The document discusses chronic obstructive pulmonary disease (COPD). It defines COPD as a disease characterized by persistent airflow limitation that is usually caused by exposure to noxious particles or gases. The main causes of COPD are cigarette smoking and exposure to environmental pollutants. Symptoms include cough, sputum production, and shortness of breath. A diagnosis is made based on patient history and spirometry testing showing airflow limitation. Treatment focuses on bronchodilators, corticosteroids, pulmonary rehabilitation, oxygen therapy, and managing exacerbations. The goal of treatment is to improve lung function and quality of life.
3. COPD – INTRODUCTION
• Chronic obstructive pulmonary disease is a global health
problem that affects millions of people
• Is an important cause of morbidity and mortality
• COPD is one of the top ten causes of death worldwide
• COPD actually represents a spectrum of disease
ranging from destruction of the alveoli and thickening of
the terminal airways on one extreme (emphysema) to
thickening of the airways with chronic inflammation and
repeated bouts of infection (chronic bronchitis) on the
other extreme.
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4. COPD – DEFINITION
1. Chronic obstructive pulmonary disease
(COPD) is a disease state characterized by
airflow limitation that is not fully reversible.
2. COPD is characterized by persistent
irreversible respiratory symptoms and airflow
limitation due to airway and/or alveolar
abnormalities, usually caused by significant
exposure to noxious particles or gases”
- Global Initiative for Chronic Obstructive
Lung Disease (GOLD; referred to as the GOLD report)
5. COPD – ETIOLOGY
1. Smoking
- 85 to 90 percent of all COPD cases caused
by cigarette smoking.
2. Surrounding Environment – Work / Home
- Long-term exposure to air pollution,
secondhand smoke and dust, fumes and
chemicals (which are often work-related)
3. Deficiency of alpha1- antitrypsin-
- Genetic cause (inherited)
- affects the body's ability to produce a protein
(Alpha-1) that protects the lungs.
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6. COPD – RISK FACTORS
1. Exposure to tobacco smoke accounts for estimated
80% to 90% of COPD.
2. Passive smoking; breathing second hand smoke.
3. Occupational exposure.
4. Exposure to air pollution.
4. Working with dust or fumes
5. History of childhood respiratory infection
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7. COPD - PATHOPHYSIOLOGY
Pathologic changes in the lung consists of:
1. Hyperplasia of mucous secreting glands in the
trachea and bronchi
2. Disappearance of cilia
3. Chronic inflammatory changes and narrowing
of small airways.
4. Altered function of alveolar macrophages
leading to increased bronchial infections.
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9. COPD INCLUDES CHANGES AS
FOLLOWS
CHRONIC BRONCHITIS EMPHYSEMA
DISEASE OF AIRWAYS IMPAIRED GAS EXCHANGE
COUGH & SPUTUM
PRODUCTION
DESTRUCTION OF WALLS OF
OVERDISTENDED ALVEOLI
3 MONTHS IN 2 YEARS
CONSECUTIVELY END STAGE – PROGRESS OF
DISEASE
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11. EMPHYSEMA – TYPES
• Destruction of
respiratory bronchiole,
alveolar duct, & alveoli
• Air spaces within the
PANLOBULAR
(PANACINAR)
lobule are enlarged
CENTRILOBUL
AR • Changes in the center
of the secondary
lobule
(CENTRIACINA
R) • Hypoemia &
Hypecapnia
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13. CHANGES IN EMPHYSEMA
EARLY STAGE
Walls of the alveoli are destroyed
(a process accelerated by recurrent infections)
the alveolar surface area in direct contact with
the pulmonary capillaries continually decreases
Causes an increase in dead space
(lung area where no gas exchange can occur)
Impaired oxygen diffusion
leads to hypoxemia
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14. CHANGES IN EMPHYSEMA
LATER STAGE
Impairment of carbon dioxide elimination
Increases carbon dioxide tension in arterial blood
(hypercapnia) and causing respiratory acidosis
As the alveolar walls continue to break down, the
pulmonary capillary bed is reduced
Causes increase in pulmonary blood flow forcing the
right ventricle to maintain a higher blood pressure in the
pulmonary artery
Hypoxemia may further increase pulmonary artery
pressure
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16. COPD – CLINICAL MANIFESTATIONS
►Frequent & CHRONIC productive cough
►Sputum production
►Dyspnea on exertion
►Broncho -spasm occur at the end of paroxysm of
coughing
►Weight loss
►Frequent respiratory infections
►Barrel chest [emphysema]
►Contraction of abdominal muscles on inspiration
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20. COPD – DIAGNOSIS
•Patient History
•Ask about onset and duration of current symptoms
•History of smoking or occupational exposure,
allergy, other lung and heart diseases, nasal
polyps, alcohol and tobacco use, unintentional
weight loss, activity restrictions, fatigue
•Sleep patterns
•Current medications. 22
21. COPD – DIAGNOSIS
• Physical Findings of Particular Interest
• Lung auscultation will identify wheezes, rales, rhonchi,
and decreased breath sounds; sputum might be
purulent in patients with acute exacerbation and
bacterial respiratory tract infection
• Dyspnea and fatigue can be evident during meals, when
walking, and even at rest
• Capacity for independence with ADLs diminished
• Patients with emphysema can be cachec23 tic
22. COPD – DIAGNOSIS
•LABORATORY TESTS
• ARTERIAL BLOOD GAS
• In Chronic bronchitis : ABGs will show hypercapnia and
hypoxia;
• In emphysema: ABGs usually show normal PaCO2 and can
show mild hypoxia
• COMPLETE BLOOD COUNT
- leukocytosis, elevated Haematocrit - indicating polycythemia
• SPIROMETRY
• Ratio of FEV1 (volume of air that the patient can forcibly exhale
in 1 second) to forced vital capacity (FVC).
