SRI GURU RAMDAS NURSING INSTITUTE

PANDHER, AMRITSAR

CASE STUDY
ON COPD

SUBJECT- ADVANCE NURSING PRACTICE

SUBMITTED TO
RESPECTED MAM
Miss Arpandeep Kaur
Associate professor
Dept. of community health Nurse

SUBMITTED BY
Pawandeep Kaur
M.SC (N) 1st YEAR
Medical surgical nursing

SUBMITTED ON -
IDENTIFICATION DATA OF THE CHILD

Name Raghu
Age 60yrs
Sex male
Address Amritsar
Dr.incharge Dr. Neha
Ward Medical ICU
Cr. Number 27894
Informant son
D.O.A 10.2.2021
Diagnosis COPD

SOCIO ECONOMIC DATA OF FAMILY

Religion Hindu
Monthly28000/month
Status Middle
Education of parents illiterate

CHIEF COMPLAINTS

The patient presented with following complaints:

 Breathlessness since morning
 Perfuse sweating since morning
 Cough *15 days
 Wheezing
 Productive cough
 Shortness of breath(dyspnea)

PRESENT HISTORY OF ILLNESS

Patient was admitted in GGS hospital on 10/2/2021 pt’s come through emergency ward with
complaints of breathlessness and perfuse sweating since morning , cough from last 15 days
with moderate amount of expectoration,no foul smell no blood stains, wheezing and shortness
of breath (dyspnea) patient feel the pressure in the chest increases the patient faces more
difficulty during exhaling air rather than inhalation.

PAST HISTORY OF ILLNESS

 MEDICAL HISTORY
Patient is a known case of chronic obstructive pulmonary disease.patient was taken treatment
in a private hospital continue last1year, but the patient did not recovered and was referred to
the GGSMCH, Faridkot.
No history of any allergies or infectious diseases present.
H/O CVA in past resolved completely.
No H/O DM, TB,Asthma etc.

 SURGICAL HISTORY

No significant past surgical history found

PERSONAL HISTORY

Addiction : Smoker * 15 years

Alcoholic * 15 years
Dietary habit: Non vegetarian
Sources of data : His son

FAMILY HISTORY

Patient with live in a nuclear family with his wife and four son.family status is midlle .No
significant family history of any genetic or hereditary disorder found. All family members are
healty .

FAMILY TREE

USED KEY:

---- PATIENT

----- FEMALE

----- MALE

65 YRS.(PT’S) 62YRS wife

35yr. 32yrs 28yrs 26yrs

SOCIOECONOMIC STATUS

Patient belongs to a middle class family. Patient that time stay at home they are no doing any
work due to old age and disease condition.Family type is nuclear. Family income is approx.
Rs.28000-40000/month.

GENERAL PHYSICAL EXAMINATION

1. GROWTH MEASUREMENTS:
a) Body built : ectomorphic
b) Weight: 65kg

2. PHYSIOLOGICAL MEASUREMENTS:
a) Temperature: 99°C
b) Pulse rate: 78 /min
c) Respiration: 26breaths/min
d) B.P: 122/95 mmhg

3. APPEARANCE: Patient appears acutely ill, pale and irritable.

4. SKIN: skin is pale, no pigmentations, no lesions, no cyanosis, no scar, tenderness, no

masses, fluffy skin, no rash, no petechiae, condition of mucous membrane healthy.

5. HAIR: color white, distribution of hair on head normal, general cleanliness maintained.

6. HEAD AND NECK: movement of head normal, no any type of injury in skull ,no
dandruff ,no enlarged thyroid etc.

8. EYES: no infection, no photophobia, and distance between the eyes normal, Normal
vision. Normal pupillary reactions to light

9. EARS: normal shape, size, position, no deformities, no discharge and no tenderness over
mastoid bone, and no hearing abilities.
10. NOSE:both nares patent, no discharge, no bleeding, no deviated septum, no depressed
nasal bridge, no foreign body, no flaring of nostrils.Condition of nasal mucous membrane
normal, andParanasal sinuses non tender.

