CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Chronic obstructive pulmonary disease (COPD) is a disease of the lung. The lungs
are the organs found in the chest which are invloved in breathing. Air enters the nose and
mouth, then travels to the lungs via the trachea, which divides into smaller airways called
bronchi and, subsequently, bronchioles. (See diagram below). The lung tissue itself is a
spongy material, consisting of a series of folded membranes (the alveoli) which are located
at the ends of very fine branching air passages (bronchioles). COPD is a disease of the
smaller airways in the lungs. COPD encompases chronic obstructive bronchitis with

obstruction of small airways and emphysema with enlargement of air spaces,

destruction of lung parenchyma, loss of lung elasticity and closure of small airways.
RISK FACTORS FOR CHRONIC OBSTRUCTIVE PULMONARY DISEASE
(COPD)

Cigarette smoke is by far the most important factor in the

development of COPD. If you smoke 30 cigarettes per day, you are 20
times more likely to die from COPD than non-smokers. The more you
smoke, the greater your risk of severe disease. Smoking a pack a day
for more than 20 years is considered a significant risk in the
development of COPD. COPD is therefore largely preventable if you do
not smoke.
Familial factors: A family history of COPD may increase your risk of
having the disease. This may relate to hyper-reactive airways, a feature
of asthma.
Alpha-1-antitrypsin deficiency: This substance is found in several
places throughout the body and is important in preventing cells from
breaking down, particularly those in the lungs and liver. People who do
not have enough of this enzyme are at increased risk of emphysema
and cirrhosis of the liver.
Exposure to air pollution.
Recurrent airway infections: This may be important in the
development
and
progression
of
COPD.
Prompt
use
of antibiotics and vaccinations may help reduce the impact of
infections.
Other factors such as urbanization, social class, occupation and diet
may also have some impact in the development of COPD, but their
overall effect is not known.

Pathogenesis
Chronic obstructive pulmonary disease (COPD) is a descriptive term given to the syndrome
seen mostly in the elderly, who have airflow obstruction, not completely relieved by therapy.
At least two distinct pathological processes may occur concurrently or separately in different
subjects lead to COPD.
These are:
1. Emphysema which is due to destruction of alveolar walls
2. Chronic bronchitis with hyper secretion of mucus,

CHRONIC BRONCHITIS Chronic bronchitis is defined as a disease characterized by

hypersecretion of mucus sufficient to cause cough and sputum on most days for at least three
months in a year for two or more consecutive years. This happens in the absence of any other
specific respiratory or cardiovascular disease.
In the initial stages the inflammation of the bronchi is intermittent and recurrent, later it
becomes established. The larger air passages are affected during the early part of the disease,
later obstructive features set in when the smaller airways are also affected. Infection leads to
periodic aggravation of the symptoms and the sputum, which is mucoid, becomes purulent
during these episodes. As the airways obstruction progresses, emphysema sets in. These two
processes become established in the majority of cases so that the condition is termed chronic
bronchitis emphysema syndrome (CBES).
The disease is more common in damp, cold, and dusty regions. Atmospheric
pollution is accompanied by a higher incidence of CBES.
PATHOGENESIS
COPD encompases chronic obstructive bronchitis with obstruction of small airways and
emphysema with enlargement of air spaces, destruction of lung parenchyma,loss of lung
elasticity and closure of small airways.
The inflammatory process in COPD differs from that in asthma in several ways. The type of
inflammatory cells,inflammatory mediators, final outcome and response to treatment are
different. In COPD the inflammation affects the peripheral airways-the bronchioles. The cells
are macrophages, CD8 lymphocytes and neutrophils. The lung parenchyma is affected.
Unlike as in asthma there is no preponderance of eosinophils.Oxidative stress also plays a
significant role in the pathogenesis. Even though the lungs bear the main brunt
of the disease, systemic effects also occur. Muscle weakness and wasting may develop as part
of the systemic disorder.

.
CLINICAL FEATURES
The clinical picture is varied depending on the severity and duration. The most frequent early
symptom is cough recurring year after year, especially so in winter months.Later the cough
becomes constant. Expectoration is mucoid and the sputum is tenacious, especially on waking
up in the morning. Main complaint is the feeling of tightness of the chest.
Physical examination reveals mild wheeze which disappears as the patient clears the bronchi
by expectoration. Variable degrees of bilateral rhonchi and coarse crepitations are heard as
adventitious sounds.

Initially acute infections give rise to fever and purulent sputum. As the infection becomes
established, fever and other general symptoms come down. At this stage the quantity and
character of the sputum are more reliable indicators of infection. The sputum becomes
copious in amount when bronchiectatic changes develop.With the development of
emphysema the chest assumes the inspiratory position and the respiratory excursions are
considerably diminished. At this stage dyspnea is far out of proportion to the physical
findings in the chest.
DIAGNOSIS
Chronic bronchitis should be diagnosed from the history of recurrent cough extending over
several years,mucopurulent sputum and the physical findings of bronchial obstruction and
emphysema. X-ray is normal in the early stages but the features of emphysema may be
evident later. X-ray may be helpful in identifying precipitating conditions like pneumonia,
pneumothorax during the time of an exacerbation. HRCT is useful in quantifying the severity
of emphysematous changes and locating areas with bronchiectatic changes. Lung function
tests show reduction in vital capacity,increase in the closing volume and features of airway
obstruction . Based on the spirometry values severity of obstruction can be categorised as
mild,moderate severe and very severe.
EMPHYSEMA Emphysema is defined as a pathological increase in the size of airspaces
distal to the terminal bronchioles, with destruction of the alveolar walls. The term
hyperinflation is used to denote non-pathological overdistension.

Etiology
Diseases of the airways: Chronic bronchitis, prolonged exposure to irritants and dusts (heavy
cigarette smoking),and chronic partial bronchial obstruction.
Conditions associated with alpha-1 antitrypsin deficiency:Persons who have alpha-1
antitrypsin deficiency develop emphysema by the third or fourth decade of life.
Chronic bronchial asthma leads on to emphysema as a sequel. Persons who have to hold
breath for prolonged periods for diving under water for collecting shells, clayand the like
develop emphysema over a period of 15-20years. Bidi or cigarette smoking and repeated
respiratory infections accelerate the process.Several pneumoconioses give rise to emphysema
as part of the pathological process or as compensatory mechanism, e.g. coal workers
pneumoconiosis, silicosis.
Occupational causes: Several occupations which require forced expiratory effort as seen in
furnace blowers,goldsmiths, and users of wind instruments predispose to the development of
emphysema in susceptible subjects.
Exposure to cadmium leads to the development of emphysema and pulmonary fibrosis.

