Chronic Obstructive

Pulmonary Disease[ COPD]

NUR/00035/022
NUR/00041/022
NUR/00043/022
NUR/00014/022
NUR/00053/022
OBJECTIVES
• 1. Describe the pathophysiology, clinical
manifestations, and treatment of chronic obstructive
pulmonary disease (COPD).
• 2. Discuss the major risk factors for developing COPD
and nursing interventions to minimize or prevent these
risk factors.
• 3. Use the nursing process as a framework for care of
patients with COPD.
 INTRODUCTION
• Chronic obstructive pulmonary disease (COPD) is a preventable and
treatable slowly progressive respiratory disease of airflow obstruction
involving the airways, pulmonary parenchyma, or both.
• The parenchyma includes any form of lung tissue, including
bronchioles, bronchi, blood vessels, interstitium, and alveoli. The
airflow limitation or obstruction in COPD is not fully reversible.
• COPD may include diseases that cause airflow obstruction (two distinct
disease process: emphysema, chronic bronchitis) or any combination
of these disorders.
• COPD can coexist with asthma. Both of these diseases have the same
major symptoms; however, symptoms are generally more variable in
asthma than in COPD
PATHOPHYSIOLOGY
• In COPD, the airflow limitation is both progressive and associated with
the lungs’ abnormal inflammatory response to noxious particles or
gases. The inflammatory response occurs throughout the proximal
and peripheral airways, lung parenchyma, and pulmonary vasculature.
• Because of the chronic inflammation and the body’s attempts to
repair it, changes and narrowing occur in the airways. In the proximal
airways (trachea and bronchi greater than 2 mm in diameter),
changes include increased numbers of goblet cells and enlarged
submucosal glands, both of which lead to hypersecretion of mucus.
 In the peripheral airways (bronchioles less than 2 mm diameter),
inflammation causes thickening of the airway wall, peribronchial
fibrosis, exudate in the airway, and overall airway narrowing
(obstructive bronchiolitis).
Over time, this ongoing injury-and-repair process causes scar tissue
formation and narrowing of the airway lumen (GOLD, 2015).
Inflammatory and structural changes also occur in the lung parenchyma
(respiratory bronchioles and alveoli).
Alveolar wall destruction leads to loss of alveolar attachments and a
decrease in elastic recoil.
• Finally, the chronic inflammatory process affects the pulmonary
vasculature and causes thickening of the lining of the vessel and
hypertrophy of smooth muscle, which may lead to pulmonary
hypertension
• Processes related to imbalances of substances (proteinases and
antiproteinases) in the lung may also contribute to airflow limitation.
• When activated by chronic inflammation, proteinases and other
substances may be released, damaging the parenchyma of the lung.
• These parenchymal changes may also occur as a consequence of
inflammation or environmental or genetic factors.
CHRONIC BRONCHITIS
• In many cases, smoke or other environmental pollutants irritate the
airways, resulting in inflammation and hypersecretion of mucus.
• Mucus plugging of the airway reduces ciliary function.
• Bronchial walls also become thickened, further narrowing the
bronchial lumen.
• Alveoli adjacent to the bronchioles may become damaged and
fibrosed, resulting in altered function of the alveolar macrophages.
 Risk Factors for Chronic Obstructive
Pulmonary Disease (COPD)
• Exposure to tobacco smoke accounts
for an estimated 80% to 90% of COPD
cases
• Passive smoking
• Occupational exposure—dust,
chemicals
• Ambient air pollution
• Genetic abnormalities, including a
deficiency of alpha1- antitrypsin, an
enzyme inhibitor that normally
counteracts the destruction of lung
tissue by certain other enzymes
 Clinical Manifestations