11. MOUTH AND THROAT:color of lips pale, no lesions at the corner of mouth, cleft
lift or cleft palate, no evidence of dental caries, staining of teeth, malocclusion and extra or
missing teeth, gum bleeding, swelling and lesions of buccal mucosa, tongue and pharynx
healthy, no infections, tonsillitis, any spot, ulcer and swelling, tongue tie or short tongue etc.

12. CHEST: shape, size and symmetry of chest normal, pesence of chest retractions,
funnel chest, condition of breast and nipples normal, wheezing sounds is present.

13. ABDOMEN:abdominal distension, swelling or enlargement present, absence of

infection or scar, cleanliness, absence of any congenital anomalies and developmental defects
like hernias.

14. LIMBS:pitting edema present over feet. no deformity, asymmetry, bow legs, knock
knees, limitation of movement of joints, paralysis, clubbing of fingers, normal number of
fingers or toes (polydactyly or syndactyly), nails, absence of deformity of feet (talipes, flat
foot), any infections, general cleanliness maintained etc.

15. SPINE AND BACK:absence of abnormal spinal curvature (kyphosis, scoliosis,

lordosis), dislocation of hip, neck stiffness etc.

16. GENITALIA: absence from any abnormality and edema.

17. ANUS AND RECTUM: patent anus, absence of fissures or fistulas, rectal prolapse,
perianal erythema.

18. NEUROLOGICAL EXAMINATION: child is irritable, normal motor

coordination, muscle tone, sense of touch or pain, absence of meningeal irritation, paresis or
paralysis etc.

SYSTEM WISE EXAMINATION

1. CARDIOVASCULAR SYSTEM: pulse rate: 78/min, B.P 122/95 mmhg.

shape and size normal, no abnormal heart sounds (murmurs), no cyanosis, no
associated congenital heart defects noted, capillary refill time normal

2. RESPIRATORY SYSTEM: respiratory rate: 26 breaths/min. Shape and size of

chest normal and symmetric. chest retractions found. Difficulty in breathing during
walking. Wheezing sounds are present.

3. GASTROINTESTINAL SYSTEM:no lesion present, bowel sounds are

present, no organ enlargement, no fluid accumulation.
 4. INTEGUMENTARY SYSTEM: skin is pale, turgor is normal, no lesions or
infections found. Other structures of skin like nails & hairs are normal and free from
infections, general cleanliness maintained.

5. GENITOURINARY SYSTEM: no any abnormality of genitourinary system

like maturation, frequency rate is more than normal.

6. REPRODUCTIVE SYSTEM: non-edema present, no infection present.

7. LYMPHATIC SYSTEM: all the lymph nodes found non-tender on palpation,

no lymphadenopathy.

8. CEREBROSPINAL SYSTEM: patient is irritable. No defects of spine found.

Patient responds to pain and has normal pupillary reactions.

DISEASE DESCRIPITION

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

INTRODUCTION

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung

disease (COLD), and chronic obstructive airway disease (COAD), among others, is a type
of obstructive lung disease characterized by chronically poor airflow. It typically worsens
over time. The main symptoms include shortness of breath, cough, and sputum  production
Most people with chronic bronchitis have COPD.

Worldwide, COPD affects 329 million people or nearly 5% of the population. In 2012, it

ranked as the third-leading cause of death, killing over 3 million peopleThe number of deaths
is projected to increase due to higher smoking rates and an aging population in many
countries.
DEFINITION

Chronic obstructive pulmonary disease (COPD) is an umbrella term used to describe chronic
lung diseases in which air flow is obstructed by emphysema , chronic bronchitis , refractory
(irreversible) asthma , and severe bronchiectasis.