Pathology: The lungs are in the inflated position occupying the whole of the pleural cavity.
Since the elastic tissue is damaged, the lungs lose their elasticity and they fail to collapse
when the chest is opened during autopsy. The diaphragm is depressed and respiratory
excursions are diminished. The alveoli are overdistended. The septa rupture and
neighbouring alveoli coalesce to form air cysts. The pulmonary vascular bed is progressively
diminished and pulmonary arterial hypertension results.Reduction of alveolar surface area
leads to impairment of gas exchange. Right ventricular hypertrophy and corpulmonale may
develop. Emphysematous bullae may rupture to produce spontaneous pneumothorax.
CLINICAL FEATURES
The main symptom is exertional dyspnea. As the condition progresses, even ordinary activity
like talking, eating or lying flat may cause dyspnea.The chest is distended in the position of
full inspiration. Expansion is diminished and the accessory muscles of respiration are active.
Expiration becomes an active process due to loss of elasticity of the lung. Infective episodes
occur frequently.
Physical examination reveals barrel-shaped chest with diminished expansion, hyperresonance on percussion,obliteration of cardiac and liver dullness and diminished breath
sounds with prolonged expiration. Due to increased intrathoracic pressure especially during
expiration, the neck veins become distended during expiration and collapse during
inspiration. The apex beat is felt feebly because of interposition of the distended lung. Right
ventricular hypertrophy produces a heaving impulse in the epigastrium and subxiphoid
region. Left parasternal heave may not be evident on account of the inflated lung covering the
heart
SPECIAL FORMS OF EMPHYSEMA
Compensatory emphysema: This is the condition in which the normal lung tissue undergoes
hypertrophy to compensate for extensive damage to the other lung or other parts of the same
lung. Being a compensatory phenomenon, this is asymptomatic. The respiratory excursion of
the normal lung is increased in this case.
Atrophic emphysema: This condition is the result of senile atrophy of inter-alveolar septa.
The total lung volume is not increased.
Bullous emphysema: In this condition air spaces exceeding 1 cm in diameter develop either
congenitally or as a part of acquired generalized emphysema. With passage of time these
bullae enlarge and become giant bullous emphysema. They may rupture to produce
pneumothorax. At times the bullae may get infected to produce abscesses
ANOTHER TYPE
There are two main types of emphysema, based on the changes taking place in
the lung: panlobular (panacinar) and centrilobular (centroacinar)
Both types may occur in the same patient.
In the panlobular (panacinar) type, there is destruction of the respiratory
bronchiole, alveolar duct, and alveoli. All air spaces within the lobule are
essentially enlarged, but there is little inflammatory disease. The patient with
this type of emphysema typically has a hyperinflated (hyperexpanded) chest
(barrel chest on physical examination), marked dyspnea on exertion, and weight
loss. To move air into and out of the lungs, negative pressure is required during
inspiration, and an adequate level of positive pressure must be attained and
maintained during expiration.The resting position is one of inflation. Instead of
being an involuntary passive act, expiration becomes active and requires mus
.
In the centrilobular (centroacinar) form, pathologic changes take place
mainly in the center of the secondary lobule, preserving the peripheral portions

of the acinus. Frequently, there is a derangement of ventilationperfusion ratios,

producing chronic hypoxemia, hypercapnia (increased CO2 in the arterial
blood),polycythemia, and episodes of right-sided heart failure. This leads to
central cyanosis, peripheral edema, and respiratory failure.The patient may
receive diuretic therapy for edema.

Alpha-1 Antitrypsin Deficiency

Alpha-1 antitrypsin (AAT) is one among the serine protein inhibitors which occurs in the
plasma. It is an inhibitor of neutrophil elastase. It has also got anti-inflammatory properties.
AAT is a glycoprotein normally secreted by the liver and circulating in blood. It moves with
the alpha-I band on serum protein electrophoresis. 90% of the trypsininhibitory activity of
serum is attributable to AAT.From the plasma, AAT diffuses into lung tissues, where it acts as
an anti-elastase, the elastase being secreted by neutrophils. Elastase is capable of destroying
the connective tissue framework of alveolar walls. Excessive destruction of alveolar walls
may lead to emphysema.Cigarette smoking which predisposes to accumulation of neutrophils
in the lung aggravates the destructive process.Cigarette smoke also inhibits AAT directly.
AAT deficiency may be congenital or acquired. The gene frequency of the defect occurs in 1
in 2000 to 1 in 5000 of the population. In the congenital form it is transmitted as an
autosomal recessive. More than 75 alleles of AAT gene are known. In the inherited form the
hepatic production of AAT is less than 15% of normal.Patients with AAT deficiency develop
panacinar emphysema by the third or fourth decade of life. The congenital form may also be
associated with hepatitis and jaundice in the newborn and cirrhosis liver in adults. Such
patients show accumulation of abnormal AAT in hepatocytes.AAT deficiency can be treated
by replacing AAT byIV infusion weekly or monthly to individuals whose serum AAT levels
are below 1 mmol/L and who have abnormal lung functions. AAT for therapeutic purposes is
obtained from pooled plasma. AAT can also be administered as an aerosol.
PATHOPHYSIOLOGY
COPD develops as a significant and chronic inflammatory response to inhaled
irritants. Chronic bacterial infections may also add to this inflammatory state. The
inflammatory cells involved include neutrophil granulocytes and macrophages, two types of
white blood cell. Those who smoke additionally haveTc1 lymphocyte involvement and some
people with COPD have eosinophil involvement similar to that in asthma. Part of this cell
response is brought on by inflammatory mediators such as chemotactic factors. Other
processes involved with lung damage include oxidative stress produced by high
concentrations of free radicals in tobacco smoke and released by inflammatory cells, and
breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited
by protease inhibitors. The destruction of the connective tissue of the lungs is what
leads to emphysema, which then contributes to the poor airflow and, finally, poor
absorption and release of respiratory gases.General muscle wasting that often occurs
in COPD may be partly due to inflammatory mediators released by the lungs into the
blood.
Narrowing of the airways occurs due to inflammation and scarring within them. This
contributes to the inability to breathe out fully. The greatest reduction in air flow
occurs when breathing out, as the pressure in the chest is compressing the airways
at this time. This can result in more air from the previous breath remaining within the lungs
when the next breath is started, resulting in an increase in the total volume of air in the lungs
at any given time, a process called hyperinflation or air trapping.Hyperinflation from exercise
is linked to shortness of breath in COPD, as it is less comfortable to breathe in when the
lungs are already partly full.
Some also have a degree of airway hyper responsiveness to irritants similar to those found
in asthma. Low oxygen levels and, eventually, high carbon dioxide levels in the blood can
occur from poor gas exchange due to decreased ventilation from airway obstruction,

hyperinflation and a reduced desire to breathe. During exacerbations, airway inflammation is

also increased, resulting in increased hyperinflation, reduced expiratory airflow and
worsening of gas transfer. This can also lead to insufficient ventilation and, eventually, low
blood oxygen levels. Low oxygen levels, if present for a prolonged period, can result
in narrowing of the arteries in the lungs, while emphysema leads to breakdown of capillaries
in the lungs. Both these changes result in increased blood pressure in the pulmonary
arteries, which may cause cor pulmonale.