• Although the natural history of COPD

is variable, it is generally a
progressive disease characterized by
three primary symptoms: chronic
cough, sputum production, and
dyspnea
• In patients with COPD that has a
primary emphysematous component,
chronic hyperinflation leads to the
“barrel chest” thorax configuration
COPD is classified into four stages
depending upon the severity (measured
by pulmonary function tests) and
symptoms
• Stage I (mild) is defined by an
FEV1/FVC less than 70% and an FEV1
greater than or equal to 80%
predicted, and the patient may be
with or without symptoms of cough
and sputum production.
• Stage II (moderate) is defined by an
FEV1/FVC less than 70%, an FEV1
50% to 80% predicted, and shortness
of breath typically developing upon
exertion.
• Stage III (severe) is defined as an
FEV1/FVC less than 70% and an FEV1
less than 30% to 50% predicted.
Severe COPD symptoms increased
shortness of breath, reduced exercise
capacity, and repeated exacerbations.
• stage IV (very severe) is defined as an
FEV1/FVC less than 70%, an FEV1 less
than 30% to 50% predicted, and
symptoms/signs of chronic
respiratory failure.
 Medical Management
• Risk Reduction-smoking cessation is the single
most cost-effective intervention to reduce the
risk of developing COPD and to stop its
progression
• Bronchodilators-Bronchodilators relieve
bronchospasm by altering smooth muscle tone
and reduce airway obstruction by allowing
increased oxygen distribution throughout the
lungs and improving alveolar ventilation. Several
classes of bronchodilators are used, including
beta-adrenergic agonists (short- and long-
acting), anticholinergic agents (short- and long-
acting), methylxanthines.
• Oxygen Therapy-Oxygen therapy can be
administered as long-term continuous therapy,
during exercise, or to prevent acute dyspnea
during an exacerbation.
• Lung Volume Reduction Surgery-Treatment
options for patients with end-stage COPD (stage
IV) with a primary emphysematous component
are limited, although lung volume reduction
surgery is a palliative surgical option in a selected
subset of patients
 Nursing Management
Assessing the Patient-Assessment involves obtaining
information about current symptoms as well as previous
disease manifestations.
Achieving Airway Clearance
Improving Breathing Patterns-Training in diaphragmatic
breathing reduces the respiratory rate, increases alveolar
ventilation, and sometimes helps expel as much air as
possible during expiration.
Improving Activity Tolerance-Education is focused on
rehabilitative therapies to promote independence in
executing activities of daily living.
Monitoring and Managing Potential Complicationssuch as
life-threatening respiratory insufficiency and failure
EMPHYSEMA
• Emphysema is a pathologic term that describes an abnormal
distention of the airspaces beyond the terminal bronchioles and
destruction of the walls of the alveoli .
• In addition, a chronic inflammatory response may induce disruption
of the parenchymal tissues.
• Destruction o the wall o the alveoli reduces the alveolar surface area
in direct contact with pulmonary capillaries causing an increase in
dead space which lead to impaired oxygen diffusion leading to
hypoxemia. In latter stages, carbon[IV]oxide elimination is impaired
resulting in hypercapnia leading to respiratory acidosis.
Empyema
• An empyema is an accumulation of thick, purulent fluid within the
pleural space, often with fibrin development and a loculated (walled-
off) area where infection is located
Pathophysiology
• Empyemas often stem from:
• Bacterial pneumonia or lung abscess.
• Penetrating chest trauma.
• Hematogenous infection of the pleural space.
• Nonbacterial infections.
• Iatrogenic causes, such as after thoracic surgery or thoracentesis.
• Initially, pleural fluid is thin with a low leukocyte count.
• Progression typically involves:
a. Advancement to a fibropurulent stage
b. Enclosure of the lung within a thick exudative membrane (loculated
empyema).
Clinical Manifestations
• Acutely ill presentation with signs and symptoms resembling acute respiratory
infection or pneumonia.
• Common symptoms include:
• Fever.
• Night sweats.
• Pleural pain.
• Cough.
• Dyspnea (shortness of breath).
• Anorexia.
• Weight loss.
• Clinical manifestations may be less obvious in patients who have received
antimicrobial therapy.
• Assessment findings:
• Decreased or absent breath sounds over the affected area on chest
auscultation. Dullness on chest percussion. Decreased fremitus.
• Diagnostic procedures:
• Chest CT scan, Diagnostic thoracentesis, Thoracentesis
Medical Management
•Treatment objectives:
1.Drain the pleural cavity.
2.Achieve complete lung expansion.
•Antibiotic therapy:
•Initial IV antibiotics prescribed in large doses based on the causative organism.
•Sterilization of the empyema cavity requires 4 to 6 weeks of antibiotics.
•Drainage methods:
1.Needle aspiration (thoracentesis) with a thin percutaneous catheter for small volume and less
purulent/thick fluid.
2.Tube thoracostomy (chest drainage using a large-diameter intercostal tube) with fibrinolytic agents
for loculated or complicated pleural effusions.
3.Open chest drainage via thoracotomy, potentially involving rib resection, to remove thickened pleura,
pus, and underlying diseased pulmonary tissue.
•Surgical intervention:
•Decortication may be necessary for long-standing inflammation, removing the
exudate trapping the lung and interfering with its expansion.
•Drainage tube left until the pus-filled space is completely obliterated,
monitored by serial chest x-rays.
•Long-term management:
•Treatment may be extended for weeks to months.
•Patients may be discharged with a chest tube and instructed to monitor fluid
drainage at home
Nursing Management
• Coping support: Providing emotional support.
• Respiratory exercises: Instructing the patient in lung-expanding breathing
exercises to restore normal respiratory function.
• Providing care tailored to the method of pleural fluid drainage, whether it's
needle aspiration, closed chest drainage, or surgical procedures like rib
resection.
• Patient and family education: Educating both the patient and their family on:
• Care of the drainage system and drain site.
• Measurement and observation of drainage.
• Signs and symptoms of infection to watch for.
• When and how to contact the primary healthcare provider for any concerns or
worsening symptoms.