Chronic Obstructive Pulmonary Disease Overview

Chronic Obstructive Pulmonary Disease (COPD)

• COPD is a preventable and treatable disease characterized by airflow limitation not fully reversible.
• Airflow limitation is usually progressive due to an abnormal inflammatory response in the lungs to noxious particles or gases, primarily cigarette smoking.
• COPD is composed of two major disease entities: emphysema and chronic bronchitis.

Chronic Bronchitis

• Chronic bronchitis is defined by the clinical manifestations associated with it, specifically a chronically productive cough due to bronchial inflammation.
• It's considered chronic when it lasts for at least 3 consecutive months in 2 successive years.
• The pathology involves enlarged bronchial mucous glands (hypertrophy), increased goblet cells, and excess mucus production.
• Reduced ciliary function leads to mucus plugging in the smaller airways, promoting infection and causing ventilation/perfusion (V/Q) mismatching, impacting gas exchange and leading to hypoxemia.
• Etiological factors include cigarette smoking, atmospheric pollutants, infection, and gastroesophageal reflux disease.
• Clinical manifestations include excessive bronchial secretions and bronchospasm.
• COPD patients with chronic bronchitis can have dusky/cyanotic color, increased sputum production, hypoxemia, hypercapnea, acidosis, edematous, increased respiratory rate, exertional dyspnea, and digital clubbing. Heavy cigarette smokers are at higher risk. Cardiac enlargement and use of accessory muscles to breathe is also observed.

Emphysema

• Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls without obvious fibrosis.
• The alveolar-capillary membrane is destroyed leading to weakening of distal airways (especially respiratory bronchioles).
• Air-trapping and hyper-inflation occur.
• Clinical symptoms include increased CO₂ retention (pink puffer), no cyanosis, non-productive cough, hyperresonance on chest percussion, barrel chest, exertional dyspnea, prolonged expiratory time, speaks in short jerky sentences, anxiety, use of accessory muscles, thin appearance, right-sided heart failure.

COPD Risk Factors

• Genetics: Alpha-1 antitrypsin deficiency
• Age and Gender: COPD increases with age.
• Exposure to particles: Tobacco smoke, occupational dusts and chemicals, indoor/outdoor air pollution.
• Socioeconomic status
• Asthma/bronchial hyperreactivity, chronic bronchitis, respiratory infections, and tuberculosis.

COPD Physical Examination

• Inspection:

  • Increased A-P diameter (barrel chest).
  • Digital clubbing
  • Peripheral edema
  • Distended neck veins.
  • Pursed lip breathing
  • Cyanosis
  • Use of accessory muscles in inspiration and expiration.

• Palpation:

  • Diminished tactile and vocal fremitus

• Percussion:

  • Hyperresonant percussion note

• Auscultation:

  • Diminished breath sounds
  • Crackles/rhonchi/wheezing

COPD Laboratory Findings

• Hematology: Increased hematocrit and hemoglobin.
• Sputum examination: Presence of Streptococcus pneumoniae or Haemophilus influenzae.
• ABG findings: (Mild to Moderate) pH increased, PaCO₂ decreased, HCO₃ slightly decreased, PaO₂ decreased. (Severe) pH normal, PaCO₂ increased, HCO₃ significantly increased, PaO₂ decreased.

COPD Radiologic Findings

• Chest Radiograph:
  • Common: Translucent (dark lung fields), depressed or flattened diaphragms, long and narrow heart, increased retrosternal air space, occasionally cor pulmonale, emphysematous bullae
• Other findings: Dark lung fields, depressed/flattened diaphragm, long/narrow heart (with pulmonary hypertension), enlarged heart.

COPD Management

• Diagnostics: Diagnosed through airflow obstruction, differentiation from asthma, chronic productive cough, and assessment of diffusing capacity and diminished vascularity on chest x-ray. Inhaling bronchodilator testing can differentiate from asthma.
• Treatment of Stable COPD: PRN bronchodilators(sympathomimetic/anticholinergic), systemic corticosteroids (only if reversibility noted with FEV1), methylxanthines, medications for exacerbations such as antibiotics, supplemental oxygen.
• Treatment of Acute Exacerbations: Inhaled bronchodilators (especially beta-2 agonists), oral antibiotics (purulent sputum), corticosteroids (systemic), supplemental oxygen (keep SaO₂ >90%), and NIV is an attractive option and intubation/mechanical ventilation.
• Maximizing Functional Status: Comprehensive pulmonary rehabilitation(to improve exercise capacity, upper body strength, ventilatory function).
• Prevention of Progression and Survival: Smoking cessation, long-term oxygen therapy (LTOT), annual influenza/pneumococcal vaccinations, lung volume reduction surgery.

Therapeutic Options

• Smoking Cessation, Prevention
• Occupational Exposure, Indoor/Outdoor Air Pollution
• Physical Activity
• Bronchodilators (stable COPD)
• Inhaled corticosteroids (stable COPD)
• Combination therapy (inhaled corticosteroids and long-acting beta2-agonists)
• Long-term oral corticosteroids (stable COPD)
• Phosphodiesterase-4 inhibitors (stable COPD)
• Methylxanthines (stable COPD)
• Vaccines, Antibiotics, Mucolytic Agents (various stages)

COPD Summary

• COPD is a serious, progressive lung disease.
• Early diagnosis and management are crucial to slow its progression and improve quality of life.
• Smoking cessation and compliance with treatment are essential for better outcomes.