The main pathological process can be summarized as follows:

1. Inflammation of the bronchi with enlargement of mucous glands and smooth muscle
hyperplasia, all leading to wall thickening
2. Acinar distension due to the destruction of lung parenchyma probably mediated by
imbalance of protease-antiprotease (alpha-1 antitrypsin) enzymes causing loss of support of
small airways
3. Fibrosis and narrowing of the airways leading to increase in airway resistance.
The capillary bed is distorted and truncated and this aggravates the progression of pulmonary
arterial hypertension. The pulmonary arteries become distended and atheromatous.
Pulmonary hypertension gives rise to right ventricular hypertrophy and dilatation. Chronic

corpulmonale

supervenes

as

time

passes.

SYMPTOMS
HISTORY

The three most common symptoms in COPD are cough, sputum production, and exertional
dyspnea. A careful history, however, usually reveals the presence of symptoms prior to the
acute exacerbation. The development of exertional dyspnea, often described as increased
effort to breathe, heaviness, air hunger, or gasping, can be insidious. It is best elicited by a
careful history focused on typical physical activities and how the patients ability to perform
them has changed.Activities involving significant arm work, particularly at or above shoulder
level, are particularly difficult for patients with COPD.
As COPD advances, the principal feature is worsening dyspnea on exertion with increasing
intrusion on the ability to perform vocational or avocational activities.In the most advanced
stages, patients are breathless doing simple activities of daily living.Accompanying
worsening airflow obstruction is an increased frequency of exacerbations (described below).
Patients may also develop resting hypoxemia and require institution of supplemental oxygen.
PHYSICAL FINDINGS

In the early stages of COPD, patients usually have an entirely normal physical examination.
Current smokers may have signs of active smoking, including an odor of smoke or nicotine
staining of fingernails. In patients with more severe disease, the physical examination is
notable for a prolonged expiratory phase and may include expiratory wheezing. In addition,
signs of hyperinflation include a barrel chest and enlarged lung volumes with poor
diaphragmatic excursion as assessed by percussion. Patients with severe airflow obstruction
may also exhibit use of accessory muscles of respiration, sitting in the characteristic tripod
position to facilitate the actions of the sternocleidomastoid, scalene, and intercostals muscles.
Patients may develop cyanosis, visible in the lips and nail beds.Although traditional teaching

is that patients with predominant emphysema, termed pink puffers, are thin and
noncyanotic at rest and have prominent use of accessory muscles, and
patients with chronic bronchitis are more likely to be heavy and cyanotic (blue bloaters),
current evidence demonstrates that most patients have elements of both bronchitis and
emphysema and that the physical examination does not reliably differentiate the two
entities.Advanced disease may be accompanied by systemic wasting, with significant weight
loss,bitemporal wasting, and diffuse loss of subcutaneous adipose tissue. This syndrome has
been associated with both inadequate oral intake and elevated levels of inflammatory
cytokines (TNF-). Such wasting is an independent poor prognostic factor in COPD. Some
patients with advanced disease have paradoxical inward movement of the rib cage with
inspiration (Hoovers sign), the result of alteration of the vector of diaphragmatic contraction
on the rib cage as a result of chronic hyperinflation.Signs of overt right heart failure, termed
cor pulmonale, are relatively infrequent since the advent of supplemental oxygen therapy.
Clubbing of the digits is not a sign of COPD, and its presence alert the clinician to initiate an
investigation for causes of clubbing. In this population, the development of lung cancer is the
most likely explanation for newly developed clubbing.
Often the cough will be associated with sputum production that is whitish
in color, mucoid in quality and is worse in the morning. During acute
exacerbations the mucus will often turn purulent and the patient may
have a fever. Some patients will have a history of hemoptysis.
Anteriorposterior diameter of the chest may be increased. cyanosis, signs
of right heart failure (cor pulmonale) including enlarged tender liver, neck
vein distention especially during expiration.
Key Indicators for Considering the Diagnosis of COPD
Chronic cough: Present intermittently or every day. Often present throughout the day;
seldom only nocturnal Chronic sputum Any pattern of chronic sputum production: production
may indicate COPD
Acute bronchitis: Repeated episodes
Dyspnea that is: Progressive (worsens over time), Persistent (present every day)
Worse on exercise, Worse during respiratory, infections
History of exposure to Tobacco smoke (including risk factors: popular local preparations)
Occupational dusts and chemicals and smoke from home cooking and heating fuel.
Diagnosis: Chronic bronchitis should be diagnosed from the history of recurrent cough
extending over several years, muco purulent sputum and the physical findings of bronchial
obstruction and emphysema. X-ray is normal in the early stages but the features of
emphysema may be evident later. X-ray may be helpful in identifying precipitating
conditions like pneumonia, pneumothorax during the time of an exacerbation. HRCT is
useful in quantifying the severity of emphysematous changes and locating areas with
bronchiectatic changes. Lung function tests show reduction in vital capacity,increase in the
closing volume and features of airway obstruction Based on the spirometry values severity
of obstruction can be categorised as mild,moderate severe and very severe.
computed tomography scan of the chest may show the distribution of emphysema
throughout the lungs and can also be useful to exclude other lung diseases.Unless surgery
is planned, however, this rarely affects management.
An analysis of arterial blood is used to determine the need for oxygen; this is
recommended in those with an FEV1 less than 35% predicted, those with a peripheral
oxygen saturation of less than 92% and those with symptoms of congestive heart failure.