COPD
Air flow obstruction

(A)
Chronic Bronchitis (C)
Asthma
Excessive accumulation
Of mucus and secretions Inflamed and
constricted
Block the airways airway obstruct airflow
(B)
Emphyema

Impaired gas exchanges results

From destruction of the walls of
Over distended alveoli

In each condition there is chronic obstruction of the flow of air through the airways and out
of the lungs , and the obstruction generally is usually progressive and irreversible and it may
be associated with airway hyperactivity . progressive means the disease gets worse over time.
RISK FACTORS

CIGARETTE SMOKING

OCCUPATION PASSIVE
EXPOSURE SMOKING

RISK
FACTORS

AIR FAMILY
POLLUTION HISTORY

GENETIC ABNORMALITIES DEFICIENCY

OF ALPHA ANTI-TRYPSIN ENZYME

CAUSES

The primary cause of COPD is tobacco smoke, with occupational exposure and pollution
from indoor fires being significant causes in some countries. Typically these exposures must
occur over several decades before symptoms develop. A person's genetic makeup also affects
the risk.
Smoking

The primary risk factor for COPD globally is tobacco smoking. Of those who smoke about
20% will get COPD and of those who are lifelong smokers about half will get COPD. In non-
smokers, secondhand smoke is the cause of about 20% of cases. Other types of smoke, such
as marijuana, cigar, and water pipe smoke, also confer a risk.Women who smoke
during pregnancy may increase the risk of COPD in their child.
Air pollution
Poorly ventilated cooking fires, often fueled by coal or biomass fuels such as wood and
animal dung, lead to indoor air pollution and are one of the most common causes of COPD
in developing countries.COPD live in large cities have a higher rate of COPD compared to
people who live in rural areas. 
Occupational exposures
Intense and prolonged exposure to workplace dusts, chemicals and fumes increase the risk of
COPD in both smokers and nonsmokers.Workplace exposures are believed to be the cause in
10–20% of cases.A number of industries and sources have been implicated, including high
levels of dust in coal mining, gold mining, and the cotton textile industry, occupations
involvingcadmium . Working in agriculture is also a risk.In some professions the risks have
been estimated as equivalent to that of half to two packs of cigarettes a day.
Genetics
Genetics play a role in the development of COPD. It more common among relatives of those
with COPD who smoke than unrelated smokers. Currently, the only clearly inherited risk
factor is alpha 1-antitrypsin deficiency (AAT).This risk is particularly high if someone
deficient in alpha 1-antitrypsin also smokes.
Other
A number of other factors are less closely linked to COPD. The risk is greater in those who
are poor, although it is not clear if this is due to poverty itself or other risk factors associated
with poverty, such as air pollution and malnutrition.There is tentative evidence that those
with asthma and airway hyperactivity are at increased risk of COPD.Birth factors such as low
birth weight may also play a role as do a number of infectious diseases
including HIV/AIDS and tuberculosis.Respiratory infections such as pneumoniado not
appear to increase the risk of COPD, at least in adults.
Exacerbations
An acute exacerbation (a sudden worsening of symptoms) is commonly triggered by infection
or environmental pollutants, or sometimes by other factors such as improper use of
medications.Infections appear to be the cause of 50 to 75% of cases, with bacteria in 25%,
viruses in 25%, and both in 25%. Environmental pollutants include both poor indoor and
outdoor air quality. Those with many exacerbations have a faster rate of deterioration of their
lung function.
PATHOPHYSIOLOGY

On the left is a diagram of the lungs and airways with an inset showing a detailed cross-
section of normal bronchioles and alveoli. On the right lungs damaged by COPD with an
inset showing a cross-section of damaged bronchioles and alveoli
COPD is a type of obstructive lung disease in which chronic incompletely reversible poor
airflow (airflow limitation) and inability to breathe out fully (air trapping) exist. The poor
airflow is the result of breakdown of lung tissue (known as emphysema) and small airways
disease known as obstructive bronchiolitis. The relative contributions of these two factors
vary between people. were destruction of small airways can lead to the formation of large air
pockets—known as bullae—that replace lung tissue. This form of disease is called bullous
emphysema.
Micrograph showing emphysema (left - large empty spaces) and lungtissue with relative
preservation of the alveoli (right).
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 haveeosinophil 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. 
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.

