CH

1. COPD
(CHRONIC OBSTRUCTIVE
PULMONARY DISEASE)
MONIKA TIMBADIYA
F.Y.M.SC. NURSING
IKDRC

2. ANATOMY OF BRONCHI AND ALVEOLI

3. INTRODUCTION
 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).
 COPD is a slowly progressive respiratory
disease of airflow obstruction involving the
airways, pulmonary parenchyma, or both.

4. DEFINITION
COPD is a chronic lung disease characterized
by chronic obstruction of lung airflow that
interfere with normal breathing and is not fully
reversible.

6. COPD MAY INCLUDE DISEASES THAT
CAUSE AIRFLOW OBSTRUCTION

7.  In COPD, less air flows in and out of the
airways because of one or more of the
following:
 The airways and air sacs lose their elastic
quality.
 The walls between many of the air sacs are
destroyed.
 The walls of the airways become thick and
inflamed.
 The airways make more mucus than usual,
which tend to clog them.

8. 1. CHRONIC BRONCHITIS

9. DEFINITION :
 Chronic bronchitis, a disease of airways, is defined
as the presence of cough and sputum production
for at least 3 months in each of 2 consecutive
years.
 Chronic bronchitis is an ongoing, serious condition.
It occurs if the lining of the bronchial tubes is
constantly irritated and inflamed, causing long
terms cough with mucus.

11. 2. EMPHYSEMA

12.  Emphysema (from the Greek word for
“inflation”) is a lung disease that involves
damage to the air sacs (alveoli) in the lungs.
 Emphysema is a long-term, progressive
disease of the lungs that primarily causes
shortness of breath due to over-inflation of
the alveoli.
 As the alveoli are destroyed the alveolar
surface area in contact with capillaries
decreases. Causing dead spaces (no gas
exchange takes place) leads to hypoxia.

13.  In later stage:
CO2 elimination is disturbed and increase in CO2
tension in arterial blood causing respiratory acidosis.

14. CAUSES AND RISK
FACTORS

15. 1. Tobacco smoke
3.Cigarette
smoking
2. Passive
smoking
8. Occupational
exposure
4. Air
pollution
5. Alpha 1-
antitrypsin
deficiency
7. Family
history
6. Age

16. PATHOPHYSIOLOGY

17. Tobacco smoke &Air pollution
Breakdown of elastin in
connective tissue of lungs
Continual bronchial
irritation & inflammation
Chronic bronchitis
bronchial edema,
hypersecretion of mucus,
chronic cough,
bronchospasm
Emphysema
destruction of alveolar
septa, airway instability
Airway obstruction, Air trapping, Dyspnea,
Frequent infections
•Abnormal ventilation – perfusion ratio
Hypoxemia & Hypoventilation, Cor pulmonale
α1 – antitrypsin
deficiency

18. STAGES OF COPD
Stage 0: At risk.
Stage 1: Mild COPD.
Stage 2 : Moderate COPD
Stage 3 : Severe COPD
Stage 4 : Very severe COPD

19. CLINICAL
MANIFESTATION

20. Chronic
coughing
– Dyspnea
Sputum
production Wheezing
Weight
loss
Chest
tightness
Fatigue

21. ADVANCED COPD SYMPTOMS
Cyanosis Barrel chest
Morning
headaches
Hemoptysis edema

22. DIAGNOSTIC EVALUATION

23.  History and Physical Examination

24.  Lung Function test:
Spirometry: it measures lung function,
specifically the amount and/or speed of air that
can be inhaled and exhaled.

25.  Chest x-ray or chest CT scan:
 Arterial blood gas analysis:
 Alpha-1- antitrypsin level

26.  Pulse Oximetry: A less invasive method to
measure oxygen levels in the blood is called
pulse oximetry. A probe is placed around a
fingertip to measure the percentages of
oxygen saturation in the blood.

27. MANAGEMENT

28. Management
Medical
Pharmacological
Non-
Pharmacological
Surgical Nursing

29. MEDICAL MANAGEMENT
 Goal :
 To prevent further deterioration in lung
function.
 To alleviate symptoms
 To improve performance of daily activities
and quality of life

30.  Pharmacological
 Smoking cessation using nicotine replacement
therapies
 Bronchodilators and anti-inflammatory agents
 Mucolytic
 Antibiotics
 Immunization
 Treatment of Alpha-1-antitrypsin deficiency

31.  Non-pharmacological
1. Nebulization

32. 2. Oxygen therapy

33. 3. Exercise
Diaphragmatic breathing Pursed lip breathing

34. PULMONARY REHABILITATION
 The primary goal of rehabilitation is to restore
patients to the highest level of independent function
possible and to improve their quality of life.
 Breathing exercises and retraining exercise
programs are used to improve functional status,
and the patient is taught methods to alleviate
symptoms.

35. LIFE STYLE CHANGES
 Clear airways- controlled coughing, drinking
plenty of water.
 Exercise regularly.
 Eat healthy foods.
 Avoid smoke.
 Avoid exposure to fumes and dust.
 Pay attention to frequent heartburn.
 Follow up regularly.

36. SURGICAL MANAGEMENT
1.Bullectomy 2. lung volume reduction
3. Lung transplant

37. NURSING MANAGEMENT
 Assessment

38.  Nursing diagnosis
 Ineffective airway clearance related to
bronchoconstriction, increased mucus
production, ineffective cough.
 Impaired gas exchange related to decreased
ventilation, chronic pulmonary obstruction,
abnormalities due to destruction of alveolar
capillary membrane.
 Ineffective breathing pattern related to shortness
of breath, mucus, bronchoconstriction, and
airway irritants.

39.  Imbalanced nutrition: less than body
requirements related to increased work of
breathing, air swallowing, drug effects with
resultant wasting of respiratory and skeletal
muscles.
 Activity intolerance related to fatigue,
inadequate oxygenation and dyspnea.
 Anxiety related to acute breathing difficulties
and fear of suffocation

40.  Intervention
 Encourage diaphragmatic and coughing
techniques.
 Change patient’s position every 2 hourly.
 Teach the patient to maintain adequate
hydration by drinking at least 8-10 glasses of
fluid per day.
 Administer low flow oxygen therapy.
 Administer bronchodilators if ordered.
 Advise the client to eat small frequent meals
that are high in protein and calories.
 Keep the environment free from pollution.