Chronic obstructive pulmonary disease (COPD) is defined by the guidelines of the Global Initiative for Chronic Obstructive Lung

Disease (GOLD) as a chronic disease characterized by airway/alveolar/systemic inflammation with measured airflow obstruction that is partially reversible with bronchodilator therapy (Fromer 1219). COPD includes two main components: chronic bronchitis, a partially reversible component, and emphysema with fibrosis, which together are an irreversible component. Chronic bronchitis and emphysema often occur together and overlap, resulting in chronic inflammation, airflow limitations, and tissue damage. Chronic obstructive bronchitis is the most prevalent COPD; about 10% of individuals with COPD have emphysema (Doherty). COPD due to chronic bronchitis is characterized by enlarged, inflamed mucus glands that block the airways (bronchi and bronchioles) with excessive mucus, resulting in a frequent, productive cough. COPD secondary to emphysema is caused by damaged lung capillaries and the destruction of air sacs at the ends of bronchioles (lung alveoli) where oxygen exchange occurs, resulting in shortness of breath and an infrequent, nonproductive cough.Asthma, although not considered a true form of COPD, is another obstructive pulmonary disease in which chronically inflamed airways become sensitized to certain triggers (pollution, smoke, stress, exertion, allergens), resulting in an accumulation of exudative debris that temporarily blocks airflow. The inflammation and muscle spasms (bronchospasm) that occur with asthma are reversible, however. Airway obstruction from COPD is progressive, but respiratory limitations once considered by clinicians to be irreversible are now believed to be partially reversible, although not to normal airflow status. Due to the similarity of COPD and asthma symptoms, certain individuals with COPD may be able to partially reverse airway obstruction with medication that opens constricted airways (bronchodilators), similar to that used by asthmatics. Conversely, those with asthma may develop true COPD if repeated airway inflammation leads to scarring and permanent airway constriction. The most common cause of COPD is inhalation of tobacco smoke and other noxious chemicals, particles, or gases. Another well-established but rare cause of COPD is the deficiency of a liver protein called alpha-1 antitrypsin (AAT). AAT deficiency is an inherited disorder that accounts for less than 5% of COPD in the United States ("Chronic"). Normal lung function depends on elastic fibers surrounding the airways and within the walls of lung alveoli where gas exchange takes place. These elastic fibers are composed of a protein called elastin. In normal individuals, AAT protects lung elastin from breakdown by the enzyme elastase, which typically functions to digest and remove old or damaged cells from the lung. With AAT deficiency, AAT does not fully release from the liver, which may allow elastase to destroy lung tissues.

Risk: Smoking is the most significant risk factor for COPD. Although not all cigarette smokers develop
COPD, an estimated 15% to 20% will develop it rapidly, and up to 70% to 90% will ultimately be diagnosed with COPD (Doherty). Smokers experience more frequent respiratory symptoms such as coughing and shortness of breath, and more deterioration in lung function than nonsmokers or exsmokers. The effects of passive smoking or secondhand smoke on the lungs are not well quantified, but inhalation of tobacco smoke increases the risk. Smoking is responsible for up to 90% of COPD in the United States (Chronic). Inhalation of other noxious substances, particles, or gases is also a major risk factor. Air pollution can result in airway inflammation and respiratory limitations in individuals with lung disease, but it is unclear whether air pollution alone contributes to the development of COPD. Some occupational pollutants, such as cadmium and silica, do increase the risk of developing COPD. Individuals at risk for this type of occupational pollution include coal miners, construction workers, metal workers, and cotton workers. Exposure to occupational pollutants is responsible for 19% of COPD cases (Chronic).

Although COPD is often thought of as a disease of elderly adults, the mean age at which a first cigarette is smoked (less than 10 years of age) has lowered the age of COPD diagnosis. A 20-year history of smoking could therefore be reached by age 30, placing even younger adults age 30 to 40 at risk (Doherty). Females have nearly twice the rate of chronic bronchitis as males, with 7.5 million females and 3.7 million males affected (Doherty). Conversely, among individuals with emphysema, 57% are male, and 43% are female (Doherty). The incidence of and deaths from emphysema are increasing among women, which is believed to be due to the greater susceptibility of women to tobacco smoke and to an increase in the number of female smokers in response to peer pressure and the idea that stopping smoking may result in weight gain or depression (Doherty).

Incidence and Prevalence: The Centers for Disease Control report that COPD affects about 10
million adults who self-report the diagnosis, and that 24 million have lung disease that may actually be COPD but has not been diagnosed by a physician (Doherty). Among these, 120,000 deaths due to COPD are recorded annually; it is the fourth leading cause of death in the United States (Doherty). In 2001, of 12.1 million COPD patients, approximately 9.2 million individuals had chronic bronchitis, 2 million had emphysema, and 0.9 million had both conditions (Doherty). Between 50,000 and 100,000 Americans have chronic lung disease due to AAT deficiency (Chronic). It is believed that COPD incidence may be significantly underestimated because not all individuals who have abnormal spirometry results are diagnosed with COPD. The prevalence of COPD has increased, and among the top 5 causes of death in the United States, COPD is the only disease whose mortality rate has increased (Doherty).