• Obstructive lung disease is defined as a FEV1/FVC ratio of24
less
23. COPD – DIAGNOSIS
•ALPHA-1 ANTITRYPSIN SCREENING
- Can be performed in patients who are < 45 years
of age or patients who have a blood relative with
COPD
•CULTURE – BLOOD & SPUTUM
- If respiratory tract infection is suspected
•B - TYPE NATRIURETIC PEPTIDE (BNP)
- if congestive heart failure is suspected
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24.
25. COPD – MEDICAL MANAGEMENT
Treatment goals:
1. Improve ventilation
2. To facilitate the removal of bronchial secretions
3. To prevent complications
4. To slow the progression of clinical manifestations.
5. To promote health maintenance
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26. MEDICAL MANAGEMENT
I. PHARMACOTHERAPY
a) Bronchodilators (beta-adrenergic agonists,
anticholinergic agents, and methylxanthines) – Via
MDI/nebulization/per oral – relieve bronchospasm &
reduce airway obstruction
For Stage I or Mild COPD – single bronchodilator
For Stage II or Moderate COPD – 1 / more bronchodilators
+ corticosteroids
b) Inhaled & Systemic Corticosteroids – For stage II or
III COPD patients
c) Antibiotics – in c/o respiratory infection contd
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27. MEDICAL MANAGEMENT
II. REMOVE BRONCHIAL SECRETIONS
ØPulmonary hygiene
ØPostural drainage
III. RESPIRATORY THERAPY
ØBreathing retraining
ØEffective coughing techniques
ØChest physiotherapy
ØAerosol nebulization therapy
contd
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30. MEDICAL MANAGEMENT
IV. OXYGEN THERAPY
►Low flow delivery devices
►High flow delivery devices
►Complications of O2 therapy
►Infection; Oxygen toxicity; CO2 narcosis; Absorption
atelectasis
V. MECHANICAL VENTILATION
In case of severe attack [acute severe exacerbation]
VI. ALPHA 1 ANTITRYPSIN THERAPY
VII. INFLUENZA AND PNEUMOCOCCAL VACCINES 32
32. SURICAL MANAGEMENT
1. BULLECTOMY
Bullae are enlarged airspaces that do not
contribute to ventilation but occupy space in the
thorax; these areas may be surgically excised. It
may help reduce dyspnea and improve lung
function
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33. SURICAL MANAGEMENT
2. LUNG VOLUME REDUCTION SURGERY
•For patients with end-stage COPD (stage III)
with a primary emphysema.
•It involves the removal of a portion of the
diseased lung parenchyma.
•This allows the functional tissue to expand,
resulting in improved elastic recoil of the lung
and improved chest wall and diaphragmatic
mechanics.
•It may decrease dyspnea, improve lung
function, and improve the patient’s overall
quality of life 35
35. SURGICAL MANAGEMENT
III. LUNG TRANSPLANTATION
•For patients with end-stage emphysema; improves
quality of life and functional capacity (NIH, 2001).
•Specific criteria exist for referral for lung
transplantation; however, organs are in short
supply and many patients die while waiting for a
transplant
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36.
37. IMPROVE GENERAL HEALTH
ØStop smoking
ØMinimize exposure to allergens
ØAvoid high altitudes
ØAdequate nutrition
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38. NURSING MANAGEMENT
1. Nursing Assessment:
q Subjective data (health information, functional
health pattern)
q Objective data (Head to foot examination)
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39. NURSING MANAGEMENT
1. Impaired gas exchange and airway clearance due to
chronic inhalation of toxins
2. Impaired gas exchange related to ventilation–perfusion
inequality
3. Ineffective airway clearance related to
bronchoconstriction, increased mucus production,
ineffective cough, bronchopulmonary infection, and
other complications
4. Ineffective breathing pattern related to shortness of
breath, mucus, bronchoconstriction, and airway
irritants
5. Activity intolerance due to fatigue, ineffective breathing
patterns, and hypoxemia
6. Deficient knowledge of self-care strategies to be
performed at home.
7. Ineffective coping related to reduced socialization,
anxiety, depression, lower activity level, and the 42
40. PATIENT EDUCATION AND HOME
CARE
1. Teach adaptive breathing techniques
2. Airway clearance technique
3. Avoid contact with persons who have URTI.
4. Importance of prescribed medications
5. Teach the family how to manage during
acute attacks of dyspnea.
6. Report any change in the health status
7. Avoid dust producing articles at home and
stop smoking.
8. Adequate fluid intake
9. Food choice modification
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41. COMPLICATIONS OF COPD
1) Respiratory insufficiency or failure
2) Atelectasis
3) Acute exacerbation of Chronic Bronchitis
4) Pulmonary infection; pneumonia
5) Pneumothorax
6) Pulmonary hypertension
7) Cor pulmonale
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![CHRONIC OBSTRUCTIVE LUNG
DISEASE [COPD]
DR. GARGEE KARADKAR
ASSOCIATE PROFESSOR
BVDUCON, NAVI MUMBAI
1](https://image.slidesharecdn.com/copd1-221204121248-b9250961/85/COPD-Chronic-obstructive-pulmonary-disease-1-320.jpg)
