Management of stable COPD

Bronchodilators

Bronchodilators are medicines that relax smooth muscle around the airways, increasing the calibre of the airways and improving air flow. They can reduce the symptoms of shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life for people with COPD. They do not slow down the rate of progression of the underlying disease. Bronchodilators are usually administered with an inhaler or via a nebulizer.

There are two major types of bronchodilator, β2 agonists and anticholinergics. Anticholinergics appear to be superior to β2 agonists in COPD. Anticholinergeics reduce respiratory deaths while β2 agonists have no effect on respiratory deaths. Each type may be either long-acting (with an effect lasting 12 hours or more) or short-acting (with a rapid onset of effect that does not last as long).

 β2 agonists

β2 agonists stimulate β2 receptors on airway smooth muscles, causing them to relax. There are several β2 agonists available. Salbutamol or albuterol (common brand name: Ventolin) and terbutaline are widely used short acting β2 agonists and provide rapid relief of COPD symptoms. Long acting β2 agonists (LABAs) such as salmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life.

Anticholinergics

Anticholinergic drugs cause airway smooth muscles to relax by blocking stimulation from cholinergic nerves. Ipratropium is the most widely prescribed short acting anticholinergic drug. Like short-acting β2 agonists, short-acting anticholinergics provide rapid relief of COPD symptoms and a combination of the two is commonly used for a greater bronchodilator effect. Tiotropium is the most commonly prescribed long-acting anticholinergic drug in COPD. It is has more specificity for M3 muscarinic receptors so may have fewer side-effects than other anticholinergic drugs. Regular use is associated with improvements in airflow, exercise capacity, quality of life and possibly a longer life.

Corticosteroids

Corticosteroids act to reduce the inflammation in the airways, in theory reducing lung damage and airway narrowing caused by inflammation. Unlike bronchodilators, they do not act directly on the airway smooth muscle and do not provide immediate relief of symptoms. Some of the more common corticosteroids in use are prednisone, fluticasone, budesonide, mometasone, and beclomethasone. Corticosteroids are used in tablet or inhaled form to treat and prevent acute exacerbations of COPD. Well-inhaled corticosteroids (ICS) have not been shown to be of benefit for people with mild COPD, however, they have been shown to decrease acute exacerbations in those with either moderate or severe COPD. They however have no effect on overall one-year mortality and are associated with increased rates of pneumonia.

Other medication

Theophylline is a bronchodilator and phosphodiesterase inhibitor that in high doses can reduce symptoms for some people who have COPD. More often, side effects such as nausea and stimulation of the heart limit its use. In lower doses, it may slightly reduce the number of COPD exacerbations. The investigative phosphodiesterase-4 antagonists, roflumilast and cilomilast have completed Phase-2 clinical trials. Tumor necrosis factor antagonists such as infliximab suppress the immune system and reduce inflammation. Infliximab has been trialled in COPD but there was no evidence of benefit with the possibility of harm.

Supplemental oxygen

Oxygen can be delivered in different forms: in large containers, in smaller containers with liquid oxygen, or with the use of a oxygen concentrator (shown here) which derives oxygen from room air. The latter two options improve mobility of people requiring long-term oxygen therapy.

Supplemental oxygen can be given to people with COPD who have low oxygen levels in the body. Oxygen is provided from an oxygen cylinder or an oxygen concentrator and delivered to a person through tubing via a nasal cannula or oxygen mask. Supplemental oxygen does not greatly improve shortness of breath but can allow people with COPD and low oxygen levels to do more exercise and household activity. Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD and arterial hypoxemia or with complications of hypoxemia such as pulmonary hypertension, cor pulmonale, or secondary erythrocytosis. High concentrations of supplemental oxygen can lead to the accumulation of carbon dioxide and respiratory acidosis for some people with severe COPD; lower oxygen flow rates are generally safer for these individuals.

Pulmonary rehabilitation

Pulmonary rehabilitation is a program of exercise, disease management and counselling coordinated to benefit the individual. Pulmonary rehabilitation has been shown to improve shortness of breath and exercise capacity. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.

Nutrition

Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation programme, this can lead to improvements in COPD symptoms.

Cause of COPD

Smoking

The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.

Occupational exposures

Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers. Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition. The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.

Air pollution

Studies in many countries have found that people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD as it is thought to slow the normal growth of the lungs although the long-term research needed to confirm the link has not been done. In many developing countries indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.

Genetics

Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers. The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.

Other risk factors

A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.[17] It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats may be related to the development of COPD.

COPD as an autoimmune disease

Autoimmunity

There is mounting evidence that there may be an autoimmune component to COPD.Many individuals with COPD who have stopped smoking have active inflammation in the lungs.  The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells

Signs and symptoms of COPD

One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: "My breathing requires effort," "I feel out of breath," or "I can't get enough air in". People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present.

Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness.

People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.

There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:

* tachypnea, a rapid breathing rate

* wheezing sounds or crackles in the lungs heard through a stethoscope

* breathing out taking a longer time than breathing in

* enlargement of the chest, particularly the front-to-back distance (hyperinflation)

* active use of muscles in the neck to help with breathing

* breathing through pursed lips

* increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).

What is COPD

Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema, a pair of two commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath. In contrast to asthma, the limitation of airflow is poorly reversible and usually gets progressively worse over time.

COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.

The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to requiring long-term oxygen therapy or lung transplantation.

Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries. [4] COPD is the 4th leading cause of death in the U.S., and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.