COPD

Definition

• A common preventable and treatable disease, is

characterized by persistent airflow limitation that is
usually progressive and associated with an enhanced
chronic inflammatory response in the airways and the
lung to noxious particles or gases.
Global Initiative for Chronic Obstructive
Lung Disease
COPD includes
• 1) Chronic Bronchitis
• 2) Emphysema
 Chronic bronchitis

• Chronic bronchitis Defined as a chronic productive

cough for three months in each of two successive years
in a patient in whom other causes of chronic cough
have been excluded
 Emphysema

• Emphysema Abnormal and permanent enlargement of the airspaces

distal to the terminal bronchioles that is accompanied by destruction
of the airspace walls, without obvious fibrosis
 Risk Factors for COPD
• Genes
• Smoking
• Occupational Exposure
• Air pollution
• Aging Populations
• Low Birth Weight and Prematurity: Impaired lung development can
predispose individuals to COPD later in life.
• Childhood Respiratory Infections: Recurrent infections in early life can
lead to reduced lung growth and function.
 Genetics
• Alpha 1-antitrypsin deficiency is a genetic condition that is
responsible for about 2% of cases of COPD.

• In this condition, the body does not make enough of a protein,

alpha 1-antitrypsin.

• Alpha 1-antitrypsin protects the lungs from damage caused by

protease enzymes, such as elastase and trypsin, that can be
released as a result of an inflammatory response to tobacco
smoke.
PATHOLOGY
 Chronic inflammation of
the airway

Increased numbers of goblet cells

Mucus gland hyperplasia

Fibrosis
Narrowing and reduction in the Airway collapse due to alveolar
number of small airways wall destruction in emphysema
In Detail
1. Chronic Inflammation
• Triggering Factors: Exposure to harmful substances, such as cigarette
smoke, air pollutants, and occupational dust and chemicals, leads to
chronic irritation of the respiratory tract

• Cellular Involvement:
• Neutrophils, macrophages, and CD8+ T lymphocytes infiltrate the
airways.
• These cells release inflammatory mediators like tumor necrosis factor-
alpha (TNF-α), interleukins (IL-8, IL-1β), and leukotrienes.

• Oxidative Stress: Harmful particles increase reactive oxygen species

(ROS), further amplifying inflammation and tissue damage.
2. Airway Remodeling
• Structural Changes: Chronic inflammation causes thickening of airway
walls, fibrosis, and narrowing of small airways.

• Goblet Cell Hyperplasia: Increased goblet cells lead to excessive

mucus production, contributing to airway obstruction.

• Smooth Muscle Hypertrophy: Prolonged inflammation leads to

thickening and stiffening of smooth muscle in the airways.
3. Parenchymal Destruction

• Emphysema:
• Destruction of alveolar walls and loss of elastic fibers due
to protease-antiprotease imbalance.

• Elevated levels of proteases (e.g., neutrophil elastase,

matrix metalloproteinases) break down elastin, while
antiproteases (e.g., alpha-1 antitrypsin) are insufficient to
counteract this damage.

• Results in enlarged alveoli, reduced surface area for gas

exchange, and impaired elastic recoil.
4. Small Airway Obstruction

• Bronchiolitis: Chronic inflammation in small airways (<2 mm in

diameter) causes thickening and obstruction.

• Loss of Elastic Support: Destruction of lung parenchyma leads to

collapse of small airways during exhalation.
5. Vascular Changes

• Pulmonary Hypertension:
• Hypoxia-induced vasoconstriction increases vascular resistance.
• Remodeling of pulmonary arteries (intimal thickening, medial
hypertrophy) exacerbates hypertension.
Clinical Correlation
• Airflow Limitation: A combination of mucus hypersecretion,
airway narrowing, and parenchymal destruction leads to
reduced expiratory airflow.

• Hyperinflation: Loss of elastic recoil traps air in the lungs,

increasing residual volume.