Due to causes and risk factors of the COPD

Affects Ciliary cleaning mechanism of respiratory tract

Airflow is obstructed and air becomes trapped behind the obstruction

Alveoli greatly distended and lung capacity decreased

 Increased accumulation of the mucus from mucus glands

Produce more irritation , infection.

CLINICAL FEATURES OF COPD (IN THEORY)

The most common symptoms of COPD are sputum production, shortness of breath and a

productive cough. These symptoms are present for a prolonged period of time and typically
worsen over time. It is unclear if different types of COPD exist. While previously divided
into emphysema and chronic bronchitis, emphysema is only a description of lung changes
rather than a disease itself, and chronic bronchitis is simply a descriptor of symptoms that
may or may not occur with COPD.
Cough
A chronic cough is usually the first symptom to occur. When it exists for more than three
months a year for more than two years, in combination with sputum production and without
another explanation, there is by definition chronic bronchitis. This condition can occur before
COPD fully develops. The amount of sputum produced can change over hours to days. In
some cases the cough may not be present or only occurs occasionally and may not be
productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum
may be swallowed or spat out, depending often on social and cultural factors. Vigorous
coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often
have a history of "common colds" that last a long time.
Shortness of breath
Shortness of breath is often the symptom that bothers people the most. It is commonly
described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air
in". Different terms, however, may be used in different cultures. Typically the shortness of
breath is worse on exertion of a prolonged duration and worsens over time. In the advanced
stages it occurs during rest and may be always present. It is a source of both anxiety and a
poor quality of life in those with COPD. Many people with more advanced COPD breathe
through pursed lips and this action can improve shortness of breath in some.
Other features
In COPD, it may take longer to breathe out than to breathe in. Chest tightness may occur but
is not common and may be caused by another problem. Those with obstructed airflow may
have wheezing or decreased sounds with air entry on examination of the chest with
a stethoscope.  A barrel chest is a characteristic sign of COPD, but is relatively
uncommon.Tripod positioning may occur as the disease worsens.Advanced COPD leads
to high pressure on the lung arteries, which strains the right ventricle of the heart.This
situation is referred to as corpulmonale, and leads to symptoms of leg swelling and bulging
neck veins. COPD is more common than any other lung disease as a cause of
corpulmonale. Corpulmonale has become less common since the use of supplemental
oxygen.
COPD often occurs along with a number of other conditions, due in part to shared risk
factors. These conditions include: ischemic heart disease, high blood pressure, diabetes
mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorder and depression. In those
with severe disease a feeling of always being tired is common.Fingernail clubbing is not
specific to COPD and should prompt investigations for an underlying lung cancer.
Exacerbation
An acute exacerbation of COPD is defined as increased shortness of breath, increased sputum
production, a change in the color of the sputum from clear to green or yellow, or an increase
in cough in someone with COPD.This may present with signs of increased work of breathing
such as fast breathing, a fast heart rate, sweating, active use ofmuscles in the neck, a bluish
tinge to the skin, and confusion or combative behavior in very severe
exacerbations.Crackles may also be heard over the lungs on examination with a stethoscope.

CLINICAL FEATURES (IN PATIENT)

 Chronic coughing (productive with sputum) phlegm

 Shortness of breath(dyspnea)
 Frequent respiratory infection
 Production of purulent (cloudy and discoloured) sputum
 Chronic coughing (productive with sputum) phlegm
 Wheezing
 Enlarged A.P diameter of chest
 Patients may develop cyanosis
 Weight loss
 Swollen feet and ankles
DIAGNOSTIC EVALUATION OF NEPHROTIC SYNDROME (IN
THEORY)

