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COPD is defined as the presence of airflow obstruction due to chronic bronchitis or emphysema. It may include a reversible component and some patients with asthma may go on to develop irreversible airflow obstruction and be included in chronic obstructive pulmonary disease.
Chronic bronchitis is defined as chronic productive cough for three months in each of two successive years when other causes of chronic cough are excluded. That includes gastroesophageal reflux disease, asthma or something like that. Emphysema is defined as abnormal permanent enlargement of air spaces distal to the terminal bronchioles. This is an airways disease, this is an alveolar disease.
The risk factors for COPD. Smoking is the most common risk factor. Passive smoking in a few patients, ambient air pollution has been implicated. We talked about hyperresponsive airways such as asthma. Gender and race, there is poor data to support these as risk.
I wanted to discuss the relationship of smoking, FEV-1 or lung function and age. This graph essentially summarizes that relationship. On the y-axis you have FEV-1 lung function and age on the x-axis. It is well-known from multiple studies that FEV-1 in everyone declines from generally about age 20-25 throughout the rest of their life.
Most of the data I showed you on the slide comes from the Lung Health study which looked at smoking cessation and COPD. What they looked at is smoking intervention versus ipratropium four times a day.
The bottom line here is that smoking cessation should be encouraged at any age to enable those patients to resume the normal rate of less rather than the accelerated loss if they continue to smoke.
These are some of the things that we use to enhance smoking cessation. We have known for a long time that behavioral approaches are probably one of the best things that we can use to get people to stop smoking.
Who you should screen if you suspect alpha1_antitrypsin deficiency? These presentations should raise your suspicions and prompt investigation. COPD in a never smoker. Very important that they were a never smoker, not a little smoker. Bronchiectasis without risk factors. Chronic sputum production without evidence of frequent infections or things that would predispose to bronchiectasis. Premature onset of emphysema. We talked about the early age. Predominance of basilar emphysema on chest x-ray.
For patients with mild to moderate disease, we usually start with a selective beta-2 agonist mainly because it has a rapid onset of action. It relieves the patient’s shortness of breath and that is why they came to see you in the first place. The problem is that if they are using it fairly frequently and this is what you need to ask them, it has more side effects than ipratropium or Atrovent and that may be an indication to add additional therapy. If you had the ipratropium or the atrovent, they can use the beta-2 agonist as needed and that may be sufficient to keep them under pretty good control. If their symptoms are uncontrolled or they complain of a lot of nighttime symptoms – they wake up, they have lots of cough, etc – you may want to add theophylline in a slow release tablet either twice a day or at bedtime or you can use salmeterol which is the long acting beta agonist, 2 puffs twice a day.
This is a list of the beta agonists. These are the specific beta-2 selective agonists on the top here. Below the line, these are the nonselective so we will have much more cardiac effects than you probably want in this age group. I just want to call your attention here to the equivalent metered dose inhaler puffs which will give you this same dose that you would be giving by nebulization. So you would have to use 27 puffs of the metered dose inhaler albuterol in order to get an equivalent dose or 2.5 mg of albuterol.
Talk about anticholinergics. Ipratropium bromide or atrovent is the only one approved. The dose in stable COPD patients is 0.5 mg. In this range, the duration is 6 to 8 hours. This was in a large study in stable COPD patients. Oxytroprium is available in Europe. It is not available in this country. Teotroprium is a longer acting anti-cholinergic.
The side effects of anticholinergics, especially inhaled anti-cholinergics, are low due to the low systemic absorption from the lungs. It reduces mucociliary clearance but it has no effect on unstimulating mucus so it is not going to change how much mucus production your chronic bronchitis patient produces on a daily basis. It may have a bitter taste. Some patients who have sprayed it into their eyes exacerbate their glaucoma problems. Paradoxic bronchoconstriction is a problem with the anti-cholinergics.