• Ventilation-Perfusion Mismatch: Impaired gas exchange

results in hypoxemia and, in advanced stages, hypercapnia.
Subtypes of emphysema
Normal acinus
 Clinical manifestations
• Respiratory symptoms

• Dyspnea
Initially occurs during exertion and progresses to at-rest dyspnea in
advanced stages.
• Chronic Cough
• Sputum Production:
• Sputum may be clear, yellow, or green, particularly during infections.
Systemic Manifestations
1.Weight Loss and Muscle Wasting:
• Increased metabolic demand due to breathing effort and systemic
inflammation.
• Loss of appetite and catabolic effects of chronic illness.
2.Fatigue: Chronic hypoxia and increased work of breathing contribute
to reduced energy levels.

3.Peripheral Edema: Indicates right-sided heart failure (cor-pulmonale)

secondary to pulmonary hypertension.
Physical Examination Findings
• General Appearance:
• Barrel-shaped chest (due to hyperinflation).
• Pursed-lip breathing (helps maintain airway patency).
• Use of accessory respiratory muscles (neck and shoulder muscles).
• Respiratory Sounds:
• Prolonged expiratory phase.
• Wheezing or crackles on auscultation.
• Decreased breath sounds in severe cases due to emphysema.
• Cyanosis:
• Bluish discoloration of lips and extremities in advanced disease due to
hypoxemia.
5. Advanced Disease Manifestations
• Hypoxemia and Hypercapnia
• Digital Clubbing:
• Signs of Cor Pulmonale:
Jugular venous distension (JVD).
Hepatomegaly (enlarged liver).
Ascites and leg swelling.
Diagnosis
Clinical History:
• Chronic symptoms of cough, sputum production, and progressive
dyspnea.
• History of smoking or exposure to risk factors.
Diagnosis
1. Pulmonary Function Tests (Spirometry)
• Gold Standard Test for COPD Diagnosis
• Forced Vital Capacity (FVC):
• Total amount of air that can be exhaled after a deep breath.
• Forced Expiratory Volume in 1 Second (FEV₁):
• Volume of air exhaled in the first second of a forceful expiration.
• FEV₁/FVC Ratio:
• A post-bronchodilator FEV₁/FVC ratio < 0.70 confirms persistent airflow
limitation and COPD diagnosis.
Classification of Severity (Based on % Predicted
FEV₁):

• Mild (FEV₁ ≥ 80% predicted).

• Moderate (50% ≤ FEV₁ < 80% predicted).
• Severe (30% ≤ FEV₁ < 50% predicted).
• Very Severe (FEV₁ < 30% predicted).
2. Imaging Studies
• Chest X-Ray:
• Helps rule out other conditions like pneumonia or lung cancer.
• May show signs of hyperinflation, flattened diaphragm, and increased
retrosternal airspace in emphysema.
• High-Resolution CT (HRCT) Scan:
• Provides detailed images to assess the extent of emphysema and airway
changes.
• Useful for detecting bullae or coexisting lung diseases.
3. Blood Tests
• Arterial Blood Gas (ABG):
• Complete Blood Count (CBC):
• Alpha-1 Antitrypsin (AAT) Levels
Management
• Medical management
a. Bronchodilators (First-line therapy)

• Short-Acting Bronchodilators (Relievers):