A person blowing into a spirometer. Smaller handheld devices are available for office use.
The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who
has shortness of breath, a chronic cough, sputum production, or frequent winter colds and a
history of exposure to risk factors for the disease.Spirometry is then used to confirm the
diagnosis.
Spirometry
Spirometry measures the amount of airflow obstruction present and is generally carried out
after the use of a bronchodilator, a medication to open up the airways.Two main components
are measured to make the diagnosis: the forced expiratory volume in one second (FEV1),
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, 75–80% of the FVC comes out in the first secondand
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.Evidence for using spirometry
among those without symptoms in an effort to diagnose the condition earlier is of uncertain
effect and is therefore currently not recommended.A peak expiratory flow (the maximum
speed of expiration), commonly used in asthma, is not sufficient for the diagnosis of COPD.
Severity

MRC shortness of breath scale

Grad
Activity affected
e

1 Only strenuous activity

2 Vigorous walking

3 With normal walking

 4 After a few minutes of walking

5 With changing clothing

GOLD grade

Severity FEV1 % predicted

Mild (GOLD 1) ≥80

Moderate (GOLD 2) 50–79

Severe (GOLD 3) 30–49

Very severe (GOLD

<30 or chronic respiratory failure
4)

There are a number of methods to determine how much COPD is affecting a given
individual. The modified British Medical Research Councilquestionnaire (mMRC) or the
COPD assessment test (CAT) are simple questionnaires that may be used to determine the
severity of symptoms.Scores on CAT range from 0–40 with the higher the score, the more
severe the disease.Spirometry may help to determine the severity of airflow limitation.This is
typically based on the FEV1 expressed as a percentage of the predicted "normal" for the
person's age, gender, height and weight.Both the American and European guidelines
recommended partly basing treatment recommendations on the FEV1.The GOLD guidelines
suggest dividing people into four categories based on symptoms assessment and airflow
limitation.Weight loss and muscle weakness, as well as the presence of other diseases, should
also be taken into account.
Other tests
A chest X-ray and complete blood count may be useful to exclude other conditions at the
time of diagnosis. Characteristic signs on X-ray are overexpanded lungs, a
flatteneddiaphragm, increased retrosternal airspace, and bullae while it can help exclude other
lung diseases, such as pneumonia, pulmonary edema or a pneumothorax. A high-
resolution 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.

Chest X-ray demonstrating severe COPD. Note the small heart size in comparison to the
lungs.
 

A lateral chest x-ray of a person with emphysema. Note the barrel chest and flat diaphragm.
 

Lung bulla as seen on CXR in a person with severe COPD

 

A severe case of bullous emphysema

 
 

Axial CT image of the lung of a person with end-stage bullous emphysema.

Differential diagnosis
COPD may need to be differentiated from other causes of shortness of breath such
as congestive heart failure, pulmonary embolism, pneumonia or pneumothorax. Many people
with COPD mistakenly think they have asthma.The distinction between asthma and COPD is
made on the basis of the symptoms, smoking history, and whether airflow limitation is
reversible with bronchodilators at spirometry. Tuberculosis may also present with a chronic
cough and should be considered in locations where it is common.Less common conditions
that may present similarly include bronchopulmonary dysplasia and obliterative
bronchiolitis. Chronic bronchitis may occur with normal airflow and in this situation it is not
classified as COPD.
DIAGNOSTIC EVALUATION (IN PATIENT)
 Medical history and physical examination
 Chest x ray or chest CT scan
 Pulmonary function test
 Arterial blood gas analysis(for checking PO2&PCO2)
 Pulse oximetry
 Spirometry is important diagnostic evaluation.it is determined by FEV1/FVC than
normal person.