In areas of the world where alpha-1 antitrypsin deficiency is common, people with COPD
(particularly those below the age of 45 and with emphysema affecting the lower parts of the
lungs) should be considered for testing.
Check pulmonary function tests (PFTs). Two main components are measured to
make the diagnosis: the forced expiratory volume in one second (FEV 1), which is the
greatest volume of air that can be breathed out in the first second of a breath, and the forced
vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single
large breath. Normally, 7580% of the FVC comes out in the first second and a FEV1/FVC
ratio of less than 70% in someone with symptoms of COPD defines a person as having the
disease.Based on these measurements, spirometry would lead to over-diagnosis of COPD in
the elderly. The National Institute for Health and Care Excellence criteria additionally require
a FEV1 of less than 80% of predicted.
MRC shortness of breath scale

Grade

Activity affected

Only strenuous activity

Vigorous walking

With normal walking

After a few minutes of walking

With changing clothing

GOLD grade

Severity

FEV1 % predicted

Mild (GOLD 1)

80

Moderate (GOLD 2)

5079

Severe (GOLD 3)

3049

Very severe (GOLD 4)

<30 or chronic respiratory failure

Prevention
Most cases of COPD are potentially preventable through decreasing exposure to smoke and
improving air quality.Annual influenza vaccinations in those with COPD reduce
exacerbations, hospitalizations and death..Pneumococcal vaccination may also be beneficial.
TREATMENT Management of chronic respiratory failure: When hypoxemia becomes severe,
i.e. PaO2 below 55 mm Hg or SaO2 below 80% at rest, continuous oxygen inhalation may have
to be instituted for at least 18 hours a day. Oxygen therapy helps to reduce pulmonary arterial tension
and allay cor pulmonale. In intractable cases lung transplantation may
have to be considered.

Table 1
SMOKES, a consultation checklist for chronic obstructive pulmonary disease

S: smoking cessation
M: medication - inhaled bronchodilator, vaccines (influenza, pneumococcus), stop
unnecessary treatment (nebuliser, inhaled corticosteroids)
O: oxygen - is it needed?
K: komorbidity - cardiac dysfunction, sleep apnoea, osteoporosis, depression, asthma
E: exercise and rehabilitation
S: surgery - lung volume reduction surgery, single-lung transplantation
general measures: Most effective single step to prevent deterioration is to stop smoking. This single
measure itself affords considerable relief of symptoms.Environmental allergens and pollutants must
be avoided
by the patient.
Other general measures include improvement in general health, regular exercise, deep-breathing
exercises,adequate sleep, treatment of obesity, and eradication of foci of sepsis in the throat, nose and
paranasal sinuses. If these measures are started during the early phase of the disease, further
progression can be arrested. Steam inhalations help to improve vital capacity, relieve

:DRUG THERAPY
Bronchodilators

Inhaled bronchodilators are the primary medications used. There are two major
types, 2 agonists and anticholinergics; both exist in long-acting and short-acting forms. They
reduce shortness of breath, wheeze and exercise limitation, resulting in an improved quality
of life. then inhaled corticosteroids are typically added. With respect to long-acting agents, it
is unclear if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs)
are better, and it may be worth trying each and continuing the one that worked best .Both
types of agent appear to reduce the risk of acute exacerbations by 1525%.While both may
be used at the same time, any benefit is of questionable significance.short-acting 2 agonists
available including salbutamol (Ventolin) and terbutaline.They provide some relief of
symptoms
for
four
to
six
hours. Long-acting
2 agonists
such
as salmeterol and formoterol are often used as maintenance therapy.
There are two main anticholinergics used in COPD, ipratropium and tiotropium. Ipratropium
is a short-acting agent while tiotropium is long-acting. Tiotropium is associated with a
decrease in exacerbations and improved quality of life, and tiotropium provides those
benefits better than ipratropium.It does not appear to affect mortality or the over all
hospitalization rate.
Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated
with increased risk of heart disease and stroke.
Corticosteroids
Corticosteroids are usually used in inhaled form but may also be used as tablets to treat and
prevent acute exacerbations. While inhaled corticosteroids (ICS) have not shown benefit for
people with mild COPD, they decrease acute exacerbations in those with either moderate or
severe disease. prednisolone 30-40 mg daily for 14 days
Other medication
Long-term antibiotics, specifically those from the macrolide class such as erythromycin,
reduce the frequency of exacerbations in those who have two or more a year. This practice
may be cost effective in some areas of the world. Concerns include that of antibiotic
resistance and
hearing
problems
with azithromycin. Methylxanthines such
as
theophylline generally cause more harm than benefit and thus are usually not
recommended, but may be used as a second-line agent in those not controlled by other
measures.
Mucolytics may be useful in some people who have very thick mucous but are generally not
needed. Cough medicines are not recommended.
alpha-1-antitrypsin deficiency, may also be treated with weekly or monthly injections of
alpha-1-antitrypsin.
Oxygen therapy
If you have severe airflow limitation you may require home oxygen therapy, sometimes for
up to 19 hours per day. Oxygen can be administered via nasal prongs (small plastic tubes
into your nose) or via a mask. This treatment has been shown to prolong life in patients with
severe COPD who have stopped smoking. The best benefit from oxygen treatment is
obtained if you have quit smoking. Furthermore, oxygen is flammable, so smoking is in fact
dangerous during this treatment. Nonpharmacological measures: Noninvasive positive pressure
ventilation and oxygen therapy at home using a simple nasal mask which eliminates the need for
endotracheal intubation is beneficial. Long-term oxygen therapy has shown improved survival with
better quality of life.
SURGICAL MANAGEMENT
Bullectomy. A bullectomy is a surgical option for select patients with bullous emphysema. Bullae are
enlarged airspaces that do not contribute to ventilation but occupy space in the thorax;

these areas may be surgically excised. Many times these bullae compress areas of the lung that do
have adequate gas exchange.Bullectomy may help reduce dyspnea and improve lung function. It can
be done thoracoscopically (with a video-assisted thoracoscope) or via a limited thoracotomy incision
Lung volume reduction surgery (LVRS): This has been found to be useful in selected cases. The
rationale for this technique is to reduce the volume of over inflated emphysematous lung by 20-30%,
in order to improve the elastic recoil of the lungs, to improve the configuration of the diaphragm,
chest wall mechanics and gas exchange.
Lung transplantation: This procedure is in vogue for more than a decade in advanced countries, it is
still not available in India. Transplantation of a single lung or both heart and lungs as a whole is
possible. Transplantation should be considered if the recipient is below 55 years of age, and is free
from underlying conditions such as advanced diabetes, malignancy, hepatic or renal failure and
conditions which impair mechanics of the chest wall.
The donor should be ABO and HLA compatible with normal lungs, preferably between 12 and 50
years of age and with normal cardiopulmonary anatomy. Usually cadaver lungs are used for
transplantation. Complications may occur as in the case of any other major organ
transplantation.
Indications
1. Incurable respiratory failurechronic or acute due to
pulmonary causes
2. Irreversible structural and functional abnormalities in
the lung such as fibrosis, extensive bronchiectasis,
cystic disease, emphysema and others.
Other

Vaccinations:
It
is
important
that
you
have
your
yearly influenza vaccination, and pneumococcal vaccine. This will help reduce
effective exacerbations from these infections;

