COPD

Chronic obstructive pulmonary disease COPD, affect about 6-7% of the US

population 11.4 million people (Lemone pg 1114) It is a non-reversible pulmonary
condition, which causes abnormal inflammation of the bronchioles. It is more common in
whites then blacks and affects men more frequently them women. COPD typically affects
middle age and older adults (Lemone pg 1114).
There are two different types of COPD the first condition is bronchitis. It is a
chronic inflammation of the bronchioles which causes an excess mucous production in
the bronchial tree, this condition manifest its self as a chronic cough that last for three
months and for two consecutive years (Porth, 2002).
This inflammation constricts the airways of the lungs and prohibits gas exchange,
along with thick mucus plugs that develop in the alveolar sacks. These plugs will obstruct
the airflow upon exhalation causes hypoxemia, CO2 retention. Over a period of many
years this condition will cause a decrease in the function of the ciliary hairs, which
further destroys the pulmonary tree. If left unchecked this condition can and most often
progress to emphysema.
The signs and symptoms of the chronic bronchitis client is as follows, chronic
productive cough, mostly noted in the morning with color change yellow to green, and
overweight (Blue bloaters) due to the manifestation of right sided heart failure secondary
to pulmonary hypertension which is brought on by physical deterioration of the
pulmonary circulation. The right-sided heart failure causes fluid retention enlarged liver,
JVD, edema and cardio megaly.
The emphysema client will present differently then the bronchitis client,
emphysema causes a physical changes in the structure of the lung tissue at the level of the
alveolar sacks and the alveoli/capillary bed. There is an enlargement of the alveolar air
spaces and destruction of the alveolar walls. The space between the capillary bed and the
alveoli wall is increased which limits or most often prohibits gas exchange from
occurring. Table 18-8.
This will show it self as impaired gas exchange, the airflow is diminished through
the bronchial and the restriction in the flow of air upon exhalation will increase the dead
space of the lungs. The normal client will have a peak flow (vital capacity) of about
4800ml of air (Lemone pg 1108), however due to air retention and decreased compliance
of the lung and chest wall the emphysema client will have about 300 to 500 ml. This air
trapping and hyperinflation will cause an increase in the anterior posterior diameter of the
chest causing barrel chest appearance and chronic tachypnea in an attempt to compensate
for the low vital capacity/tidal volume. This in turn will make it difficult for the client to
eat and an anorexic condition (pink puffers, figure 23.14).
Hypoxic drive is the condition that the emphysema client develops over a period
of years; it is a change in the normal body functions of the regulatory system of the
respiratory drive in the brain stem and chemoreceptors. Due to the physical changes in
the lungs and alveolar sacks, there is an increase in the space between the capillary beds
and the alveoli were gas exchange occur (figure 23.12). Under normal conditions the
space is not present and there are only four cell layers between the gas O2 and CO2 and

1
the red blood cell. Due to this space there is retention of CO2 in the blood stream and a
lack of O2 uptake from the lungs. These conditions along with the barrel chest, which
prohibits an adequate amount of airflow further, decrease the gas exchange.
Now that we realize that there is an increase in CO2 in the emphysema client how
does this affect the chemoreceptors? The normal ABG will have a PaO2 of 80-100 and a
PaCO2 of 35-45, along with a Ph of 7.35 to 7.45. The chemoreceptors located in the
carotid bodies and the aortic arch will sense changes in the level of CO2 in the blood and
increase their impulses to the respiratory center of the brain which in turn increase the
impulse and contraction the skeletal muscle of the chest notability the diaphragm,
external intercostals, scalenes and the sternocleidomastoid muscles (fig 23.14, 23.18, and
23.27).
However with an emphysema client it is not uncommon to have a CO2 level of
50-70mmHg and an O2 less an 88mmHg, which causes a drop in the Ph to below 7.35
during in exacerbation of their emphysema. Because of the increase CO2 level in the
blood it will bind to the H2O form carbonic acid H2CO3 that will rapidly convert to
Hydrogen and H2CO3 (hydrogen and bicarbonate). There needs to be a 20:1 ratio
between bicarbonate and hydrogen to cancel them selves out, it is only a matter of time
until all buffer systems fails and the client become acidotic. The over accumulation of
CO2 in the blood for a chronic period of time eight to ten years causes the chemoreceptor
to become desensitized and they no longer see changes in the CO2 level. The desensitized
receptors how change their focus from CO2 to O2 levels. Remember that the COPD
client O2 levels are normally below 92mmHg and if the level drops the receptors will
increase the impulses to the brain stem, which in turn will increase the respiratory rate.
However the Inspiratory center of the brain is more strongly stimulated by an increase of
CO2 then it is by a drop in O2 levels in the arteriole blood. As an example if a diver were
to hyperventilate cause a drop in the CO2 level and a rise in the O2 level, while
swimming under water he would consume the O2 at a faster rate then he would produce
carbon dioxide, thus causing him to pass out under water due to the lack of O2 by for the
CO2 would have a chance to rise to alert him to breath. (Tortora PG 839)
If the emphysema client is in acute distress we will administer high flow O2 along
with bronchial dilators while closely watching for changes in the respiratory effort, rate
and depth. With this is in mind it is important to remember that an emphysema client
can’t handle high flow O2 for prolong periods of time because the increase in the blood
PaO2 levels above 95-100mmHg will in fact suppress the respiratory function an stop
any and all desire to breath. The client will cease to breath and develop a life threatening
respiratory arrest. This in turn will cause the client to be placed on a ventilator, and they
will have to be weaned off of it, which in some cases is nearly impossible because of the
hypoxic drive. Any attempt to decrease the O2 level to encourage them to breath will
cause an increase in the CO2 levels, however do to the fact that an increased CO2 level
will not stimulate them to breath and before the O2 level can drop low enough to
stimulate respiration the client will develop respiratory acidosis; it causes a self-perpetual
problem.

2
Treatments:
 Albuteral inhaler Q 4-6hrs prn
 Xopenex inhaler Q 4-6 hrs
 Atrovent inhaler Q6 hrs prn
 Digoxin QD
 Lasix QD
 K-Dur 20 MEq QD
 Cipro prn
 Biaxin prn
 Advair disk
 Prednisone 10 mg alternating cycle
 Flovent inhaler
 Diflucan prn

References:
 Principles of anatomy and physiology tenth edition Tortora and Grabowski
 Medical surgical nursing third edition Lemone and Burke
 Anatomy and physiology by professor Bryan h Derrickson PH.D.
 Physical examination fourth edition Saunders by Carolyn Jarvis
 http://www-medlib.med.utah.edu/WebPath/ORGAN.html
 http://www-medlib.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html