Chronic obstructive pulmonary disease (COPD) refers to a clinical syndrome of chronic dyspnea as a result of expiratory airflow obstruction due to chronic bronchitis or emphysema (often both). Chronic bronchitis is defined clinically and is associated with chronic cough, resulting from excessive tracheobronchial mucus production and impaired mucus elimination, lasting for at least three months of the year for more than two consecutive years. Emphysema is defined anatomically and is characterized by enlarged air spaces distal to the terminal bronchioles with destruction of the alveolar walls; there is also a loss of elastic recoil in the lung. In the United States, COPD affects an estimated 15 million people and is the fifth leading cause of death.

• Smoking is the number one cause of COPD. Obstruction of airflow in the small airways has been shown to be the earliest detrimental effect of smoking.
• Exposure to environmental air pollutants
• Alpha1-antitrypsin deficiency, the only known inherited form of the disease

• History of smoking or passive smoke exposure
• History of working with high levels of airborne particulates (e.g., dusts), gases, and fumes (such as coal and gold miners; farmers; and cement, cadmium, and cotton workers)
• Low socioeconomic status
• Male gender
• Allergy and airway hyper-responsiveness (e.g., asthma)
• Women in undeveloped countries exposed to open fires for cooking and heating
• Living in heavily industrialized urban areas
• Recurrent respiratory illnesses
• Family history of chronic bronchitis and emphysema (e.g., alpha1-antitrypsin deficiency)
• Emotional stress and repressed emotions have also been shown to contribute

Patients with emphysema present with a long history of dyspnea on exertion. Patients with chronic bronchitis present with chronic cough productive of sputum.

• Cough
• Cyanosis
• Weight gain
• Dyspnea on exertion (and eventually at rest)
• Excessive sputum production
• Wheezing
• Recurrent bronchial infections
• Weight loss in late stages
• Peripheral edema secondary to cor pulmonale

• Asthma
• Bronchiolitis obliterans
• Pneumonia
• Lung cancer
• Cystic fibrosis
• Congestive heart failure
• Interstitial lung disease
• Primary pulmonary hypertension
• Acute viral infection

There is considerable variability in the clinical presentation of COPD, which can range from simple chronic bronchitis (cough without airway obstruction) to severe respiratory disability and fatal respiratory failure. The classic patient with emphysema is often very thin and barrel chested and shows obvious difficulty breathing, manifesting tachypnea (rapid respirations) with prolonged expiration through pursed lips. Patients often assume a "tripod" position, leaning forward while sitting, bracing with the arms. Cyanosis is not present so the patient is considered a "pink puffer." The classic patient with bronchitis is often overweight, even obese, and appears cyanotic. The respiratory rate is normal, and there is no obvious distress. These patients are called "blue bloaters." In reality most patients with COPD have a combination of chronic bronchitis and emphysema.

Show moderate to severe hypoxia

In bronchitis:

• Hyperplastic and hypertrophied mucous glands in the submucosa of large bronchi
• Increased Reid index (ratio of bronchial gland thickness to bronchial wall thickness)
• Small airways: mucus plugging, goblet-cell metaplasia, airway thickening, peribronchial fibrosis, mucosal and submucosal inflammatory changes, increased smooth muscle, and accumulation of macrophages and neutrophils in respiratory bronchioles
• Large airways: mucous gland enlargement, goblet-cell hyperplasia, and squamous metaplasia

In emphysema:

• Enlargement of air spaces distal to the nonrespiratory bronchioles
• Destruction of the alveolar walls

• Chest X ray may show hyperinflation (flattened diaphragm, increased retrosternal air space, outwardly bowed lower ribs), bulbous or cystic change, especially in upper lung, and wide pulmonary diameter (due to pulmonary hypertension).
• High-resolution CT can show areas of anatomic emphysema, bronchiectasis, and allow measurement of pulmonary artery diameter.
• Echocardiography (two-dimensional, M-mode, or transesophageal) may show characteristic changes of cor pulmonale, right atrial and ventricular hypertrophy, and tricuspid regurgitation. It may allow estimation of the severity of pulmonary hypertension.

• Pulmonary function tests define the physiologic abnormalities of COPD. Spirometry before and after bronchodilator administration confirms airflow obstruction and helps in assessing the severity and reversibility of lung damage. Lung volume measurements (e.g., plethysmography) show characteristic overinflation. Diffusion capacity is impaired in COPD.
• Arterial blood gases may show hypoxemia, hypercapnea, or both.
• Exercise testing (i.e., on a treadmill or stationary bicycle, 6- or 12-minute tests) will show reduced exercise tolerance and exercise-induced hypoxemia.

Smoking cessation is the key to preventing exacerbations and progression. Management is dependent on the degree of obstruction, the severity of disability, and reversibility of the illness. Respiratory infections must be treated aggressively.

• Alpha1-antitrypsin replacement therapy
• Supplemental oxygen (1 to 3 liters/min)—dosage should be appropriate to relieve hypoxemia (i.e., to maintain a PaO2 of 55 to 60 mm Hg)
• Bronchodilators—to increase airflow and reduce dyspnea
• Anticholinergic agents (e.g., ipratropium, 0.18 mg, 2 puffs qid)
• Beta₂-adrenergic agonists (e.g., metaproterenol, terbutaline, or albuterol, 2 to 6 puffs every three to six hours)
• Theophylline (200 to 400 mg bid)—requires frequent blood monitoring for toxicity
• Corticosteroids (e.g., prednisone, 40 mg/day for two weeks then reduce to 0 to 10 mg every day or on alternate days)
• Broad-spectrum antibiotics (e.g., ampicillin or amoxicillin, 2 g/day; erythromycin, 2 g/day; or trimethoprim-sulfamethoxazole, 1 double-strength capsule/day)—for treatment of exacerbations
• N-acetylcysteine—for mucolytic therapy; however, it may cause bronchospasm
• Magnesium can also be markedly helpful as an IV infusion of 5 to 10 g of elemental magnesium over 6 to 10 hours.

