Shree sahAjanand institute of nursing,
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Presented by
Mr. AKRAM KHAN
M.S.N. (HOD)
ASST. PROFESSOR
SSIN, BHAVNAGAR

INTRODUCTION
• Chronic obstructive pulmonary disease (COPD)is
a preventable & treatable disease state
characterised by airflow limitation that is not
reversible .The airflow limitation is usually
progressive & associated with an abnormal
inflammatory response to lungs to noxious
particles caused by cigarette smoking .

• The term chronic obstructive pulmonary disease
encompasses 2 types of obstructive airway diseases,
chronic bronchitis , emphysema . Chronic bronchitis
is the presence of chronic productive cough for 3
months in each of 2 consecutive years in a patient .
Emphysema is an abnormal permanent enlargement
of the air spaces distal to the terminal bronchioles,
accompanied by the destruction of their walls and
without obvious fibrosis.only 10% of patients with
COPD have pure Emphysema.

DEFINITION:-
• Chronic obstructive pulmonary disease
(COPD) is a disease state characterized
by the presence of airflow obstruction
caused by chronic Bronchitis or
emphysema. The airflow obstruction is
generally progressive, may be
accompanied by airway hyperactivity,
and may be partially reversible.

CHRONIC BRONCHITIS
• Chronic bronchitis, a disease of the
airways, is defined as the presence of
cough and sputum production for at
least 3 months in each of two
Consecutive years. In much case,
smoke or other environment
pollutants irritates the airways,
resulting in hyper secretion of mucus
and inflammation.

EMPHYSEMA:
• In emphysema, impaired gas
exchanges results from destruction of
the walls of over distended alveoli
“emphysema in a pathological form
that describes an abnormal distention
of the air spaces beyond the terminal
bronchioles, with destruction of the
walls of the alveoli.

TYPES
There are two main type of emphysema.
• 1. Pan lobular (Panacinar)
• There is destruction of the respiratory
bronchiole, alveolar duct, and alveoli.
All air space within the lobule are
essentially enlarged, but there is little
inflammatory disease. The patient
shows hyper inflated (hyper expended)
chest (barrel chest on physical
examination), dyspnea and weight loss.

2. Centrilobular
• In this from, pathologic changes takes
place mainly in the center of the
secondary lobule. In which the
respiratory bronchioles enlarge, the
walls are destroyed and the bronchioles
became inflamed. Frequently, there is a
derangement of ventilation- perfusion
ratios, producing chronic hypoxemia,
hypercapnia, poly cythemia and
episode of right side heart failure.

Causes and risk factors
• 1) Cigarette Smoking: -
• It is major risk factors. The prevalence of
cigarette smoking in the United States has
decreased since 1964. Nearly all-first use of
tobacco occurs before high school graduation,
and each day 3000 teenagers start to smokes.
• Clinically significant airway obstruction
develops in 15% of smokers, and 80-90% of
COPD deaths in united sates related to tobacco
smoking, when cigarettes are smoked.
Approximately 4000 chemicals and gases are
inhaled into the lungs.

• 2) Infection: -
• Recurrent respiratory tract infections.
• 3) Passive smoking
• 4) Occupational exposure
• 5) Air pollution
• 6) Heredity: - Genetic abnormality including a
deficiency of alpha1, ( 1) antitrypsin (AAT), an
enzyme inhibitor that normally counteracts the
destruction of lung tissue by certain other enzyme.
• Bronchial edema
• Hyper secretion of mucus
• Broncho spasm
• 7) Aging

INCIDENCE
• COPD is the fifth leading causing
factor of death in the united stated
states for all ages and both genders;
fifth for men and fourth for women.
More than 15 million persons in the
united status suffer from emphysema
and chronic bronchitis.

Chronic Bronchitis
Bronchial edema
Hyper secretion of mucus
Broncho spasm
Tobacco Smoke
Air Pollution
1Anti trypsin
Deficiency
Break down of elastin in
Connective tissue of lungs
Continual bronchial
Irritation and
inflammation
Emphysema
Destruction of alveolar septa
Air way instability
Airway obstruction
Dyspnea
Frequent infections

Abnormal ventilation – Perfusion ratio
Hypoxemia
Hypoventilation
Cor pulmonale
Hypoxia
Reduction of
Pulmonary
Vascular bed
Acidosis and
Hypercapnia
Pulmonary
Vasoconstriction
Polycythemia
Pulmonary Vasoconstriction
increase Pulmonary
vasculature Resistance
Pulmonary Hypertension
Right Ventricular Hypertrophy
Cor Pulmonale
Congestive heart Failure (Right Sided)//

• MECHANISM INVOLVED IN
THE PATHOPHYSIOLOGY OF
• COR PULMONALE
SECONDCERY TO CHRONIC
OBSTRUCTIVE PULMONARY
DISEASE

CLINICAL MANIFESTATION
•
• COPD is characterized by three primary symptoms
• Cough (mucopurulent, scanty, mucoid)
• Sputum production
• Dyspnea on exertion
• Weight loss because dyspnea interferes with eating
• Barrel chest
• Hypoxemia during exercise
• Cyanosis

