 60s, when FEV1 has declined to a symptomatic range, and when quality of life is rapidly deteriorating.

Therefore, the goal of any physician treating patients with COPD is to help prevent and relieve their patients’ symptoms and to help patients better manage the effects of their disease and live as full and active lives as possible.

If patients work closely with physicians to develop a complete respiratory care program, they can:

  • Improve lung function
  • Reduce hospitalizations
  • Prevent acute episodes
  • Minimize disability
  • Prevent early death

How Is Chronic Obstructive Pulmonary Disease Treated?

Although there is no cure for COPD, the disease can be prevented in many cases. And, in almost all cases the disabling symptoms can be reduced. Because cigarette smoking is the most important cause of COPD, not smoking almost always prevents COPD from developing, and quitting smoking slows the disease process.

If the patient and medical team develop and adhere to a program of complete respiratory care, disability can be minimized, acute episodes prevented, hospitalizations reduced, and some early deaths avoided. On the other hand, none of the therapies has been shown to slow the progression of the disease, and only oxygen therapy has been shown to increase the survival rate.

Home oxygen therapy can improve survival in patients with advanced COPD who have hypoxemia, low blood oxygen levels. This treatment can improve a patient’s exercise tolerance and ability to perform on psychological tests, which reflect different aspects of brain function and muscle coordination. Increasing the concentration of oxygen in blood also improves the function of the heart and prevents the development of cor pulmonale. Oxygen can also lessen sleeplessness, irritability, headaches, and the overproduction of red blood cells. Continuous oxygen therapy is recommended for patients with low oxygen levels at rest, during exercise, or while sleeping. Many oxygen sources are available for home use; these include tanks of compressed gaseous oxygen or liquid oxygen and devices that concentrate oxygen from room air. However, oxygen is expensive with the cost per patient running into several hundred dollars per month, depending on the type of system and on the locale.

Medications frequently prescribed for COPD patients include:

  • Bronchodilators help open narrowed airways. There are three main categories: sympathomimetics (isoproterenol, metaproterenol, terbutaline, albuterol) which can be inhaled, injected, or taken by mouth; parasympathomimetics (atropine, ipratropium bromide); and methylxanthines (theophylline and its derivatives) which can be given intravenously, orally, or rectally.
  • Corticosteroids or steroids (beclomethasone, dexamethasone, triamcinolone, flunisolide) lessen inflammation of the airway walls. They are sometimes used if airway obstruction cannot be kept under control with bronchodilators, and lung function is shown to improve on this therapy. Inhaled steroids given regularly may be of benefit in some patients and have few side effects.
  • Antibiotics (tetracycline, ampicillin, erythromycin, and trimethoprim-sulfamethoxazole combinations) fight infection. They are frequently given at the first sign of a respiratory infection such as increased sputum production with a change in color of sputum from clear to yellow or green.
  • Expectorants help loosen and expel mucus secretions from the airways.
  • Diuretics help the body excrete excess fluid. They are given as therapy to avoid excess water retention associated with right-heart failure. Patients taking diuretics are monitored carefully because dehydration must be avoided. These drugs also may cause potassium imbalances, which can lead to abnormal heart rhythms.
  • Digitalis (usually in the form of digoxin) strengthens the force of the heartbeat. It is used very cautiously in patients who have COPD, especially if their blood oxygen tensions are low, because they are vulnerable to abnormal heart rhythms when taking this drug.
  • Other drugs sometimes taken by patients with COPD are tranquilizers, pain killers (meperidine, morphine, propoxyphene, etc.), cough suppressants (codeine, etc.), and sleeping pills (barbiturates, etc.). All these drugs depress breathing to some extent; they are avoided whenever possible and used only with great caution.

A number of combination drugs containing various assortments of sympathomimetics, methylxanthines, expectorants, and sedatives are marketed and widely advertised. These drugs are undesirable for COPD patients for several reasons. It is difficult to adjust the dose of methylxanthines without getting interfering side effects from the other ingredients. The sympathomimetic drug used in these preparations is ephedrine, a drug with many side effects and less bronchodilating effect than other drugs now available. The combination drugs often contain sedatives to combat the unpleasant side effects of ephedrine. They also contain expectorants, which have not been proven to be effective for all patients and may have some side effects.