Diuretics: If your chronic bronchitis is complicated by right heart failure,

you may be treated with tablets to remove the excess fluid;

Acute exacerbations of COPD: Acute attacks should be treated with

bronchodilators, supplemental oxygen, antibiotics and glucocorticoids;

Depression: COPD is a chronic disease that may lead to significant

disability, so some patients may become depressed. Counselling
and antidepressant medications may help you overcome this;

Weight control: It is important that you maintain a healthy weight and

nutrition. In advanced disease you may notice marked weight loss. You should
have a high fat content and nutritious diet to prevent muscle wasting.
Alternatively, if you are markedly overweight or obese you should try to
reduce your weight to a healthy range with diet an exercise, in order to reduce
demands on your lung function.
COPD OF COMPLICATIONS:
Secondary polycythaemia: This is an increase in the number of red blood cells
in the blood to try to compensate for reduced oxygen levels. The blood
subsequently becomes thicker with sluggish flow which can lead to clotting;
Hypoxaemic respiratory failure (type I respiratory failure): PaO2 is less than 60 mm Hg
(8 kPa) with a normal or low PaCO2. This is caused by ventilation-perfusion mismatch with
either/both:

Under-ventilated
asthma).

alveoli

(eg pulmonary

oedema, pneumonia or acute

Venous blood bypasses ventilated alveoli (eg right to left cardiac shunts).

Hyperventilation increases CO2 removal but does not increase oxygenation,

as blood leaving unaffected alveoli is almost fully saturated.

Hypercapnic respiratory failure (type II respiratory failure): PaCO2 is more than 50

mm Hg (6.5 kPa) and indicates inadequate alveolar ventilation. Any ventilationperfusion mismatch will affect PaO2 and therefore hypoxaemia is also common.
Respiratory failure may be acute or chronic

Acute hypercapnic respiratory failure develops over minutes to hours. The pH is

usually therefore less than 7.3.

Chronic respiratory failure develops over several days or longer. There is sufficient
time for renal compensation and an increase in bicarbonate so the pH is usually only
slightly

decreased.

Clinical

markers

of

long-standing

polycythaemia and cor pulmonale.

Causes-Common causes of type I respiratory failure

Chronic obstructive pulmonary disease (COPD).

Pneumonia.

Pulmonary oedema.

Pulmonary fibrosis.

Asthma.

Pneumothorax.

Pulmonary embolism.

Pulmonary hypertension.

Cyanotic congenital heart disease.

Bronchiectasis.

hypoxaemia

include

Acute respiratory distress syndrome.

Kyphoscoliosis.

Obesity

Add notes to aCommon causes of type II respiratory failure

COPD.

Severe asthma.

Drug overdose, poisoning.

Myasthenia gravis.

Polyneuropathy.

Poliomyelitis.

Muscle disorders.

Head injuries and neck injuries.

Obesity.

Pulmonary oedema.

Adult respiratory distress syndrome.

Hypothyroidism.

Pneumothorax: This is leakage of air from the lung into the surrounding
pleural space due to rupture of a bulla (dilated air space). This can lead to
collapse of the lung and may require insertion of a chest drain;
Respiratory failure: This is often caused by acute infective exacerbations.
Death can sometimes occur from a severe decline in respiratory function.
Cor pulmonale is failure of the right side of the heart, the side that pumps blood to the
lungs. This problem occurs when the heart has to work harder to pump blood through
damaged lungs, such as when a person's lungs are damaged because of chronic obstructive
pulmonary disease (COPD).People with cor pulmonale are short of breath because of their
damaged lungs. They may have swollen legs and a swollen abdomen because of fluid

retention (edema).Pneumonia is a lung infection that can make you very sick. You may
cough, run a fever, and have a hard time breathing. It can usually be treated at home, but
some people need to go to the hospital. Pneumonia can be caused by bacteria or a virus.
Antibiotics are used to treat pneumonia caused by bacteria.

NURSING MANAGEMENT
patient education

Patient education is a major component of pulmonary rehabilitation and includes

a broad variety of topics. Depending on the length and setting of the program,
topics may include normal anatomy and physiology of the lung, pathophysiology
and changes with COPD, medications and home oxygen therapy, nutrition,
respiratory therapy treatments, symptom alleviation, smoking cessation,
sexuality and COPD, coping with chronic disease,communicating with the health
care team, and planning for the future (advance directives, living wills, informed
decision making about health care alternatives).

Pulmonary rehabilitation
Chest physiotherapy has been shown to help remove fluid in the airways. Various
techniques are available such as steam inhalation, which assists sputum removal and
improves your ventilation. Your doctor will also enter you into exercise or pulmonary
rehabilitation programs which have been shown to increase exercise tolerance, relieve
symptoms and improve your quality of life. Blowing into an air pillow repeatedly for 10-15 times
twice a day and bending over a pillow held firmly on to the abdomen, in order to push the diaphragm
up during expiration are simple maneuvers which can be practised at home.
Breathing Exercises.
The breathing pattern of most people with COPD is shallow, rapid, and
inefficient; the more severe the disease, the more inefficient the breathing
pattern. With practice,this type of upper chest breathing can be changed to
diaphragmatic breathing, which reduces the respiratory rate, increases alveolar
ventilation, and sometimes helps expel as much air as possible during expiration
(technique). Pursedlip breathing helps to slow expiration, prevents collapse of
small airways, and helps the patient to control the rate and depth of respiration.It
also promotes relaxation, enabling the patient to gain control of dyspnea and
reduce feelings of panic.
Inspiratory Muscle Training.
Once the patient masters diaphragmatic breathing, a program of inspiratory
muscle training
may be prescribed to help strengthen the muscles used in breathing. This
program requires that the patient breathe against resistance for 10 to 15
minutes every day. As the resistance is gradually
increased, the muscles become better conditioned. Conditioning of the
respiratory muscles takes time, and the patient is instructed to continue
practicing at home
Activity Pacing.
A patient with COPD has decreased exercise tolerance during specific periods of
the day. This is especially true on arising in the morning, because bronchial
secretions collect in the lungs during the night while the person is lying down.
The patient may have difficulty bathing or dressing. Activities requiring the arms
to be supported above the level of the thorax may produce fatigue or respiratory
distress but may be tolerated better after the patient has been up and moving
around for an hour
or more. Working with the nurse, the patient can reduce these limitations by
planning self-care activities and determining the best time for bathing, dressing,
and daily activities.
Self-Care Activities.

