COPD (Chronic Obstructive Pulmonary Disease) is a serious lung disease that, over time, makes it hard to breathe. It is the 4th leading cause of death in the United States and causes serious, long-term disability. The number of people with COPD is increasing. More than 12 million people are currently diagnosed with COPD and an additional 12 million likely have the disease and don't even know it.
You may have heard COPD called other names, like emphysema or chronic bronchitis. In people who have COPD, the airways—tubes that carry air in and out of your lungs—are partly blocked, which makes it hard to get air in and out.
Chronic obstructive pulmonary disease, or COPD, is a long-lasting obstruction of the airways that occurs with chronic bronchitis, emphysema, or both. This obstruction of airflow is progressive in that it happens over time.
Chronic bronchitis is defined as a chronic (ongoing, long-term) cough not caused by another condition that produces sputum (mucus) for 3 or more months during each of the 2 consecutive years. In chronic bronchitis, the mucous glands in the lungs become larger. The airways become inflamed, and the bronchial walls thicken. These changes and the loss of supporting alveolar (air space) attachments limit airflow by allowing the airway walls to deform and narrow the airway lumen (the inside of the airway tube).
Emphysema is an abnormal, permanent enlargement of the air spaces (alveoli) located at the end of the breathing passages of the lungs (terminal bronchioles). Emphysema also destroys the walls of these air spaces.
There are 3 types of emphysema: centriacinar emphysema, panacinar emphysema, and distal acinar emphysema or paraseptal emphysema.
In the United States, approximately 14.2 million people have been diagnosed with COPD, 12.5 million people have chronic bronchitis, and 1.7 million people have emphysema. It is estimated that there may be an additional equal number of US citizens that have COPD but who have not been diagnosed with the disorder. The number of people with COPD has increased by 41.5% since 1982.
Most people with COPD have smoked at least 10-20 cigarettes per day for 20 or more years before experiencing any symptoms. Thus, COPD is typically not diagnosed until the fifth decade of life (in people aged 40-49 years).
Common signs and symptoms of COPD are as follows:
1. A productive cough or an acute.
2. Breathlessness or being short of breath (called dyspnea) is the most significant symptom, but it does not usually occur until the sixth decade of life (in people aged 50-59 years).
3. Wheezing is a musical, whistling, or hissing sound with breathing. Some people may wheeze, especially during exertion and when their condition worsens.
The following may occur as COPD worsens:
1. Intervals between acute periods of worsening of dyspnea (exacerbations) become shorter.
2. Cyanosis (discoloration of the skin) and failure of the right side of the heart may occur.
3. Anorexia and weight loss often develop and suggest a worse prognosis.
The 3 major goals of the comprehensive treatment of COPD are as follows:
1. Lessen airflow limitation.
2. Prevent and treat secondary medical complications (eg, hypoxemia, infection).
3. Decrease respiratory symptoms and improve quality of life.
Acute exacerbation of COPD is one of the major reasons for hospital admission in the United States.
You may need to be hospitalized if you develop severe respiratory dysfunction, if your disease progresses, or if you have other serious respiratory diseases (eg, pneumonia, acute bronchitis). The purpose of hospitalization is to treat symptoms and to prevent further deterioration.
You may be admitted to an intensive care unit (ICU) if you require invasive or noninvasive mechanical ventilation or if you have the following symptoms: Confusion, lethargy, respiratory muscle fatigue, worsening hypoxemia (not enough oxygen in the blood), respiratory acidosis (retention of carbon dioxide in the blood).
Care provider will determine if you need medication to relieve symptoms of COPD.
Smoking cessation using nicotine replacement therapies:
The supervised use of medications is an important adjunct to smoking cessation programs.
Nicotine is the ingredient in cigarettes primarily responsible for the addiction. Withdrawal from nicotine may cause you to have unpleasant side effects, such as anxiety, irritability, difficulty concentrating, anger, fatigue, drowsiness, depression, and sleep disruption. These effects usually occur during the first several weeks after you stop smoking.
Nicotine replacement therapies reduce these withdrawal symptoms. If you require your first cigarette within 30 minutes of waking up, you are most likely highly addicted and would benefit from nicotine replacement therapy.
Several nicotine replacement therapies are available.