TEST PETIENT VALUE NORMAL VALUE REMARKS

HB 10.3gm/dl 14-16gm/dl Decrease
BUN 39mg/dl 15-45mg/dl Normal
S.CRETININE 0.9mg/dl 0.8-1.3mg/dl Normal
T.S.BILIRUBIN 0.7mg/dl 0.3-1.1mg/dl Normal
SODIUM 138meq/l 135-155meq/l Normal
CLORIDE 99.0meq/l 98-107meq/l Normal
T.S.PROTEIN 7.4mg/dl 6.5-8g/dl Normal
ALBUMIN 4.5mg/dl 3.5-5.5g/dl Normal
GLOBULIN 2.4mg/dl 2-3.5g/dl Normal
POTASSIUM 3.7meq/l 3.5-5.5mwq/l Normal
S.CHOLESTEROL 160mg/dl 150-200mg/dl Normal

PREVENTION
Most cases of COPD are potentially preventable through decreasing exposure to smoke and
improving air quality.Annual influenza vaccinations in those with COPD reduces
exacerbations, hospitalizations and death. Pneumococcal vaccination may also be beneficial.
Smoking cessation
Keeping people from starting smoking is a key aspect of preventing COPD. The policies of
governments, public health agencies and anti-smoking organizations can reduce smoking
rates by discouraging people from starting and encouraging people to stop smoking. Smoking
bans in public areas and places of work are important measures to decrease exposure to
secondhand smoke and while many places have instituted bans more are recommended.
In those who smoke, stopping smoking is the only measure shown to slow down the
worsening of COPD. Even at a late stage of the disease, it can reduce the rate of worsening
lung function and delay the onset of disability and death.Smoking cessation starts with the
decision to stop smoking, leading to an attempt at quitting. Often several attempts are
required before long-term abstinence is achieved. Attempts over 5 years lead to success in
nearly 40% of people.Some smokers can achieve long-term smoking cessation through
willpower alone. Smoking, however, is highly addictive,and many smokers need further
support. The chance of quitting is improved with social support, engagement in a smoking
cessation program and the use of medications such as nicotine replacement
therapy, bupropion orvarenicline.
Occupational health
A number of measures have been taken to reduce the likelihood that workers in at-risk
industries—such as coal mining, construction and stonemasonry—will develop
COPD.Examples of these measures include: the creation of public policy, education of
workers and management about the risks, promoting smoking cessation, checking workers
for early signs of COPD, use of respirators, and dust control. Effective dust control can be
achieved by improving ventilation, using water sprays and by using mining techniques that
minimize dust generation. If a worker develops COPD, further lung damage can be reduced
by avoiding ongoing dust exposure, for example by changing the work role.
Air pollution
Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the
worsening of existing disease. This may be achieved by public policy efforts, cultural
changes, and personal involvement.A number of developed countries have successfully
improved outdoor air quality through regulations. This has resulted in improvements in the
lung function of their populations. Those with COPD may experience fewer symptoms if they
stay indoors on days when outdoor air quality is poor.One key effort is to reduce exposure to
smoke from cooking and heating fuels through improved ventilation of homes and better
stoves and chimneys. Proper stoves may improve indoor air quality by 85%. Using
alternative energy sources such as solar cooking and electrical heating is effective, as is using
fuels such as kerosene or coal rather than biomass.

LIFE STYLE AND HOME REMIDIES

If you have COPD, you can take steps to feel better and slow the damage to your
Lungs :-
CONTROL BREATHING : Talk to doctor or respiratory therapist about techniques
for breathing more efficiently throughout the day .also be sure to discuss breathing position
and relaxation techniques that you can use when you are short of breath.
CLEAR AIRWAYS : In COPD , mucus tends to collect in air passages and can be
difficult to clear .controlled coughing , drinking plenty of water and using a humidifier may
help.

EXERCISE REGULARLY : It may seem difficult to exercise when you have trouble
breathing but regular exercise can improve overall strength and endurance and strengthen
respiratory muscles.

EAT HEALTHY FOODS : A healthy diet can help you maintain strength .if you are
under weight your doctor may recommended nutritional supplements.if you are over weight
losing weight can significantly help your breathing especially during times of exertion .
AVOID SMOKE : In addition to quitting smoking , it is important to avoid places where
other smoke . second hand smoke may contribute to further lung damage.

