COPD-

Chronic obstructive pulmonary

diseases
• COPD is also known as chronic obstructive lung
disease (COLD), chronic obstructive airway disease
(COAD), chronic airflow limitation (CAL) and chronic
obstructive respiratory disease (CORD)
• Chronic obstructive pulmonary disease (COPD)
refers to chronic bronchitis and emphysema, a pair
of two commonly co- existing diseases of the lungs
in which the airways become narrowed which leads
to a limitation of the flow of air to and from the
lungs causing shortness of breath.
 Causes
• Smoking is primary risk factors for COPD. The numerous
irritants found in cigarette smoke stimulate excess mucus
production and coughing, destroy ciliary function and lead to
inflammation and damage of bronchiolar and alveolar walls.
• Air pollution high levels of urban air pollution are harmful to
persons with existing lung disease. Another risk factor for COPD
development is fossil fuels that used for indoor heating and
cooking.
• Occupational exposures- exposure to workplace dusts found in
coal mining, gold mining, and the cotton textile industry and
chemicals such as cadmium, and fumes from welding have
been implicated in the development of airflow obstruction.
Exposure of these irritants causes the airway to be hyper
responsive.
• Infection :infections is risk factor for developing COPD.
Severe recurring respiratory tract infection in childhood
have been associated with reduced lung function and
increased respiratory symptoms in adulthood. Recurring
infections impair normal defense mechanisms, making
bronchioles and alveoli more susceptible to injury.
• Genetics-Alpha 1-antitrypsin deficiency is a genetic
condition that is responsible for about 2% of cases of
COPD. In this condition, the body does not make
enough of a protein, alpha 1-antitrypsin. Alpha 1-
antitrypsin protects the lungs from damage caused by
protease enzymes, such as elastase and trypsin, that
can be released as a result of an inflammatory response
to tobacco smoke
 CLINICAL FEATURES
• Chronic cough
• sputum production
• Wheezing
• Chest tightness
• Dyspnoea on exertion
• Wt.loss
• Respiratory insufficiency
• Respiratory infections
• Barrel chest- chronic hyperinflation leads to loss of lung
elasticity.
 Bronchitis
• Bronchitis results from inflammation of bronchi
leading to increased musus production, cough and
eventual scaring of the bronchial lining.
• acute (short term) Infections or lung irritants cause
acute bronchitis.
• chronic is an ongoing, serious condition. It occurs if
the lining of the bronchial tubes is constantly irritated
and inflamed, causing a long-term cough with mucus
– It is defined as the presence of cough and sputum
production for atleast 3 months.
• Chronic bronchitis is characterized by the
following :
– A increased in size and number of submucus
glands in the large bronchi, which increase mucus
production.
– An increased number of goblet cells which also
secrete mucus.
– Impaired cillary function which reduce mucus
clearance.
 PATHOPHYSOPLOGY- bronchitis
• Irritants irrritate the airway
• Excess mucus production
• Inflammation
• Cause the mucus secreting glands and goblet cells to
increase in number.
• Ciliary function is reduced
• More mucus production
• Bronchial walls become thickened and lumen narrows and
mucus plug the airway
• Alveoli adjacent to the bronchioles may become damaged
and fibrosed.
• Alter function of alveolar macrophages.
Chronic bronchitis
 Signs and symptoms-Acute
• sore throat, fatigue (tiredness)
• Fever
• body aches
• stuffy or runny nose
• vomiting, and Diarrhea
• persistent cough
• cough may produce clear mucus
• shortness of breath
 Chronic symptoms
• Coughing
• Wheezing
• Chest discomfort.
• The coughing may produce large amounts of
mucus.
• This type of cough often is called a smoker's
cough.
 EMPHYSEMA
• Definition:- Emphysema is defined as
enlargement of the air spaces distal to the
terminal bronchioles, with destruction of their
walls of the alveoli.
• As the alveoli are destroyed the alveolar surface
area in contact with the capillaries decreases.
Causing dead spaces (no gas exchange takes
place) Leads to hypoxia.
• In later stages: CO2 elimination is disturbed and
increase in CO2 tension in arterial blood causing
respiratory acidosis
 There are three types of emphysema
• 1. Centriacinar 2. Panacinar 3. Paraseptal
• Centriacinar(centrilobular) emphysema the
most common type produce destruction in
bronchioles usually in the upper lung region.
– Inflammation begins in the bronchioles and spread
peripherally but usually the alveolar sac remains
intact.
– This form of emphysema occurs most often in
smokers.
• Panaicnar emphysema destroys the entire
alveolus and most commonly involves the
lower portion of the lung.
• This form of disease is generally observed in
individuals with ATT deficiency.
• Paraseptal or distal acinar emphysema
primarily involves the distal airway structures
alveolar ducts and alveolar sacs.
