Chronic Obstructive

Pulmonary Disease
Christine Loren T. Laya
BSN 3-1
Chronic Obstructive
Pulmonary Disease (COPD)
A preventable and treatable slowly
progressive respiratory disease of
airflow obstruction involving the:
-Airways
-Pulmonary Parenchyma
(functional tissue of an organ as distinguished from the
connective and supporting tissue) Alveoli. Alveolar ducts.
Bronchioles.

-Both
Airflow obstruction:
 Pulmonary Parenchyma
Chronic pulmonary disorders:
 Cystic fibrosis – produces thick sticky mucus
 Bronchiectasis - condition where the bronchial
tubes of your lungs are permanently damaged,
widened, and thickened.
 Pathophysiology
Inflammatory and structural changes occur in:

 Proximal airways – changes include increased numbers

of goblet cells and enlarged submucosal glands which lead
to hypersecretion of mucus.
Trachea
Bronchi (greater than 2 mm diameter)

 Peripheral airways – inflammation causes thickening of

the airway wall, exudate in the airway & overall narrowing.
Bronchioles (less than 2 mm diameter)
 Lung Parenchyma (portion of the lung involved in gas transfer)

Respiratory bronchioles
Alveoli
-loss of alveolar attachments
-decrease in elastic coil

 Pulmonary Vasculature
-Thickening of the vessel wall
-Increased vascular smooth muscle
-Pulmonary Hypertension
 Disease of the airways
 presence of cough and sputum production for at least
3 months in each 2 consecutive years
(Smoke or other environmental pollutants irritate
airways)
Cilia – sweeps mucus and dirt
out of the lungs

Bronchial walls become

thickened; further narrowing
bronchial lumen

Alveolar adjacent to the

bronchioles may be damaged
and fibrosed resulting in
altered function of Alveolar
Macrophages.

Chronic Bronchitis
Emphysema
 long-term, progressive disease of the
lungs that primarily causes shortness of
breath due to over-inflation of the alveoli
 Pulmonary Capillaries allow rapid exchange of respiratory gases

 As the walls of the alveoli are destroyed, the pulmonary

capillaries continually decreases.

 Hypoxemia – impaired oxygen diffusion

 Dead space – lung area where no gas exchange can occur and
impaired O2 diffusion which leads to Hypoxemia.
 Hypercapnia – increased CO2 tension in
arterial blood which can lead to
respiratory acidosis.

 Cor Pulmonale – right sided heart failure

brought on by long term high blood
pressure in the pulmonary arteries

Signs and Symptoms:

Edema
Distended neck veins
Pain in the region of the liver
 2 Main Types of Emphysema:
 Panlobular (panacinar)
type:
Destruction of respiratory
bronchiole, alveolar duct,
and alveolus.
Signs and Symptoms:
 Hyperinfalted chest
 Dyspnea
 Weight loss
•Centrilobular
(centroacinar) form:
There are changes in the
center of the secondary
lobule.
Derangement of
ventilation-perfusion.
Signs and Symptoms:
Chronic hypoxemia
Hypercapnia
Polycythemia
Right sided heart failure
Risk Factors
 Expossure to tobacco smoke
 Passive smoking (secondhand smoke)
 Increased age
 Occupational exposure (dust, chemicals)
 Indoor and outdoor pollution
 Genetic abnormalities, including a
deficiency of alpha-1 antitrypsin (an
enzyme inhibitor that protects lung
parenchyma)
Treatment
 Alpha-protease Inhibitor replacement
therapy, which slows progression of the
disease

Clinical Manifestations
 Chronic cough
 Sputum production
 Dyspnea
 Weight loss
 “barrel chest” thorax
Assessment and Diagnostic
Findings
 Spirometry
 Arterial blood gas measurements
 Chest x-ray
 CT chest scan
 Screening for alpha1-antitrypsin
deficiency for patients younger than 45
years and for those with strong family
history of COPD.
 Pulmonary function test
Complications
 Respiratory insufficiency and failure
 Pneumonia
 Chronic atelectasis
 Pneumothorax
 Pulmonary arterial hypertension (cor
pulmonale)
 Medical Management
 Risk reduction – smoking cessation

Pharmacologic Therapy
•Bronchodilator
a. Metered-dose inhaler
b. Long-acting B2 agonist
bronchodilators
c. Nebulized medications (wet nebulizers)
•Corticosteroids
Management of Exacerbations

 Roflumilast – oral tablet taken once daily

 Antibiotics
 Oxygen Therapy – to increase the
baseline resting partial pressure of arterial
oxygen
Surgical Management
 Bullectomy
 Lung transplantation
 Pulmonary Rehabilitation
 Patient education
 Breathing exercises
Nursing Management

 Assess the patient

 Achieving airway clearance
 Improving breathing patterns
 Improving activity tolerance
Bronchiectasis
 Chronic, irreversible dilation of bronchi
and bronchioles that results from
destruction of muscles and elastic
connective tissue.
Causes:
 Airway obstruction
 Diffuse airway injury
 Complications of long-term pulmonary
infections
(measles, influenza, tuberculosis)
Pathophysiology
 Usually localized, affecting a segment or
lobe of a lung, most frequently the lower
lobes.

 ATELECTASIS
Clinical Manifestation
 Chronic cough
 Production of purulent
sputum in copious
amounts
 Clubbing of the fingers
 Repeated episodes of
pulmonary infection
(pneumonia/measles,
influenza, TB)
Assessment and diagnostic
findings
 Prolonged history of productive cough
with sputum consistently negative for
Tubercle Bacilli

 CT scan – bronchial dilation

Medical Management
Treatment objectives to promote:

 Bronchial drainage
 Clear excessive secretions from the
affected portion of the lungs
 Prevent or control infection
Medical Management:
1. Postural drainage
2. Bronchoscopy
3. Chest physiotherapy
-percussion and postural drainage
4. Smoking cessation
5. Antibiotics
Pseudomonas Aeruginosa
6. Vaccine against influenza & pneumococcal
pneumonia
7. Bronchodilators
8. Surgical treatment
9. Segmental Resection
10. Lobectomy
11. Pneumonectomy
Nursing Management
 Patient education
 Patient and families are thought to
perform postural drainage
Asthma
 A chronic inflammatory disease of the airways
that causes hyperresponsiveness, mucosal
edema, and mucus production.

 A reversible diffuse airway inflammation that

leads to airway narrowing.

Symptoms:
-cough
-chest tightness
-Wheezing
-dyspnea
 Pathophysiology
Inflammation of asthma
-Mast cells
-Macrophages
-T lymphocytes
-neutrophils
-eosinophils

MEDIATORS – perpetuate the inflammatory response

•Histamine
•Bradykinin
•Prostanoids
•Cytokines
Clinical Manifestations

 Cough
 Dyspnea
 Wheezing
Assessment and diagnostic
Findings
 Sputum and blood tests (elevated
eosinophils)
 Arterial blood gas analysis
 Pulse oximetry reveal hypoxemia
 PaCO2 may increase
Medical management
 Pharmacologic therapy
-quick relief meds

Ventolin – to treat or prevent bronchospasm

Levalbuterol – to relieve wheezing, shortness of breath

Anticholinergics – to prevent muscle bands around the

airways from tightening

-long acting meds

Corticosteroids – to provide relief for inflamed areas of

the body
Nursing management
 Assess the patient’s respiratory status by
monitoring the severity of symptoms,
breath sounds, peak flow pulse oximetry
and vital signs.
 Administer meds as prescribed
 Administer fluids if the patient is
dehydrated.