Bullectomy, or surgical removal of large air spaces called bullae that are filled with stagnant air, may be beneficial in selected patients. Recently, use of lasers to remove bullae has been suggested.

Lung transplantation has been successfully employed in some patients with end-stage COPD. In the hands of an experienced team, the 1-year survival in patients with transplanted lungs is over 70 percent.

Pulmonary rehabilitation programs, along with medical treatment, are useful in certain patients with COPD. The goals are to improve overall physical endurance and generally help to overcome the conditions which cause dyspnea and limit capacity for physical exercise and activities of daily living. General exercise training increases performance, maximum oxygen consumption, and overall sense of well-being. Administration of oxygen and nutritional supplements when necessary can improve respiratory muscle strength. Intermittent mechanical ventilatory support relieves dyspnea and rests respiratory muscles in selected patients. Continuous positive airway pressure (CPAP) is used as an adjunct to weaning from mechanical ventilation to minimize dyspnea during exercise. Relaxation techniques may also reduce the perception of ventilatory effort and dyspnea. Breathing exercises and breathing techniques, such as pursed lips breathing and relaxation, improve functional status.

Keeping air passages reasonably clear of secretions is difficult for patients with advanced COPD. Some commonly used methods for mobilizing and removing secretions are the following:

  • Postural bronchial drainage helps to remove secretions from the airways. The patient lies in prescribed positions that allow gravity to drain different parts of the lung. This is usually done after inhaling an aerosol. In the basic position, the patient lies on a bed with his chest and head over the side and his forearms resting on the floor.
  • Chest percussion or lightly clapping the chest and back, may help dislodge tenacious or copious secretions.
  • Controlled coughing techniques are taught to help the patient bring up secretions.
  • Bland aerosols, often made from solutions of salt or bicarbonate of soda, are inhaled. These aerosols thin and loosen secretions. Treatments usually last 10 to 15 minutes and are taken three or four times a day. Bronchodilators are sometimes added to the aerosols.

How Can Patients With Chronic Obstructive Pulmonary Disease Cope Best With Their Illness?

In most instances of COPD, some irreversible damage has already occurred by the time the doctor diagnoses the disease. At this point, the patient and the family should learn as much as possible about the disease and how to live with it. The patient must understand the goals, limitations, and techniques of treatment so that symptoms can be kept under control, and daily living can proceed as normally as possible. The doctor and other health care providers are good sources of information about COPD education programs. Patients and family members can usually take part in educational programs offered at a hospital or by a local branch of the American Lung Association.

Patients with COPD can help themselves in many ways. They can:

  • Stop smoking. Many programs are available to help smokers quit smoking and to stay off tobacco. Some programs are based on behavior modification techniques; others combine these methods with nicotine gum or nicotine patches as aids to help smokers gradually overcome their dependence on nicotine.
  • Avoid work-related exposures to dusts and fumes.
  • Avoid air pollution, including cigarette smoke, and curtail physical activities during air pollution alerts.
  • Refrain from intimate contact with people who have respiratory infections such as colds or the flu and get a one-time pneumonia vaccination (polyvalent pneumococcal vaccination) and yearly influenza shots.
  • Avoid excessive heat, cold, and very high altitudes. (Note: Commercial aircraft cruise at high altitudes and maintain a cabin pressure equal to that of an elevation of 5,000 to 10,000 feet. This can result in hypoxemia for some COPD patients. However, with supplemental oxygen, most COPD patients can travel on commercial airlines.)
  • Drink a lot of fluids. This is a good way to keep sputum loose so that coughing can bring it up.
  • Maintain good nutrition. Usually a high protein diet, taken as many small feedings, is recommended.
  • Consider “allergy shots.” COPD patients often also have allergies or asthma which complicate COPD.

Of all the avoidable risk factors for COPD, smoking is by far the most significant. Cessation of smoking is the best way to decrease one’s risk of developing COPD.

What Types of Research on Chronic Obstructive Pulmonary Disease Is the National Heart, Lung, and Blood Institute Supporting?