PAY ATTENTION TO FREQUENT HEARTBURN : Constant heartburn can

indicate gastro-esophageal reflux disease , a condition in which stomach acid or occasionally
bile flows back into esophagus . this constant backwash of acid can aggravate COPD but
treatment for GERD can help .talk to doctor if you have frequent heart burn.

SEE DOCTOR REGULARLY : Stick to your appointment schedule even if you are
feeling fine. It is important to steadily monitor lung function.

NON-PHARMACOLOGIC MANAGEMENT
There is no known cure for COPD, but the symptoms are treatable and its progression can be
delayed.The major goals of management are to reduce risk factors, manage stable COPD,
prevent and treat acute exacerbations, and manage associated illnesses.The only measures
that have been shown to reduce mortality are smoking cessation and supplemental
oxygen. Stopping smoking decreases the risk of death by 18%.Other recommendations
include: influenza vaccination once a year, pneumococcal vaccination once every 5 years,
and reduction in exposure to environmental air pollution. In those with advanced
disease, palliative care may reduce symptoms, with morphine improving the feelings of
shortness of breath.Noninvasive ventilation may be used to support breathing.

Exercise
Pulmonary rehabilitation is a program of exercise, disease management and counseling,
coordinated to benefit the individual. In those who have had a recent exacerbation,
pulmonary rehabilitation appears to improve the overall quality of life and the ability to
exercise, and reduce mortality.It has also been shown to improve the sense of control a
person has over their disease, as well as their emotions. Breathing exercises in and of
themselves appear to have a limited role.Being either underweight or overweight can affect
the symptoms, degree of disability and prognosis of COPD. People with COPD who are
underweight can improve their breathing muscle strength by increasing their calorie
intake. When combined with regular exercise or a pulmonary rehabilitation program, this can
lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those
who are malnourished.
Nebulization
Inhaled bronchodilators are often used to provide direct bronochodilators often to the airway ,
thereby improving airflow.
Oxygen therapy
Long term oxygen therapy ultimately improves the quality of life & survival, oxygen is used
when the client has severe exertional or resting hypoxemia (PaO2 below40 mmHg), 1-
3LOxygen by nasal cannula may be required to raise the PaO2 60-80mmHg.
Removeing bronchial secretions
Client may be treated with nebulized bronchodilators and positive pressure air flow or
positive end-expiratory pressure(PEEP) device to increase the calibre of airways.
In addition,postural drainage & chest-physiotherapy may be prescribed to move the
secretions foam small to large airways,from which they can be expelled.
MEDICAL MANAGEMENT

Bronchodilators
Inhaled bronchodilators are the primary medications usedand result in a small overall
benefit. There are two major types, β2 agonists and anticholinergicsboth exist in long-acting
and short-acting forms. They reduce shortness of breath, wheeze and exercise limitation,
resulting in an improved quality of life. It is unclear if they change the progression of the
underlying disease.
In those with mild disease, short-acting agents are recommended on an as needed basis.In
those with more severe disease, long-acting agents are recommended. If long-acting
bronchodilators are insufficient, 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 15–
25%.While both may be used at the same time, any benefit is of questionable significance.
There are several short-acting β2 agonists available including salbutamol (Ventolin)
and terbutaline. They provide some relief of symptoms for four to six hours. Long-acting
β2 agonists such as salmeterol and formoterol are often used as maintenance therapy. Some
feel the evidence of benefits is limitedwhile others view the evidence of benefit as
established. Long-term use appears safe in COPD with adverse effects
include shakiness and heart palpitations. When used with inhaled steroids they increase the
risk of pneumonia. While steroids and LABAs may work better together. it is unclear if this
slight benefit outweighs the increased risks.
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 strokeAclidinium, another long acting
agent which came to market in 2012, has been used as an alternative to tiotropium.
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.When used in combination with a LABA they decrease mortality more than
either ICS or LABA alone.By themselves they have no effect on overall one-year mortality
and are associated with increased rates of pneumonia. It is unclear if they affect the
progression of the disease. Long-term treatment with steroid tablets is associated with
significant side effects.
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
astheophylline 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.