Nicotine polacrilex is a chewing gum. Chewing pieces come in 2 strengths (ie, 2 mg, 4 mg). If you smoke 1 pack per day, you should use 4-mg pieces. If you smoke less than 1 pack per day, you should use 2-mg pieces. You should chew hourly and also chew when needed for any initial cravings within the first 2 weeks. You should gradually reduce the amount chewed over the next 3 months.
Transdermal nicotine patches are also available. Patches are well tolerated. The most common side effect is slight skin irritation where the patch is placed. Nicotine replacement therapy patches are sold under the following trade names: Nicoderm, Nicotrol, and Habitrol. Each product has a scheduled decrease in nicotine over 6-10 weeks.
The use of the antidepressant Bupropion (Zyban) is effective. It is a nonnicotine aid to smoking cessation. Bupropion may also be effective for those people who have not been able to quit smoking with nicotine replacement therapies.
Inhaled steroids: Some people with COPD who respond well to oral corticosteroids can be maintained on long-term inhaled steroids.
The use of these drugs is widespread, despite little evidence of efficacy in the treatment of COPD. Inhaled corticosteroids do not slow the decline in lung function. They do, however, decrease the frequency of exacerbations and improve disease-specific and health-related quality of life issues for some people with COPD. Inhaled corticosteroids have fewer side effects than oral steroids, but they are less effective than oral steroids, even at high doses.
Beta2 Agonists - Bronchodilators: Inhaled beta2-agonist bronchodilators relax and open the breathing passages. They work rapidly, typically within minutes. Beta2 agonists are primarily used to relieve symptoms of COPD. Inhaled beta2 agonists are the treatment of choice for acute exacerbations of COPD.
Two long-acting beta2 agonists (ie, formoterol, salmeterol) are available. They may be useful if you frequently use short-acting beta2-bronchodilators or if you experience symptoms at night.
Anticholinergic agents - Bronchodilators Maintenance treatment with aerosolized anticholinergic agents (eg, ipratropium bromide) may be more effective than beta2 agonists for people with COPD, particularly in relieving shortness of breath.
Ipratropium bromide opens the breathing passages and has minimal side effects.
It is administered by a metered-dose inhaler, at 2-4 puffs 4 times a day. Beta2 agonists can be added as needed. Although it is slower to take effect (eg, 30-60 min) than inhaled beta2 agonists, ipratropium bromide lasts longer. Because of this, it is less suitable for use on an as-needed basis.
People undergoing exacerbations of COPD respond well to inhaled beta2-agonists and anticholinergic aerosols (eg, ipratropium bromide). Treatment usually begins with an inhaled beta2-agonist delivered via a spacer or a nebulizer, which creates a mist of the drug. Delivering the drug this way also reduces the side effects. Inhaled ipratropium bromide is also usually added.
Methylxanthines, such as theophylline, are a group of medications chemically related to caffeine. They work in COPD by opening the breathing passages. In addition, methylxanthines reduce inflammation, improve respiratory muscle function, and stimulate the brain respiratory center.
Adding theophylline to the combination of bronchodilators can be beneficial, although the response to theophylline may vary among people with COPD. Their use has decreased over the last decade because of the risks of unwanted side effects. Side effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and seizures.
Oral steroids: Corticosteroids are used for people who do not improve sufficiently after trying other drugs or who develop an exacerbation. Oral steroids have been used successfully to treat acute exacerbations. They improve symptoms and lung function in this circumstance. Oral corticosteroids are generally not recommended for long-term use because of their potential side effects.
Antibiotics: In people with COPD, chronic infection of the lower airways is common. The goal of antibiotic therapy is not to eliminate organisms but to treat acute exacerbations. This therapy is most beneficial for people whose exacerbations are characterized by at least 2 of the following (ie, Winnipeg criteria): increased shortness of breath, increased sputum production, and increased sputum purulence.
First-line treatment choices include amoxicillin, cefaclor, or trimethoprim/sulfamethoxazole. Second-line treatment choices include azithromycin, clarithromycin, and fluoroquinolones.
Mucolytic agents: Mucolytic agents not only reduce sputum viscosity (resistance to its flow) but also improve sputum clearance.
Oxygen therapy: COPD is commonly associated with worsening oxygenation of the blood (hypoxemia).
