The disease can lead to an array of lungsounds caused by narrowed airways and secretions from very diminished, to tight inspiratory wheezes, to rhonchi, to crackles (particularly in the bases).
It can lead to chest pain due to muscle soreness from using accessory muscles (those used only when you're working very hard to breath) or cardiac anomalies caused by the heart working extra hard to pump blood through constricted vessels in the lungs.
COPD is now the 4th leading cause of death in the United States, effecting 32 million Americans. Likewise, of the top 10 diseases, it's the only one that is on the rise. It's a disease that effects about 12% of all people who smoke cigarettes, and is occasionally caused by occupational inhaled chemicals, and in some rare instances asthma gone bad. The #1 cause of COPD, however, is cigarette smoking, as about 80% of current COPDers are former or current smokers.
The term chronic means you will always have it. The obstruction is in the lungs and it causes air to become trapped in the lungs making it feel as though you can't get air out. The obstruction can be partially reversed by using bronchodilators like Albuterol, although permanant damage to the lungs means some shortness of breath may always be present.
For the most part, in the hospital the term COPD is usually reserved for people who smoked and developed either chronic bronchitis or emphysema. Asthma, however, has been identified as a major contributor of COPD. Egan's Fundamentals of Respiratory Care notes that "increased airway reactivity (asthma) is present in 15-70% of patients with COPD." Thus, if you smoke and you have asthma, there is a good chance you will develop COPD (see my post on Recovered Asthmatics).
Chronic bronchitis is where the chemicals from smoking or other polutants (and perhaps the smoke itself) causes the cilia in the lungs to burn down to cinders.
You have to realize that your lungs are generally kept sterile by your body's defense mechanisms. One such defense mechanism is cilia, or microscopic hairlike structures that line your respiratory tract from your lungs all the way up to your nose. The purpose of cilia is to act like an escalator to bring up any microscopic object -- like bacteria -- that try to enter the lungs.
Ideally, your immune system balls up the unwanted object into a mucus ball, which sits on the cilia. The cilia vibrates and works the mucus to the upper airway by this so-called escalator system (you can view a picture here). Once the mucus reaches your upper airway you have an urge to cough and spit. Once you spit the mucus it is called sputum.
In the case of a normal patient with a normal escalator system you should expect very little sputum production. Most of the time, COPDers produce thick yellow sputum. It's yellow because it usually has bacteria in it, as I will explain below.
In the case of chronic bronchitis, your cilia is gone or greatly damaged. As irritants get into the lungs and are balled up into mucus, it has no place to go, and therefore much of it stays in the lungs. Since the escallator system is weakened you may feel a constant or chronic urge to cough. In fact, it's this chronic cough that is used to diagnose chronic bronchitis.
Couple this with the fact that many chronic bronchitis patients also have inflammed airways that are more sensitive to irritants such as strong smells, smoke, pollutants, etc. This is where chronic bronchitis is similar to asthma. Asthmatics have chronically inflammed lungs that are increasingly sensitive to asthma triggers. The best way to treat this inflammation is with inhaled corticosteroids and, in some instances, systemic corticosteroids.
Untreated inflammation, or inflammation that is non-responsive to steroids or slow to resond, can result in lung cells producing excessive mucus that becomes trapped in the lungs.
Since it's hard for your body to bring up this mucus, your lungs can become breeding grounds for various bacteria, making you susceptible to catching pneumonia (which may be the leading cause of COPD exacerbations). This is also the leading cause of hospital visits.
The chronic inflammation and excessive mucus production may also lead to airway narrowing (bronchoconstriction) or airway spasming (bronchospasm) that lead to blocked air passages causing air to become trapped in the lungs. The way to treat such acute episodes of chronic bronchitis is with bronchodilators like Albuterol and Xopenex. Corticosteroids are also used for acute episodes to control the inflammation.