As gas exchange, airway clearance, and the breathing pattern improve, the
patient is encouraged to assume increasing participation in self-care activities.
The patient is taught to coordinate diaphragmatic breathing with activities such
as walking, bathing, bending, or climbing stairs. The patient should bathe, dress,
and take short walks, resting as needed to avoid fatigue and excessive dyspnea.
Fluids should always be readily available, and the patient should begin to drink
fluids without having to be reminded. If postural drainage is to be done at home,
the nurse instructs and supervises the patient before discharge or in the
outpatient setting.
Physical Conditioning.
Physical conditioning techniques include breathing exercises and general
exercises intended to conserve energy and increase pulmonary ventilation. There
is a close relationship between physical fitness and respiratory fitness.Graded
exercises and physical conditioning programs using treadmills, stationary
bicycles, and measured level walks can improve symptoms and increase work
capacity and exercise tolerance. Any physical activity that can be done regularly
is helpful. Lightweight portable oxygen systems are available for ambulatory
patients who require oxygen therapy during physical
activity.
Oxygen Therapy. Oxygen supplied to the home comes in compressed gas,
liquid, or concentrator systems. Portable oxygen systems allow the patient to
exercise, work, and travel. To help the
patient adhere to the oxygen prescription, the nurse explains the proper flow
rate and required number of hours for oxygen use as well as the dangers of
arbitrary changes in flow rates or duration
of therapy. The nurse cautions the patient that smoking with or near oxygen is
extremely dangerous. The nurse also reassures the patient that oxygen is not
addictive and explains the need for regular evaluations of blood oxygenation
by pulse oximetry or arterial blood gas analysis.
Nutritional Therapy.
Nutritional assessment and counseling are important aspects in the rehabilitation
process for the patient with COPD. Approximately 25% of patients with COPD are
undernourished .A thorough assessment of caloric needs and counseling about
meal planning and supplementation are part of the
rehabilitation process.
Coping Measures.
Any factor that interferes with normal breathing quite naturally induces anxiety,
depression, and changes in behavior. Many patients find the slightest exertion
exhausting.Constant shortness of breath and fatigue may make the patient
irritable and apprehensive to the point of panic. Restricted activity(and reversal
of family roles due to loss of employment), the frustration of having to work to
breathe, and the realization that the disease is prolonged and unrelenting may
cause the patient to
react with anger, depression, and demanding behavior. Sexual function may be
compromised, which also diminishes self-esteem. In addition, the nurse needs to
provide education and support to
the spouse/significant other and family because the caregiver role in end-stage
COPD can be difficult.
NURSING PRIORITIES
1.

Maintain airway patency.

2.

Assist with measures to facilitate gas exchange.

3.

Enhance nutritional intake.

4.

Prevent complications, slow progression of condition.

5.

Provide information about disease process/prognosis and treatment

regimen.

Discharge Goals
1.

Ventilation/oxygenation adequate to meet self-care needs.

2.

Nutritional intake meeting caloric needs.

3.

Infection treated/prevented.

4.

Disease process/prognosis and therapeutic regimen understood.

5.

Plan in place to meet needs after discharge.

1. Ineffective Airway Clearance

Nursing Diagnosis

Ineffective Airway Clearance

May be related to

Bronchospasm

Increased production of secretions; retained secretions; thick, viscous

secretions

Allergic airways

Hyperplasia of bronchial walls

Decreased energy/fatigue

Possibly evidenced by

Statement of difficulty breathing

Changes in depth/rate of respirations, use of accessory muscles

Abnormal breath sounds, e.g., wheezes, rhonchi, crackles

Cough (persistent), with/without sputum production

Desired Outcomes

Maintain airway patency with breath sounds clear/clearing.

Demonstrate

behaviors

to

improve

effectively and expectorate secretions.

airway

clearance,

e.g.,

cough

Nursing Interventions

Rationale

Auscultate breath sounds. Note adventitious breath

Some degree of bronchospasm is present

sounds (wheezes, crackles, rhonchi).

obstructions in airway and may or may n

manifested in adventitious breath sounds su

scattered, moist crackles (bronchitis); faint so

with expiratory wheezes (emphysema); or a

breath sounds (severe asthma).
Assess and monitor respirations and breath sounds,

Tachypnea is usually present to some degree an

noting rate and sounds (tachypnea, stridor, crackles,

be pronounced on admission or during stre

wheezes). Note inspiratory and expiratory ratio.

concurrent acute infectious process. Respiration

be shallow and rapid, with prolonged expirat

comparison to inspiration.
Note presence and degree of dyspnea as for reports

Respiratory dysfunction is variable depending o

of air hunger, restlessness, anxiety, respiratory

underlying process such as infection, allergic rea

distress, use of accessory muscles. Use 010 scale or

and the stage of chronicity in a patient

American Thoracic Societys Grade of Breathlessness

established COPD. Note: Using a 010 scale t

Scale

Ascertain

dyspnea aids in quantifying and tracking chan

precipitating factors when possible. Differentiate acute

respiratory distress. Rapid onset of acute dy

episode from exacerbation of chronic dyspnea.

may reflect pulmonary embolus.

Assist patient to assume position of comfort (elevate

Elevation of the head of the bed facilitates resp

head of bed, have patient lean on overbed table or sit

function by use of gravity; however, patient in s

on edge of bed).

distress will seek the position that most

to

rate

breathing

difficulty.

breathing. Supporting arms and legs with

pillows, and so on helps reduce muscle fatigu

can aid chest expansion.
Keep environmental pollution to a minimum such

Precipitators of allergic type of respiratory rea

as dust, smoke, and feather pillows, according to

that can trigger or exacerbate onset of acute epis

individual situation.
Encourage

abdominal

or

pursed-lip

breathing

Provides

patient

with

some

means

to

Nursing Interventions

Rationale

exercises.

with or control dyspnea and reduce air-trapping.

Observe characteristics of cough (persistent, hacking,

Cough can be persistent but ineffective, espec

moist). Assist with measures to improve effectiveness

patient is elderly, acutely ill, or debilitated. Cough

of cough effort.

most effective in an upright or in a head-down po

after chest percussion.

Increase fluid intake to 3000 mL per day within cardiac

Hydration helps decrease the viscosity of secre

tolerance. Provide warm or tepid liquids. Recommend

facilitating expectoration. Using warm liquids

intake of fluids between, instead of during, meals.

decrease bronchospasm. Fluids during meal

increase gastric distension and pressure o

diaphragm.
Monitor and graph serial ABGs, pulse oximetry, chest

Establishes baseline for monitoring progressi

x-ray.

regression of disease process an complications.