Many people with COPD who are not hypoxemic at rest have worsening of their blood oxygen level during exertion. Even though studies to determine the long-term benefit of oxygen solely for exercise have not yet been conducted, home supplemental oxygen is commonly recommended for people whose blood oxygen level falls with exercise. Oxygen supplementation during exercise can prevent increases in pulmonary artery pressure, reduce shortness of breath, and improve exercise tolerance.
Oxygen therapy for people with COPD may be needed during air travel because of low airplane cabin pressure. If flying, you should arrange supplemental oxygen prior to the flight directly through the airline or through an airline agent (at an extra expense).
Supplemental oxygen may also be needed for people with COPD whose sleep is disturbed by its symptoms.
Oxygen therapy is generally safe. Toxicity from high concentrations of oxygen is well recognized, but little is known about the long-term effects of low concentrations of supplemental oxygen. Because providing oxygen reduces the death rate of people with advanced COPD, the increased survival and quality of life benefits of long-term oxygen therapy outweigh the possible risks.
The major physical hazards of oxygen therapy are fires or explosions. People with COPD, their family members, and their caregivers are warned not to smoke when supplemental oxygen is in use. Overall, major accidents are rare and can be avoided by proper training.
Oxygen delivery systems: Long-term oxygen therapy (LTOT) is typically delivered by continuous flow nasal cannula. This method is the standard means of oxygen delivery because it is simple, reliable, and generally well tolerated. At home, a machine called an oxygen concentrator is the usual means through which oxygen is delivered. Portable tanks provide the opportunity for people with COPD to continue their oxygen therapy while away from home.
Oxygen-conserving devices enable the use of smaller, lighter, and more portable oxygen tanks. Oxygen-conserving devices function by delivering all of the supplemental oxygen during early inhalation (breathing in). In addition, they may reduce overall costs.
Three oxygen-conserving devices exist: reservoir cannulas, demand pulse delivery devices, and transtracheal oxygen delivery. Transtracheal oxygen delivery is invasive and requires special training by you, your health care provider, and your caregiver.
Assisted ventilation: Progressive airflow obstruction may impair oxygenation and/or ventilation to the point where you may require assisted ventilation.
General guidelines that are used in determining the ideal time to begin ventilatory support are as follows:
Surgery: Over the past 50-75 years, various surgical approaches have been tried to improve symptoms and to restore lung function in people with emphysema. Only giant bullectomy and, possibly, lung volume reduction surgery have proven useful.
Causes and Risk factors:
Tobacco smoking: Tobacco smoking causes 80% to 90% of COPD cases. Smokers are more than ten times as likely to die from COPD than non-smokers (US DHHS, 2004). Chemicals found in tobacco smoke stimulate inflammation in the lungs, leading to destruction of the alveoli and narrowing of the airways. While smoking is related to most COPD cases, only 15% to 20% of smokers develop the disease.
Environmental factors: Exposure to outdoor and indoor air pollutants increases the prevalence of COPD by an estimated 2% for each 10 g/m3 increase in particulate matter. The use of biomass fuels (e.g. use of wood for cooking and heating) increases the risk of COPD by three to four times, contributing significantly to COPD prevalence, especially in rural regions.
Age: COPD is rarely found below the age of 40. Lung function deteriorates with age. Ageing may therefore increase the susceptibility for the development of COPD and its exacerbations. As previously stated, COPD prevalence is higher in elderly people; it is not the physiological decline of the function which predispose to COPD.
Sex: Sex does not seem to have a specific meaning in the development of COPD in the general population, except when related to smoking behavior. Male smoking rates still exceed female, although prevalence rates for European women are increasing while male rates have either reached a plateau or are decreasing. It is likely that the COPD prevalence will follow this pattern.
Recent research indicates that estrogen plays a role in maintaining the lung function in women, putting postmenopausal women at higher risk of developing COPD, having a severe form, and dying from COPD. This may explain the higher prevalence of COPD among older women non-smokers, compared to the male non-smoking population.
Genetic factors: A rare inherited condition and the only currently known genetic risk factor for COPD, alpha1-antitrypsin (AAT) deficiency is due to the inability to produce enough of the lung-protective protein AAT in the liver. Severe AAT-deficiency leads to emphysema at an early age.
Socio-economic inequalities: Deprivation, measured by income and education can negatively affect lung function, independently of smoking. Underlying reasons include childhood infections, occupational exposure and poor housing conditions. Impaired lung function can increase the susceptibility to COPD and its exacerbations.