• Short-Acting Beta-2 Agonists (SABAs): e.g., Salbutamol, Levalbuterol.
• Short-Acting Muscarinic Antagonists (SAMAs): e.g., Ipratropium.
• Used for symptom relief in acute episodes.
• Long-Acting Bronchodilators (Maintenance therapy):
o Long-Acting Beta-2 Agonists (LABAs): e.g., Salmeterol, Formoterol.
o Long-Acting Muscarinic Antagonists (LAMAs): e.g., Tiotropium,
Glycopyrrolate.
o Improve lung function, reduce symptoms, and prevent exacerbations.
b. Inhaled Corticosteroids (ICS)
• e.g., Budesonide, Fluticasone.
• Indicated for patients with frequent exacerbations or evidence of
asthma-COPD overlap (ACO).
• Often combined with LABAs for synergistic effects.
c. Combination Therapy
• LABA + LAMA: For moderate to severe COPD to optimize
bronchodilation.
• LABA + ICS: For patients with high eosinophil counts or frequent
exacerbations.
d. Phosphodiesterase-4 (PDE4) Inhibitors
• e.g., Roflumilast.
• Reduces inflammation and exacerbations in severe COPD with chronic
bronchitis.
e. Methylxanthines
• e.g., Theophylline.
• Used less frequently due to narrow therapeutic window and side
effects.
f. Antibiotics
• Long-term use of macrolides (e.g., Azithromycin) may reduce
exacerbations in select patients with frequent infections.
g. Mucolytics
• e.g., N-acetylcysteine, Carbocysteine.
• May help in patients with chronic productive cough by thinning
mucus.
• 2. Oxygen Therapy
• Long-Term Oxygen Therapy (LTOT):
• Indicated for patients with chronic hypoxemia (PaO₂ ≤ 55 mmHg or SpO₂ ≤
88%).
• Improves survival in severe COPD with resting hypoxemia.
• Ambulatory Oxygen:
• For patients with exercise-induced desaturation.
• Surgical Interventions (For Severe COPD)
• Lung Volume Reduction Surgery (LVRS):
• Removes diseased lung tissue to improve lung function in selected patients
with emphysema.
• Bullectomy:
• Removes large air-filled spaces (bullae) that compress healthy lung tissue.
• Lung Transplantation:
• Considered for younger patients with end-stage COPD.
Non-Pharmacological
Management
• Smoking Cessation:
• The most effective intervention to slow disease progression.
• Includes behavioral counseling, nicotine replacement therapy (NRT), or medications
like Varenicline and Bupropion.
• Pulmonary Rehabilitation:
• A multidisciplinary program including exercise training, education, and psychological
support.
• Improves exercise tolerance and quality of life.
• Vaccinations:
• Annual influenza vaccine and pneumococcal vaccines (PCV13, PPSV23) to prevent
infections.
• Nutritional Support:
• Proper nutrition to manage weight loss or obesity.
• Patient Education:
• Training in proper inhaler techniques and self-management strategies.
Management of Exacerbations
• Bronchodilators:
• Increase dose or frequency of SABAs or add SAMAs.
• Systemic Corticosteroids:
• e.g., Prednisone (30-40 mg daily for 5-7 days).
• Reduces inflammation and accelerates recovery.
• Antibiotics: Indicated for exacerbations with purulent sputum or signs
of infection (e.g., Amoxicillin-Clavulanate, Azithromycin, Doxycycline).

• Oxygen Therapy: Titrated to maintain SpO₂ between 88-92%.

• Non-Invasive Ventilation (NIV):For acute respiratory failure to reduce

the need for intubation.
• Monitoring and Follow-Up

• Regular follow-up to:

• Monitor symptoms and lung function (spirometry).
• Assess adherence to treatment.
• Identify and address complications or comorbidities.
 Nursing Management
1. Impaired gas exchange related to alveolar-capillary membrane changes, air trapping

and bronchoconstriction as evidenced by dyspnea and low oxygen saturation levels

• Interventions:
1. Assess respiratory rate, depth, and effort regularly.
2. Monitor oxygen saturation using pulse oximetry.
3. Administer oxygen therapy as prescribed (e.g., nasal cannula at 1–2 L/min).
4. Position the patient in a semi-Fowler’s or high Fowler’s position to facilitate lung
expansion.
5. Encourage pursed-lip breathing to promote alveolar ventilation.
6. Administer prescribed bronchodilators and corticosteroids.
2. Ineffective airway clearance related to excessive mucus production
and inability to clear secretions as evidenced by persistent cough,
abnormal breath sounds (e.g., wheezing, crackles),use of accessory
muscles for breathing

Interventions:
1.Assess for the presence of sputum (color, consistency, and amount).
2.Encourage adequate hydration (if not contraindicated) to thin
secretions.
3.Teach controlled coughing techniques to mobilize secretions.
4.Perform chest physiotherapy or postural drainage as needed.
5.Administer mucolytic agents or expectorants as prescribed.
• 3. Activity intolerance related to imbalance between oxygen supply
and demand dyspnea during exertion as evidenced by complaints of
fatigue

• Interventions:
1.Assess baseline activity level and response to activities.
2.Plan care to include rest periods between activities.
3.Assist with activities of daily living (ADLs) as needed.
4.Encourage participation in pulmonary rehabilitation exercises.
5.Monitor vital signs before, during, and after activities.
• 4. Risk for Infection
• 5. Anxiety