• The process is localized around the septa of
the lung or pleura.
• It is believed to be the likely cause of
spontaneous pneumothorax
 DIAGNOSIS
• Blood Test Blood tests can help determine if
symptoms are being caused by an infection.
• An arterial blood gas test will measure the amount
of oxygen in blood.
• This is one indication of how well lungs are working.
This can help doctor determine how severe COPD is
and whether need oxygen therapy.
• Chest X-ray or CT scan A CT scan is a type of X-ray
that creates a more detailed image than a standard
X-ray.
• Sputum Examination :if the client has a
productive cough. Sputum is the mucus the
client cough up.
• Analyzing sputum can help identify the cause
of breathing difficulties and may rule out
some lung cancers. If there is a bacterial
infection, it can be identified and treated
• Pulmonary Function Test : pulmonary function tests
(PFTs) measure how well the lungs are moving air in
and out.
• They also measure how well the lungs are moving
oxygen to the blood.
• Spirometry (meaning the measuring of breath) is the
most common of the pulmonary function tests (PFTs).
– It measures lung function, specifically the amount
(volume) and/or speed (flow) of air that can be inhaled
and exhaled
 MEDICAL MANAGEMENT
• The treatment goal for the client with COPD
are:
– To improve ventilation
– To facilitate the removal of bronchial secretions
– To promote health maintenance
– To reduce complications, and
– To slow progression of the disease
• Smoking cessation Cessation of cigarette
smoking is single most effective and cost
effective intervention to reduce the risk of
developing COPD and stop the progression of
the disease.
• Bronchiodilator : are agents that widen the
air passages by relaxing the bronchial smooth
muscle and improve the ventilation of lungs.
– The principal bronchiodilator treatment are Beta2
agonists, anticholinergics, and methylxanthines
used singly or combination.
• Oxygen therapy O2 therapy is frequently used
in the treatment of COPD another problem
associated with hypoxemia. Long term o2
therapy improves survival, exercise capacity,
cognitive
• Oral corticosteroids are used in acute
exacerbations for anti-inflammatory effect
• Methylxanthines, such as theophylline given orally
as sustained-release formulation for chronic
maintenance therapy (less commonly used)
• Chest physical therapy, including postural drainage
for secretion clearance and breathing retraining for
improved ventilation and control of dyspnea.
• Treatment for alpha1-antitrypsin deficiency:
– Regular I.V. infusions (every 1 to 2 weeks) of
human alpha1-antitrypsin (Prolastin) as
replacement therapy to correct the antiprotease
imbalance in the lungs.
 SURGICAL MANAGEMENT
• Bullectomy :Bullae are enlarged airspaces that
do not contribute to ventillation but occupy
space in the thorax
• These areas may be surgically excised lung
volume reduction surgery It involves the
removal of a portion of the diseased lung
parenchyma.
• This allows the functional tissue to expand.
• Lung transplantation
• Impaired gas exchange related to decreased
ventilation
• Objectives Improve ventilation Intervention
– Monitor lung sounds every 4 to 8 hours.
– Perform chest physiotherapy
– Advice the client to drink at least 8 to 10 glasses
of fluid per day unless contraindicated
– Teach the client in coughing technique
– Asses the condition of oral mucus membrane and
perform oral care
• Disturbed sleep pattern related to dyspnea
Objectives Getting adequate rest Intervention
– Promote relaxation by providing a darkened, quiet
environment, ensure adequate room ventilation.
– Avoid use of sleeping pills
– Schedule care activities to allow periods of
uninterrupted sleep.
• Activity intolerance related to inadequate
oxygenation
• Objective :Improve to perform daily activity
Intervention
– Monitor the severity of dyspnea
– Stop or slow any activity that leads to change in
respiratory rate
– Advice the client to avoid conditions that increase
oxygen demand
 Nursing diagnosis
• Ineffective airway clearance related to excessive
secretions and ineffective coughing Objective Effective
airway clearance Intervention
• Monitor lung sounds every 4 to 8 hours.
• Perform chest physiotherapy
• Advice the client to drink at least 8 to 10 glasses of
fluid per day unless contraindicated
• Teach the client in coughing technique
• Asses the condition of oral mucus membrane and
perform oral care
• Anxiety related to acute breathing difficulties
and fear of suffocation
• Objectives :Relieve fear of dying Intervention
– Provide a quiet, calm environment.
– During acute episodes, open doors and curtains and
limit the number of people in the room.
– Encourage the use of breathing retraining and
relaxation technique
– Give sedative and tranquilizers with extreme
caution.
– Nonpharmacological methods of anxiety reduction
are more useful
 Complications
• Respiratory failure.
• Pneumonia, overwhelming respiratory
infection.
• Right-sided heart failure, dysrhythmias
• Depression
• Skeletal muscle dysfunction