The National Heart, Lung, and Blood Institute (NHLBI) is supporting a number of research programs on COPD with the following objectives: 1) to understand its underlying causes, 2) to develop methods of early detection, 3) to improve treatment, and 4) to help patient’s and their families better manage the disease.

A study completed several years ago examined the use of oxygen therapy for people who, because of COPD, cannot get enough oxygen into their blood by breathing air. This study has determined that continuous oxygen therapy is more beneficial in extending life than giving oxygen only for 12 hours at night.

Another clinical study compared inhalation therapy using a machine, which administers medication to the lungs by intermittent positive pressure breathing (IPPB) with one that delivers the medicine by relying on the patient’s own breathing. Although home use of IPPB machines is widespread, previous studies had not been able to show conclusively whether they were effective. In this study, 985 ambulatory patients with COPD were randomly assigned to a treatment group which received a bronchodilator aerosol solution by IPPB, or to a control group which received the medication via a compressor nebulizer. The only difference between the two groups was the positive pressure applied by the IPPB. There was no statistically significant difference between the two treatment groups in numbers of deaths, frequency and length of hospitalization, change in lung function tests, or in measurements of quality of life. This study suggests that the use of IPPB devices may be unnecessary.

An intervention trial called the Lung Health Study, which began in 1983, has enrolled approximately 6,000 smokers in a study to determine whether an intervention program incorporating smoking cessation and use of inhaled bronchodilators (to keep air passages open) in men and women at high risk of developing COPD can slow the decline in pulmonary function compared to a group receiving usual care. When this study is completed, it should help to determine the extent to which identification and treatment of asymptomatic subjects with early signs of obstructive lung disease would be useful as a preventive health measure. In addition, the study will test some of the current theories about behavior and smoking cessation. Early results indicate that cigarette smoking may be more harmful to women than to men. Furthermore, smoking cessation results in greater weight gain in women than in men, and to avoid weight gain women are less likely to quit smoking and more likely to revert to their smoking habit.

Because familial emphysema results from a deficiency of AAT in affected individuals, efforts to minimize the risk of emphysema have been directed at increasing the circulating AAT levels either by promoting or increasing the production of AAT within the individual, or augmenting it from the outside. One strategy for improving the production of AAT is by pharmacological means (e.g., by administration of drugs such as danazol or estrogen/ progesterone combinations), but this has not been found to be effective. Genetic engineering to correct the defective gene or introduce the functional gene in the deficient individuals is being attempted by several NHLBI-supported investigators. The normal gene for AAT as well as the mutant genes causing AAT deficiency have been characterized and cloned, and animal models carrying the mutant gene have been developed. The resulting animals displayed many of the physical and histologic changes seen in human neonatal AAT deficiency. These studies should provide the groundwork for future development of gene replacement therapy for AAT deficiency.

In the meantime, attention is being focused on AAT augmentation therapy for familial emphysema. Studies have shown that intravenous infusion of AAT fractionated from blood is safe and biochemically effective, that is, the needed blood levels of AAT can be maintained by the continued administration of AAT at appropriate intervals.

Because of the practical and fiscal limitations to mounting a clinical trial for establishing the clinical efficacy of AAT augmentation therapy for emphysema, the NHLBI sponsored a national registry of patients with AAT deficiency to assess the natural history of severe AAT deficiency and to examine whether the disease course is altered by the augmentation therapy. This program is enrolling, at various medical centers both in the U.S. and Europe, at least 1,000 adult patients with AAT deficiency satisfying certain other eligibility criteria. The patients will be followed for 3 to 5 years (chest x rays, lung function, blood and urine analysis, etc.) at one of 37 participating clinical centers. The evaluation of the data and the release of the conclusions are expected by early 1995.

Methods to treat emphysema before it becomes disabling remain an important research objective of programs supported by NHLBI. Since it is believed that either excess protease (elastase), or too little useful antiprotease, can lead to development of the disease, scientists have also been attempting to use other approaches to develop animal models which will mimic the human condition of inherited alpha-l-protease inhibitor deficiency and using such models to test if natural or synthetic antiproteases can be used safely to prevent development of emphysema-like lesions in these animals. If found safe and effective in animals, these agents can be tried in humans.

National Heart, Lung and Blood Institute, Division of Lung Diseases