• DIAGNOSTIC FINDING:
– Extensive history collection.
• Exposure to risk factors – types, intensity, duration
• Past medical history – respiratory disease, allergy, asthma
• Family history of COPD
• Pattern of symptoms development
• History of previous hospitalizations for respiratory problems.
• Current medical treatments
• Potential for reducing risk factors (eg. Smoking cessation)
– Physical examination
– Spirometry: - to evaluate airflow obstruction.
– ABG analysis
– Chest X-Ray
– Bronchodilator reversibility Test
– Alpha1, antitrypsin deficiency screening
– Pulmonary function Test
– ECG
• Echo – cardiogram

MANAGEMENT
• Risk reduction
• Smoking cessation is the single most effective intervention to
prevent COPD.
• Pharmacological therapy
• A) Broncho dilators
• Several classes of Broncho dilators are used
• Beta-adrenergic agonist agents
• Albuterol , Pirbuterol, Terbutaline
• b) Anticholinergic Agents
• Ipratropium bromide
• Oxitropium bromide
• c) Methylxanthines
• Aminophylline, Theophylline

• B) Corticosteroids
• Beclomethasone
• Budesonide
• Flunisolide
•
• C) Alpha1antitrypsin augmentation therapy
• D) Antibiotic agents
• E) Anti tussive agents
• F) Oxygen therapy: - it can be administered
to prevent dyspnea.

SURGICAL
MANAGEMENT
• 1. BULLECTOMY
• Bullae are enlarged air spaces that do
not contribute to ventilation but occupy
space in the thorax. These areas may be
surgically excised. Many times this
area has adequate gas exchanges.
Bullectomy may help reduce dyspnea
and improve lung function. It can be
done thoraco scopically or via a limited
thoracotomy incision.

2. LUNG VOLUME
REDUCTION SURGERY
• This is used in end stage COPD (STAGE-
III). It involves the removed of a portion
of the diseased lung parenchyma. This
allows the functional tissue to expend,
resulting in improved elastic recoil of the
lungs and improved chest wall. This type
of surgery does not cure disease, but it
may decrease dyspnea, improve lung
function and improve the patient overall
quality of life.

3. LUNG TRANSPLANTATION
• Lung transplantation is a viable
alternative for definitive surgical
treatment of end stage emphysema. It
has been shown to improve quality
of life and functional capacity but
organs are short supply and many
patient die while waiting for a
transplant.

DIETARY MANAGEMENT
• Liquid, blenderized diet may be given
• Foods that require a great deal of
chewing should be avoided
• Avoid exercise for at least 1 hour
before and after eating
• Avoid gas-forming foods such as
cabbage, beans)
• High protein and calorie diet given
• Avoid high CHO diet
• Avoid sodium if this is heart failure.

• NURSING MANAGEMENT

ASSESSMENT
• The nurses play a key role to manage
the client condition.
• Assess the general and respiratory
condition of the patient.
• Collect the important health
information
• Assess the functional health patterns
• Physical examination.

NURSING DIAGNOSIS: -
1.Impaired gas exchange and airway clearance due to
chronic inhalation of toxin.
• Goal: - improvement in gas exchange
• Intervention:
• Evaluates current smoking status,
educate regarding smoking cessation
• Provide comfortable position
• Administer and teach appropriate use
of bronchodilators
• Administer O2 to increase O2
saturation.

2. Impaired gas exchange related to
ventilation – perfusion inadequately
• Goal: - improvement in gas exchange.
• Intervention:
– Administer bronco dilators
– Evaluate effectiveness of nebulizer
– Instruct and encourage patient in
diaphragmatic breathing and effective
coughing.
– Administered O2
– Instruct the patient to avoid smoking
– Provide comfortable position.

3.Ineffective airway clearances related to bronco
constriction, increased mucus production.
• Goal: - Achievement of airway
clearance.
• Intervention:
• Adequately hydrate the patient
• Teach and encourage the use of
diaphragmatic breathing and coughing
techniques.
• Assist in nebulizer.
• Avoid the smoking
• Administer antibiotic

4.Ineffective breathing pattern related to shortness of
breath, mucus and airway irritants.
• Goal: - improvement in breathing
pattern.
• Intervention:
• Facilitate deep breathing by
elevating head
• Provide semi fowler position
• Encourage alternating activity with
rest period

5. Imbalance nutrition: less than body
requirement related to poor appetite
• Goal: - improve the nutritional status
• Intervention:
• Monitor calorie intake, weight.
• Provide menu suggestion for high
protein & calorie foods
• Give high protein and calorie diet.
• Provide liquid and frequent diet

Thanks to all