An asthmatic who has a reversible obstruction that does return to normal does not have COPD under the new guidelines." See COPD: New Treatments for an Old Disease Source: Medical Association Communications. Also see Emphysema and Other Obstructive Lung Diseases
The following represents actual discussions on the EFFORTS list in reference to this topic. Mark Mangus is a Respiratory Care Practitioner and active member of EFFORTS as well as on our Medical Board of Directors.

Question: Can someone explain a few things about the Asthma component of COPD? As I see it, it's not the same as 'real' or 'just ' asthma since our airways don't completely reverse. Also if it is reflected in the FEF 25 75 #s in our PFT results , representing small airways , then don't all of us have SEVERE small airway obstruction? (regardless of severity of FEV1?) I heard that was the 'first to go with smoking ' (small airways) and ...IF this is so then what is the difference in those of us considered to have this A component ? (Is it just the fact that there is significant post dilator response ?) Answer 1: I believe that Mark is going to have to answer this question. I too have an

Asthma component even though the specialists say there is no longer an asthma component to Emphysema. I cannot understand why this was changed. It used to be that the definition of COPD was a combination of Asthma and Emphysema or Bronchitis and Emphysema but this is no longer so. They say because Asthma can be reversed, well in all reality Bronchitis can also be reversed in some people until it becomes chronic. I never had Asthma prior to getting Emphysema, but I am here to tell you that this so called Asthma I have is just as chronic as any Bronchitis. I thought that Wheezing was part of Asthma but now I hear a lot of members with NO Asthma say they have a wheeze. It can't be both ways. If Asthma is a result of the emphysema than it is not going to go away as long as we are alive unless they find a cure for the big E. In my estimation this is chronic at that point and becomes part of the big E process. Makes no sense to me and even physiologically, it makes no sense. Mark Mangus: Which came first? - - - . . . the chicken or the egg? ? ? ? ? ? Asthma that is acute and "completely" reversible is NOT a component of COPD. Asthma which is "INcompletely" reversible IS indeed a component of COPD. The differences and key here are the terms "chronic" versus "acute" and "completely" versus "INcompletely". Asthma is NOT "caused by Emphysema", but rather as a long term and poorly controlled problem, is attributable as a "cause" of emphysema. Wheezing is the result of air moving through the airways in a turbulent fashion - - - FOR WHAT EVER CAUSE. In Asthma, wheezing is the result of inconsistently narrowed and spasmed airways, which can be further blocked by mucus (the "spasm" being the key determinant of the presence of Asthma). BUT wheezing can result from airways that are NOT spasms, but are otherwise inconsistently narrowed due to mucus and swelling from non asthmatic reasons. Clearing the airways reduces wheezing. reducing swelling reduces wheezing. All the wheezes is NOT Asthma! This is a very old and true 'axiom'. Remark: I had asthma since childhood. It was episodic, always brought on by exposure to an allergen, and reversible in that medication (usually adrenaline chloride) made it go away. Then in my 60s I began having it all the time, without any exposure to allergens. At least, that is what I thought was going on and I called it Chronic Asthma -- a label the doctors agreed with. Then I was tested and they called it COPD Emphysema with an Asthma component. So it seems to me that the asthma we have as emphysema patients is not the same as the asthma that was "reversible."

When they do the PFTs and dose me with albuterol my testing is marginally better, but the effect never lasts more than two or three hours. So if it comes right back, why call it reversible? Maybe they just want to make a distinction between the other kind of asthma and the asthma component of COPD. Mark Mangus: Your presumption is correct - - - the chronic asthmatic component is NOT the same as the "reversible" Asthma you speak of having had long ago. It is p-r-e-c-i-s-e-l-y because your asthma WON'T completely reverse that it is called 'chronic' and is included as a component of your COPD. This has been explained several ways, several times. Perhaps you missed it before, or the bell just didn't ring. In any case, you NOW have it! Remark: You know I don't get it. I started out with the Emphysema and he said there was no way to test to see if I also had Asthma because they were so much alike. So - I didn't question him. He tested me for the inherited emphysema and I did not have that kind. Now years later I am tested at my regular doctor's office and they tell me I have severe asthma. I thought a while back that it might be asthma even though I have not had asthma for years and never never was it really bad. Now they say they are very concerned about the asthma attacks. I am confused as always. There is still no doubt I have the emphysema but now it is more complicated because of the asthma - I think. I also have this doctor telling me to take this and that and giving me the prescriptions and then this woman from the insurance company calls and says Oh you use that medicine as a "rescue Inhaler" when the doctor has just told me to take 2 puffs x 2 a day. Then she says no - you take this stuff for that. I feel like there are 20 people telling me 20 different things over the medicine Mark Mangus: To distinguish Asthma from emphysema on you pulmonary functions test is 'easily' done and fairly straight forward. Once again, we have an example of either incompetence OR poor communication skills (to give the physician the benefit of the doubt!) In any case, the Asthma problem DOES pose the greater concern for you and your current doctor(s), as it can result in rapid compromise, hospitalization and worse. It is most pressing to be able to

achieve effective control to reduce and/or prevent serious or acute difficulties because of the Asthma. This means good compliance with an effective medication plan AND good communication between you and your doctor to make changes when indicated.
Question: Mark Will you please explain how they are able to distinguish between a flare up of emphysema or an asthma attack when you have both? What value on the PFT tells you that you have an asthma component along with emphysema? Thanks for all your valuable information. I have learned more from you about respiratory than in all the years I spent in college in the practice of Nursing. Thanks in advance. Mark Mangus:

NOW you're get down to asking about distinguishing the difficult to distinguish. The O-N-L-Y thing you can definitively distinguish - - - with regard to an 'acute episode' - - - IS Asthma. The fact that you have flows that are reduced (FEV1, FVC and the FEF's) from your stable values AND have a clinically significant response to bronchodilator define the asthmatic component of your exacerbation and give information as to momentary degree of severity. Your description of the emphysema component couldn't have been better put, presenting an opportunity to make a point to - - - hopefully - - - clear up a long-standing misconception many folks have, though I hope I don't create more/different confusion in attempting to do so. Emphysema is R-E-A-L-L-Y a "physical" description of 'characteristic' destructive changes in the 's-t-r-u-c-t-u-r-e' of the lungs. The term carries over to designate the condition many of you suffer as part of your COPD. BUT - - - per se - - - Emphysema is N-O-T a series of, or a descriptor for any "group of s-y-m-p-t-o-m-s", such that you can correctly and/or meaningfully say "my Emphysema is 'flaring up' ". With that point in mind, you need THEN to understand that it is your 'Chronic Bronchitis', Bronchiectasis, Asthma or other airway reactivity or an 'infection', or something along those lines that, on top of having emphysematous changes in your lungs, is causing you to feel worse, or have a "flare-up". BUT, Emphysema, in and of itself, cannot " flare up", or be said to be 'flaring up', as it is not the symptom, but rather the physical condition. It is under this rationale that we label such 'flare-ups' "AECOPD" - - - or, Acute Exacerbation of COPD symptoms. So, in the end, it is neither clinically helpful or of any definitive consequence to attempt to distinguish 'cause of symptoms', with respect to 'equating them with' or 'attributing them to' emphysema versus the symptom-causing conditions 'associated' with having the condition of

clinically significant pulmonary emphysema. At the same time, you can also consider that the more AECOPD's you have, the worse they will likely make your Emphysema! Make sense?
Question:

So, basically, what you are saying is that when we have a flare-up of some kind, it is probably not the emphysema, because that is actually the "condition" of our lungs, but rather, it is something such as asthma, bronchitus, etc that is causing the symptoms? Is that right? Mark Mangus: Basically, "Yup"! It is the conditions that cause symptoms that are making you feel bad - - - not the Emphysema "flaring up". Remark: Thanks for making it perfectly clear that Chronic Asthma IS a component of COPD. For solong most of us have been hearing that it was NOT a component and my doctor (exdoctor)kept telling me it was. Now I understand why he kept saying that it was theAsthma that was causing most of my problems. I have asthma attacks daily, usuallyhelped with bronchodilators but when it is not, I know that it is time to go to the hospital. Mark Mangus: I wouldn't characterize what I said as making it perfectly clear that (the formal/standard l-a-b-e-l) "Chronic Asthma" is a component of COPD. I do agree that "incompletely reversible" Asthma is a component of COPD and it is indeed 'chronic' in nature. But I do not use, nor do I like the idea of using the label/name "Chronic" with regard to the asthma we include as a component of COPD. It has not been endorsed as a standard 'name' by those responsible for establishing terminological standards While we speak of the asthma we see as a component of COPD as 'b-e-i-n-g' 'chronic', we don't call it "Chronic Asthma" (notice placement of capitals, versus deliberate omission of capital letters when chronic and asthma are 'adjectives'). Because too many folks get confused with the use of nonstandard terms and in this case also confusing terms, I would prefer to stick to the more accurate and accepted standard term "incompletely reversible Asthma". Question: To distinguish Asthma from emphysema on you pulmonary functions test is 'easily' done and fairly straight forward. How does one do it?

Mark Mangus: Significant improvement (> 15 %) in FEV-1 on a pre-and postbronchodilator Pulmonary Functions Test! Simple!
Question: In other words, there can be no significant improvement of 15% or more with emphysema --only with asthma --right? That's what you mean Mark? Mark Mangus:

What you extrapolate from what I said is absolutely correct! Emphysema is NOT confirmed by changes in response to bronchodilators! (There shouldn't BE any changes - - - unless there is and Asthma component!) The presence of Emphysema is determined by generally decreased expiratory airflow rate and characteristic and/or classic changes in lung volumes and diffusion capacities. Other information goes into making the diagnosis, but here I am referring only to PFT's. Regards,