Alpha1-antitrypsin level: Of the approximately 75 different alleles for AAT variants, 10-15 are associated with serum levels below the protective threshold of 11 mmol/L. The most common severe variant is the Z allele, which accounts for 95% of the clinically recognized cases of severe AAT deficiency. The diagnosis of severe AAT deficiency is confirmed when the serum level falls below the protective threshold value (ie, 3-7 mmol/L). Specific phenotyping is reserved for cases in which serum levels are 7-11 mmol/L or when genetic counseling or family analysis is needed.
Measure the AAT level in all patients younger than 40 years or with a family history of emphysema at an early age.
The defining laboratory features of HVUS are decreased levels of C1q and detectable immunoglobulin G antibodies to C1q. Laboratory evaluation also demonstrates decreased serum complement levels consistent with the characteristic feature of complement activation. A positive serum antinuclear antibody test result is observed in 61% of these individuals.
Polycythemia may develop in severe COPD or in patients who smoke excessively. A hematocrit greater than 52% in men and greater than 47% in women is indicative of the condition. Patients should be evaluated for hypoxemia at rest, with exertion, or during sleep. Correction of hypoxemia should reduce secondary polycythemia in patients who have quit smoking.
Sputum evaluation: In stable chronic bronchitis, the sputum is mucoid, and the predominant cells are macrophages. With an exacerbation, the sputum becomes purulent, with excessive neutrophils and a mixture of organisms visualized through a Gram stain.
Streptococcus pneumoniae and Haemophilus influenzae are pathogens that are cultured frequently during exacerbations.
Chest Radiograph: Frontal and lateral chest radiographs reveal signs of hyperinflation, which involves flattening of diaphragms, increased retrosternal air space, and a long narrow heart shadow. Rapid tapering vascular shadows accompanied by hyper-lucency of the lungs are signs of emphysema.
With complicating pulmonary hypertension, the hilar vascular shadows are prominent; with right ventricular enlargement, opacity in the lower retrosternal air space may occur.
CT scan: A high-resolution CT (HRCT) scan is more sensitive than a standard chest radiograph. HRCT scan is highly specific for diagnosing emphysema and outlines bullae that are not always observed on radiographs. This information does not alter therapy; therefore, a CT scan has no place in the routine care of patients with COPD. Studies are underway to assess the role of CT scans in early detection of lung cancer in patients with COPD and in predicting response to lung reduction surgery.
Pulmonary function tests: These measurements are necessary for the diagnosis of obstructive airway disease and assessment of its severity. In addition, spirometry is helpful for assessing response to treatment and disease progression.
FEV1 is a reproducible test and is the most common index of airflow obstruction. Lung volume measurements show an increase in total lung capacity (TLC), functional residual capacity, and residual volume. The vital capacity is decreased.
DLCO is decreased in proportion to the severity of emphysema.
Arterial blood gases reveal mild-to-moderate hypoxemia without hypercapnia in the early stages. As the disease progresses, hypoxemia becomes more severe and hypercapnia supervenes. Hypercapnia is observed commonly as the FEV1 falls below 1 L/s or 30% of predicted. Some patients may have hypercapnia without a significant increase in the alveolar-arterial oxygen gradient.
Lung mechanics and gas exchange worsen during acute exacerbations.
As many as 30% of patients have an increase in FEV1 of 15% or more after inhalation of a bronchodilator. The absence of bronchodilator response does not justify withholding bronchodilator therapy.
Medicine and medications:
Oral and inhaled medications are used for patients with stable disease to reduce dyspnea and improve exercise tolerance. Most of the medications used are directed at the 4 potentially reversible mechanisms of airflow limitation: (1) bronchial smooth muscle contraction, (2) bronchial mucosal congestion and edema, (3) airway inflammation, and (4) increased airway secretions.
Albuterol (Proventil, Ventolin).
Theophylline (Aminophylline, Theo-24, Theo-Dur, Slo-bid).
Formoterol (Oxis, Foradil).
Fluticasone (Flovent, Cutivate, Flonase).
Budesonide (Pulmicort Turbuhaler).
Prednisone (Deltasone, Orasone, Meticorten).
Nicotine transdermal system (Nicotrol, Habitrol, Nicoderm CQ).
Nicotine polacrilex (Nicorette).
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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