Pulse oximetry readings detect changes in satu

as they are happening, helping to identify

before patient is symptomatic. However, studies

shown that the accuracy of pulse oximetry m

questioned

if

patient

has

vasoconstriction.
2. Impaired Gas Exchange
Nursing Diagnosis

Impaired Gas Exchange

May be related to

Altered

oxygen

supply

(obstruction

bronchospasm; air-trapping)

Alveoli destruction

Alveolar-capillary membrane changes

Possibly evidenced by

Dyspnea

of

airways

by

secretions,

severe

peri

Abnormal breathing

Confusion, restlessness

Inability to move secretions

Abnormal ABG values (hypoxia and hypercapnia)

Changes in vital signs

Reduced tolerance for activity

Desired Outcomes

Demonstrate improved ventilation and adequate oxygenation of tissues by

ABGs within patients normal range and be free of symptoms of respiratory
distress.

Participate in treatment regimen within level of ability/situation.

Nursing Interventions

Rationale

Assess and record respiratory rate, depth. Note use of

Useful in evaluating the degree of respiratory d

accessory muscles, pursed-lip breathing, inability to

or chronicity of the disease process.

speak or converse.
Elevate head of bed, assist patient to assume position

Oxygen delivery may be improved by upright po

to ease work of breathing. Include periods of time in

and breathing exercises to decrease airway co

prone position as tolerated. Encourage deep-slow or

dyspnea,

pursed-lip

research supports use of prone position to inc

breathing

as

individually

needed

or

and

work

of

breathing.

Note: R

tolerated.

Pao2.

Assess and routinely monitor skin and mucous

Cyanosis may be peripheral (noted in nailbe

membrane color.

central (noted around lips/or earlobes). Duskines

central cyanosis indicate advanced hypoxemia.

Encourage expectoration of sputum; suction when

Thick, tenacious, copious secretions are a

indicated.

source of impaired gas exchange in small ai

Deep suctioning may be required when cou

ineffective for expectoration of secretions.
Auscultate breath sounds, noting areas of decreased

Breath sounds may be faint because of decr

airflow and adventitious sounds.

airflow or areas of consolidation. Presence of wh

may indicate bronchospasm or retained secre

Nursing Interventions

Rationale

Scattered moist crackles may indicate interstitia

or cardiac decompensation.
Palpate for fremitus.

Decrease of vibratory tremors suggests fluid col

or air-trapping.

Monitor level of consciousness and mental status.

Restlessness and anxiety are common manifest

Investigate changes.

of

hypoxia.

Worsening

ABGs

accompanie

confusion/ somnolence are indicative of ce

dysfunction due to hypoxemia.
Evaluate level of activity tolerance. Provide calm, quiet

During severe, acute or refractory respiratory dis

environment. Limit patients activity or encourage bed

patient may be totally unable to perform basic

or chair rest during acute phase. Have patient resume

care activities because of hypoxemia and dys

activity

Rest interspersed with care activities remain

gradually

and

increase

as

individually

tolerated.

important part of treatment regimen. An ex

program is aimed at increasing endurance

strength without causing severe dyspnea an

enhance sense of well-being.
Evaluate sleep patterns, note reports of difficulties and

Multiple external stimuli and presence of dyspne

whether patient feels well rested. Provide quiet

prevent relaxation and inhibit sleep.

environment, group care or monitoring activities to

allow

periods

of

uninterrupted

sleep;

limit

stimulants such as caffeine; encourage position of

comfort.
Monitor vital signs and cardiac rhythm.

Tachycardia, dysrhythmias, and changes in B

reflect effect of systemic hypoxemia on c

function.
3. Imbalanced Nutrition
Nursing Diagnosis

Nutrition: imbalanced, less than body requirements

May be related to

Dyspnea; sputum production

Medication side effects; anorexia, nausea/vomiting

Fatigue

Possibly evidenced by

Weight loss; loss of muscle mass, poor muscle tone

Reported altered taste sensation; aversion to eating, lack of interest in

food

Desired Outcomes

Display progressive weight gain toward goal as appropriate.

Demonstrate

behaviors/lifestyle

changes to regain

and/or maintain

appropriate weight.
Nursing Interventions

Rationale

Ascertain understanding of individual nutritional needs

To determine informational needs of client and S

Assess dietary habits, recent food intake. Note degree

Patient in acute respiratory distress is often ano

of difficulty with eating. Evaluate weight and body size

because

(mass).

medications.
habitually

of

dyspnea,
In

eat

sputum

addition,
poorly,

production,

many

even

COPD

though

pa

resp

insufficiency creates a hypermetabolic state

increased caloric needs. As a result, patient o

admitted with some degree of malnutrition. P

who have emphysema are often thin with w

musculature.
Auscultate bowel sounds.

Diminished or hypoactive bowel sounds may

decreased gastric motility and constipation (co

complication) related to limited fluid intake, poo

choices, decreased activity, and hypoxemia.
Give

frequent

oral

care,

remove

expectorated

secretions promptly, provide specific container for

Noxious

tastes,

smells,

and

sights

are

deterrents to appetite and can produce nause

Nursing Interventions

Rationale

disposal of secretions and tissues.

vomiting with increased respiratory difficulty.

Encourage a rest period of 1 hr before and after

Helps reduce fatigue during mealtime, and pr

meals. Provide frequent small feedings.

opportunity to increase total caloric intake.

Avoid gas-producing foods and carbonated beverages.

Can produce abdominal distension, which ha

abdominal breathing and diaphragmatic mov

and can increase dyspnea.
Avoid very hot or very cold foods.

Extremes in temperature can precipitate or agg

coughing spasms.

Weigh as indicated.

Useful in determining caloric needs, setting

goal,

and

evaluating

adequacy

of

nutr

plan. Note:Weight loss may continue initially, d

adequate intake, as edema is resolving.
Administer supplemental oxygen during meals as

Decreases dyspnea and increases energy for e

indicated.

enhancing intake.

4. Risk for Infection

Nursing Diagnosis

Risk for Infection

Risk factors may include

Inadequate

primary

defenses

(decreased

ciliary

action,

stasis

of

secretions)

Inadequate

acquired

immunity

(tissue

destruction,

environmental exposure)

Chronic disease process

Malnutrition

Desired Outcomes

Verbalize understanding of individual causative/risk factors.

Identify interventions to prevent/reduce risk of infection.

increased

Demonstrate techniques, lifestyle changes to promote safe environment.

Nursing Interventions

Rationale

Monitor temperature.

Fever

may

be

present

because

of

inf

or dehydration.
Review importance of breathing exercises, effective

These

activities

cough, frequent position changes, and adequate fluid

expectoration

intake.

developing pulmonary infection.

Observe color, character, odor of sputum.

Odorous, yellow, or greenish secretions sugge

of

promote
secretions

mobilization
to

reduce

ris

presence of pulmonary infection.