MEDICAL MANAGEMENT (IN PATIENT)

DRUGS SALT DOSE ROUTE ACTION

Inj.Gramocef Sulbactum 1gm IV Antibiotics
Ceftrixone
Inj.Dexon Dexamethasone 80mg IV Antihistamine

Inj.Deriphyillin etiphylline 2ml IV Bronchodilators

e Frusemide 2ml IV Diuretic
Inj.Lasix

SURGICAL MANAGEMENT

Surgery is an option for some people with some forms of severe emphysema who aren't
helped sufficiently by medications alone :
Bullectomy

When the walls of the air sacs are destroyed , larger air spaces called bullaeform.these air
spaces can becomes so large that they interfere with breathing , in a bullectomy , doctors
remove one or more very large bullae from the lungs.

Lungs volume reduction surgery

In this surgery , surgeon removes small wedges damaged lung tissue . this creates extra space
in chest cavity so that the remaining lung tissue and the diaphragm work more efficiently.
The surgery has a number of risks and long term results may be no better than for non
surgical approaches.

Lung transplant

Single lung transplantation may be an option for certain people with severe emphysema who
meet specific criteria .transplantation can improve ability to breath and be active , but it does
not appear to prolong life and patient may have to wait for a long time to receive a donated
organ . so the decision to undergo lung transplantation is complicated.

COMPLICATIONS OF COPD

A person with COPD is at increased risk of a number of complications, including:

• chest infections – a common cold can easily lead to a severe infection

• pneumonia – a lung infection that targets the alveoli and bronchioles

• collapsed lung – the lung may develop an air pocket. If the air pocket bursts during a
coughing fit, the lung will deflate

• heart problems – the heart has to work extremely hard to pump blood through the lungs

• osteoporosis – where bones become thin and break more easily. Steroid use in people with
COPD is thought to contribute to osteoporosis

• anxiety and depression – breathlessness or the fear of breathlessness can often lead to
feelings of anxiety and depression

• oedema (fluid retention) – problems with blood circulation can cause fluid to pool,
particularly in the feet and ankles

• hypoxaemia – caused by lack of oxygen to the brain. Symptoms include cognitive
difficulties such as confusion, memory lapses and depression

• risks of sedentary lifestyle – as symptoms of COPD progress, many people adjust their
lifestyle to avoid symptoms. For example, they reduce their physical activity to avoid
breathlessness. As they reduce their physical activity, they become less fit and even more
breathless on exertion. This downward spiral of inactivity means the person is prone to a
range of potentially serious health problems, such as obesity and cardiovascular disease.

NURSING MANAGEMENT

ASSESSMENT

 Assess nursing history ,family history and obtains a through smoking history of the
patient.
 Assess respirations note quality,rate,pattern,depth and breathing effort.
 Assess lung sounds noting areas of decreased ventilation and the presence of
adventious sound.
 Inspects the chest to determine breathing rate & pattern and auscultates the chest to
determine depth of inspiration & to listen breath sounds.
 Assess for signs and symptoms of hypoxemia, tachycardia, restlessness,
diaphoresis,headache,lethargy and confusion.
 Monitor ABG’s and note change.increasing PaCO2 and decreasing PaO2 are signs of
respiratory failure.
 Use pulse oximetry to monitor oxygen saturation and pulse rate. Pulse oximetry is a
useful tool to detect changes in oxygenation.
 Assess patient ability to cough effectively to clear secretions.notequantity,color,and
consistency of sputum.
 Monitor for changes in orientation, increased restlessness , anxiety and air
hunger .restlessness is an early sign of hypoxia.
 Assess skin color , temperature , capillary refill , note central versus peripheral
cyanosis.
 Assess the ability of activities both before illness or condition now and also the use of
aids such as canes, wheel chairs and others.
 Ask the patient daily sleep habits , how long sleep.often wake up during sleep caused
by pain , itching, urination, difficulty and others.