May be very helpful at decreasing the symptoms and preventing infections. Since smoking cessation is very important, the alternative treatments for this will be listed. Psychotherapy and support groups can be very helpful in learning to cope with chronic disease.

• Dairy products and bananas increase mucus buildup and should be avoided. Garlic, onions, and horseradish may actually decrease mucus production. IgG ELISA food allergy testing can determine other foods that can cause inflammation in the lungs.
• Some essential fatty acids are anti-inflammatory, dose is 1,000 to 2,000 IU, mixed omega-3 and omega-6 oils (flaxseed, fish, borage, and/or evening primrose oil; avoid vegetable oils and saturated fats)
• Coenzyme Q10 prevents fatty acid oxidation and increases exercise tolerance as a cardio-protective antioxidant. Dose is 10 to 50 mg tid.
• Other important antioxidants: selenium (200 mcg/day), vitamin E (400 IU/day), vitamin C (1,000 mg tid), L-carnitine (750 mg bid). Note that beta-carotene increases the risk of lung cancer in smokers.
• Bromelain is a mucolytic, 250 to 500 mg tid away from meals. People with pineapple allergy may be sensitive to this product. Bromelain may also aggravate gastritis.
• N-acetylcysteine is a mucolytic, 400 mg tid.
• Magnesium promotes muscle relaxation in bronchial smooth muscle and blood vessels (100 to 500 mg bid). Magnesium may cause diarrhea in some sensitive individuals.

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

• Mullein (Verbascum densiflorum): expectorant, soothes irritation
• Ginger (Zingiber officinale): dissolves secretions, relieves bronchial spasms
• Fennel (Foeniculum vulgare): dissolves secretions, mild antispasmodic, calming digestive stimulant
• Coltsfoot (Tussilago farfara): anticatarrh, demulcent. Prolonged use may cause liver damage due to pyrrolizidine alkaloids.
• Licorice (Glycyrrhiza glabra): antiviral, antidepressant, soothing, anticatarrh, contraindicated in hypertension
• Hawthorn (Crataegus monogyna): protective of blood vessels, increases cardiac output without increasing cardiac load

Mix equal parts of herb, or tincture of four to six of the above herbs. Dose is 1 cup tea tid, or 30 to 60 drops tincture tid.

Essential oils: eucalyptus (Eucalyptus globulus), thyme (Thymus vulgaris), rosemary (Rosmarinus officinalis), and/or lavender (Lavandula angustifolia): place 3 to 5 drops in 2 cups of water in a humidifier to prevent infection.

Constitutional treatment by a homeopathic prescriber may help with symptoms and address underlying emotional issues that will aid patients in smoking cessation.

• Castor oil pack: Used externally, castor oil is a powerful anti-inflammatory. Apply oil directly to skin, cover with a clean soft cloth (e.g., flannel) and plastic wrap. Place a heat source (hot water bottle or heating pad) over the pack and let sit for 30 to 60 minutes. For best results use three consecutive days in one week. When placed over the lungs, castor oil packs decrease inflammation and stimulate drainage.
• Postural drainage, yogic breathing, and pulmonary rehabilitation programs may all be helpful.

Has been shown to have great benefit in smoking cessation.

Serial monitoring of pulmonary function is performed annually or as symptoms dictate. If patient is unstable or if home oxygen is required, more frequent visits are needed.

Cessation of smoking is the single best way to prevent disease progression. Respirators of the appropriate type can reduce the risk to workers exposed to dusts, fumes, and gases.

Negative air ion generators are frequently helpful. Electronic air cleaners and HEPA filters are helpful in highly polluted environments and for persons who have a marked allergic basis for their chronic bronchitis contribution to COPD.

The most common complication of COPD is pulmonary infection. Prophylactic influenza vaccination (annually) and pneumococcal vaccination (every six to eight years) can be effective. Patients on steroid therapy are at risk for steroid-related complications—adrenal suppression, capillary fragility, easy bruisability, glucose intolerance, weight gain in the face, and muscle wasting.

By the time dyspnea develops with simple daily activity, patients may have lost two-thirds of their pulmonary function. The diagnosis is often made very late in the course of the disease. Thus, the mortality rate after diagnosis is high (>50% after 10 years).

With the exception of patients with alpha₁-antitrypsin deficiency, women are usually diagnosed with COPD well beyond the reproductive years.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:423, 468.

Bordow RA, Moser KM. Manual of Clinical Problems in Pulmonary Medicine. 4th ed. Boston, Mass: Little, Brown; 1996:212-215.

Celli BR. Pulmonary rehabilitation in patients with COPD. Am J Respir Crit Care Med. 1995;152:861-864.

Duke JA. The Green Pharmacy. Emmaus, Pa: Rodale Press; 1997:93-95, 179-183.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:1451-1457.

Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med. 1993;328:1017-1022.

Snider GL. Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease. Washington Crossing, Pa: Scientific Frontiers; l996:1-12.

Woodley M, Whelan A. Manual of Medical Therapeutics. 27th ed. Boston, Mass: Little, Brown; 1992:200-202.