Demonstrate and assist patient in disposal of tissues

Prevents spread of fluid-borne pathogens.

and sputum. Stress proper handwashing (nurse and

patient), and use gloves when handling or disposing of
tissues, sputum containers.
Monitor visitors; provide masks as indicated.

Reduces potential for exposure to infectious illn

such as upper respiratory infection (URI).

Encourage balance between activity and rest.

Reduces oxygen consumption or demand imba

and

improves

patients

resistance

to

infe

promoting healing.
Discuss need for adequate nutritional intake.

Malnutrition can affect general well-being and

resistance to infection.

Recommend rinsing mouth with water and spitting, not

Reduces localized immunosuppressive effect o

swallowing, or use of spacer on mouthpiece of inhaled

and risk of oral candidiasis.

corticosteroids.
Obtain sputum specimen by deep coughing or

Done to identify causative organism and suscep

suctioning for Grams stain, culture and sensitivity.

to various antimicrobials.

Administer antimicrobials as indicated.

May be given for specific organisms identifi

Nursing Interventions

Rationale

culture and sensitivity, or be given prophylac

because of high risk.
5. Knowledge Deficit
Nursing Diagnosis

Knowledge Deficit

May be related to

Lack of information/unfamiliarity with information resources

Information misinterpretation

Lack of recall/cognitive limitation

Possibly evidenced by

Request for information

Statement of concerns/misconception

Inaccurate follow-through of instructions

Development of preventable complications

Desired Outcomes

Verbalize understanding of condition/disease process and treatment.

Identify relationship of current signs/symptoms to the disease process and

correlate these with causative factors.

Initiate necessary lifestyle changes and participate in treatment regimen.

Nursing Interventions

Rationale

Explain and reinforce explanations of individual disease

Decreases

process. Encourage patient and SO to ask questions.

participation in treatment plan.

Instruct and reinforce rationale for breathing exercises,

Pursed-lip and abdominal or diaphragmatic bre

coughing effectively, and general conditioning exercises.

exercises strengthen muscles of respiration,

anxiety

and

can

lead

to

imp

minimize collapse of small airways, and provid

individual with means to control dyspnea. G

conditioning

exercises

increase

activity

muscle strength, and sense of well-being.

tole

Nursing Interventions

Rationale

Stress importance of oral care and dental hygiene.

Decreases bacterial growth in the mouth, whic

lead to pulmonary infections.

Discuss importance of avoiding people with active

Decreases exposure to and incidence of acquired

respiratory infections. Stress need for routine influenza

URIs.

and pneumococcal vaccinations.

Discuss individual factors that may trigger or aggravate

These environmental factors can induce or agg

condition (excessively dry air, wind, environmental

bronchial irritation, leading to increased sec

temperature extremes, pollen, tobacco smoke, aerosol

production and airway blockage.

sprays, air pollution). Encourage patient and SO to

explore ways to control these factors in and around the
home and work setting.
Review the harmful effects of smoking, and advise

Cessation of smoking may slow or halt progress

cessation of smoking by patient and SO.

COPD. Even when patient wants to stop sm

support groups and medical monitoring ma

needed. Note: Research studies suggest that

stream or second-hand smoke can be as detrim

as actually smoking.
Provide information about activity limitations and

Having this knowledge can enable patient to

alternating activities with rest periods to prevent fatigue;

informed choices or decisions to reduce dys

ways to conserve energy during activities (pulling

maximize activity level, perform most desired act

instead of pushing, sitting instead of standing while

and prevent complications.

performing tasks); use of pursed-lip breathing, sidelying position, and possible need for supplemental
oxygen during sexual activity.
Discuss importance of medical follow-up care, periodic

Monitoring disease process allows for alteratio

chest x-rays, sputum cultures.

therapeutic regimen to meet changing needs an

help prevent complications.

Review oxygen requirements and dosage for patient

Reduces risk of misuse (too little or too much

Nursing Interventions

Rationale

who is discharged on supplemental oxygen. Discuss

resultant complications. Promotes environmenta

safe use of oxygen and refer to supplier as indicated.

physical safety.

Instruct patient and SO in use of NIPPV as appropriate.

NIPPV may be used at night or periodically durin

Problem-solve

identify

to decrease CO2 level, improve quality of sleep

dyspnea,

enhance functional level during the day. Sig

possible

side

adverse

signs and symptoms

fatigue,

daytime

effects

and

(increased

drowsiness,

or

headaches

on

increasing CO2 level indicate need for more aggr

awakening).

therapy.

Instruct asthmatic patient in use of peak flow meter, as

Peak flow level can drop before patient exhibit

appropriate.

signs and symptoms of asthma during the first

after exposure to a trigger. Regular use of the pea

meter may reduce the severity of the attack beca

earlier intervention.
Provide information and encourage participation in

These patients and their SOs may experience a

support groups (American Lung Association, public

depression, and other reactions as they deal

health department).

chronic disease that has an impact on their d

lifestyle. Support groups or home visits may be d

or needed to provide assistance, emotional su

and respite care.
Refer for evaluation of home care if indicated. Provide

Provides for continuity of care. May help r

frequency of rehospitalization.

detailed

plan

of

care

and

baseline

physical

assessment to home care nurse as needed on

discharge from acute care.
Discuss respiratory medications, side effects, adverse

Frequently these patients are simultaneously on s

reactions.

respiratory drugs that have similar side effect

potential drug interactions. It is important that p

understand the difference between nuisance

effects (medication continued) and untoward or ad

side effects (medication possibly discontinue

dosage changed).

Nursing Interventions

Rationale

Demonstrate technique for using a metered-dose

Proper administration of drug enhances deliver

inhaler (MDI), such as how to hold it, taking 25 min

effectiveness.

between puffs, cleaning the inhaler.

Devise system for recording prescribed intermittent drug

Reduces risk of improper use and overdosage

and inhaler usage.

medications, especially during acute exacerba

when cognition may be impaired.

Recommend avoidance of sedative antianxiety agents

Although patient may be nervous and feel the ne

unless specifically prescribed or approved by physician

sedatives, these can depress respiratory drive

treating respiratory condition.

protective cough mechanisms. Note: These drug

be used prophylactically when patient is unable to

situations known to increase stress or trigger resp

response.
Other Possible Nursing Diagnoses
1.

Self-Care

deficit,

specifyintolerance

to

activity,

decreased

strength/endurance, depression, severe anxiety.

2.

Home

Maintenance,

ineffectiveintolerance

to

activity,

inadequate

support system, insufficient finances, unfamiliarity with neighborhood

resources.
3.

Infection, risk fordecreased ciliary action, stasis of secretions, tissue

destruction, increased environmental exposure,chronic disease process,
malnutrition.