Chronic bronchitis patients are often referred to as blue bloaters because their lungs have lost some of their ability to get inhaled oxygen to the blood and to tissues. With less oxygenated blood getting to tissues, their bodies naturally increases cardiac output (blood flowing through the heart) and decreases the respiratory rate. This results in less CO2 being exhaled by the lungs, and results in an increase in CO2 retained by their bodies to go with their chronic hypoxia (low oxygen in the blood).
In more severe cases, such COPDers have a normal resting CO2 of about 50 and a normal resting PO2 of about 50. We RTs refer to these patients as members of the 50/50 club.
Thinking the reason for the low amount of oxygen to the blood (hypoxemia) is due to a lack of red blood cells (RBCs), the bodies of such COPDers are tricked into producing extra RBCs.
But in the case of chronic bronchitis, this technique doesn't work. Instead, these patients remain in the 50/50 club, remain hypoxic and cyanotic, and have a condition called polycythemia, which is the medical term for too many RBCs.
Each RBC has hemoglobin on it to carry oxygen. When an oxygen molecule sits on this hemoglobin, it turns the blood red. This, in turn, turns your skin its normal pink color. In the case of chronic bronchitis patients, they have many extra RBCs that are not carrying an oxygen molecule. Thus, their skin tends to be blue until they are wearing supplemental oxygen (hence the term blue bloater).
Blue bloaters, therefore, have a tendency to develop lungs that are constricted, and due to lack of oxygen the veins in the lungs become constricted too. The heart, therefore, has to work extra hard to pump blood to the lungs. After this goes on for several years, the heart can tire, and often reverts to chronic Atrial Fibrillation.
Of course, you know that when you work a muscle extra hard it gets bigger. The heart is no different. The heart is a muscle. After working hard to pump blood to chronic bronchitis lungs, the right side of the heart gets bigger (called cor pulmonale). This ultimately results in the left heart working extra hard too, resulting in a larger left heart. Now the heart is a weaker pump that sometimes has trouble moving blood through the body, thus causing edema to build up throughout their system. This causes the patient to look puffy.
The bloater part of blue bloater comes from this edema.
Emphysema is a disease where the inhaled smoke (or other chemicals, or anti-trypson deficiency, or age itself) causes the lungs to break down. The National Heart and Lung Institute describes emphysema this way:
"The 'airways' are the tubes that carry air in and out of the lungs through the nose and mouth. Healthy airways and air sacs in the lungs are elastic—they try to bounce back to their original shape after being stretched or filled with air, just the way a new rubber band or balloon does. This elastic quality helps retain the normal structure of the lung and helps to move the air quickly in and out.
In people with (emphysema), the air sacs no longer bounce back to their original shape."
Their bodies compensate with an increased respiratory rate and decreased cardiac output. While the lungs are well oxygenated, there is poor blood flow through them. So, these patients have a normal pink color, have normal blood gases (CO2 and oxygen levels), and normal pressure in their lungs.
Due to the low cardiac output the tissues of the body receive less of the oxygen the patient breaths in, resulting in low oxygen to the tissues (hypoxia). Over time, these patients develop muscle wasting and they lose weight, and are therefore called pink puffers.
It has been noted that 1/3 of men and 1/4 of women have emphysema at the time of death. So, in time, many of us will develop it. However, people who smoke, and have the COPD gene (which may also be the asthma gene), will speed up the aging process, which will result in early emphysema.
Men are more likely to get COPD, yet when women get it some studies show it progresses faster, perhaps because it is not "diagnosed" soon enough. While either emphysema or chronic bronchitis may dominate, most COPDers have a combination of the two.
You can still get COPD if you quit smoking. And while you cannot undo damage already done to your lungs, stopping smoking will prevent further damage. Thus, the best way to treat COPD is by stopping smoking.
Proper diagnosis and proper treatment can delay progression of the disease. The goal of physicians in treating COPD is to provide the least amount of medicines necessary to allow the patient to maintain a productive and active member of society.
Treatment for COPD is to reverse acute chronic episodes. When the damage to the lungs is permanent (as in emphysema), treatment is generally supportive.