Contents
Respiratory disease 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 (GOLD) definintion of COPD
- World COPD Day: November 20th
Phenotypes:
COPD has both airway (central and small airways) and airspace abnormalities.
- Chronic bronchitis: Daily productive cough for at least 3 consecutive months for more than 2 successive years
- Emphysema: Anatomic alteration of lung characterized by abnormal enlargement of air spaces distal to terminal, non-respiratory bronchiole, accompanied by destructive changes of alveolar walls.

Etiology
The development of COPD is multifactorial and the risk factors of COPD include genetic and environmental factors. The interplay of these factors is important in the development of COPD.
- Smoking hisotry (biggest risk factor, 90% cases): Directly inhibits α-1 antitrypsin
- Age > 35 years with significant smoking history
- α1-antitrypsin deficiency (1-2% cases)
- Exposure to indoor/outdoor air pollution, occupational dusts, or chemicals
Pathophysiology
Airway changes:

Disease progression:


Emphysema “pink puffer”:
Anatomic alteration of the lung characterized by abnormal enlargement of air spaces distal to terminal, non-respiratory bronchiole, accompanied by destructive changes of alveolar walls.
Centriacinar | Panacinar |
Most frequently associated with cigarette smoking
Characterized by enlarged air spaces found (initially) in association with respiratory bronchioles Most prominent in the upper lobes and superior segments of lower lobes | Observed in patients with α1-AT deficiency
Abnormally large air spaces evenly distributed within and across acinar units Predilection for the lower lobes |

Chronic bronchitis “blue bloater”:
Daily productive cough for at least 3 consecutive months for more than 2 successive years.

Presentation
In the clinical setting, emphysema and bronchitis/bronchiolitis often coexist with different degree of severity in the same patient making it very difficult to physiologically and clinically identify the contribution of each. Thus, such overlap led to the terminology of COPD.
Type A: Emphysema “pink puffer”
- Progressive dyspnoea (dominant symptom) and cough & hypersecretion (modest symptom)
- ↑ Lung volumes
- ↓ Carbon monoxide (DLCO) diffusing capacity
Type B: Chronic bronchitis “blue bloater”
- Mucous hypersecretion (dominant symptom), while dyspnea (modest symptom)
- Hypercapnia and hypoxemia with secondary pulmonary hypertension and cardiovascular comorbidities
General symptoms:
- Diffuse bilateral wheezing
- Tripod position
- Arms serve as extra anchor for accessory respiratory muscles
- Pursed lips (prolonged expiration)
- Helps maintain pressure to inflate distal airways
- Weight loss
Severe COPD:
- Pulsus paradoxus: Exaggerated negative intrathoracic pressure leads to > 10 mmHg decrease in systolic pressure during inspiration
- Hoover’s sign: Paradoxical inward movement of the rib cage with inspiration
- Distant heart sounds
- Diminished lung/breath sounds

Complications
Acute exacerbation of COPD (AECOPD):
Episodes of increased dyspnea and cough and change in the amount and character of sputum.

- May/may not be accompanied by other signs of illness, including fever, myalgias, and sore throat.
- Chronic hypoxemia → Hypoxic vasoconstriction → Pulmonary arterial hypertension
- Pulmonary hypertension → Right heart failure (Cor pulmonale)
- RHF due to lung pathology


Diagnosis

GOLD & NIH Severity based classification:

Reid index:
Ratio of the thickness of the mucous gland layer to the thickness of the bronchial wall.
- > 0.4 suggests mucous gland hyperplasia
Body plethysmography:
Measures the volume of any gas containing space in the thorax, including bullae. It is accurate in both restrictive as well as obstructive lung diseases.

Blood gas analysis:
- Early emphysema “pink face”:
- Hyperventilation → Normal arterial oxygen (PaO2)
- Respiratory alkalosis
- Late emphysema “blue face”:
- ↑ PaCO2 (Hypercarbia)
- Respiratory acidosis
- ↓ DLCO → ↓ PaO2 (hypoxemia) → Cyanosis
- Early chronic bronchitis:
- ↑ PaCO2 (Hypercarbia)
- Respiratory acidosis
- Mucus plugs limit oxygenation → ↓ PaO2 (hypoxemia) → Cyanosis
Chest X-ray:
- Hyperinflated lung:
- Flat diaphragm
- 10+ posterior rib shadows
- ↑ Parenchymal radiolucency
- Lengthened cardiac silhouette (vertical heart appearance)
- Due to loss of parenchyma

Management

Medical management:
- Anticholinergic agents: Ipratropium bromide improves symptoms and produces acute improvement in FEV1.
- Long-acting inhaled β agonists: Salmeterol or formoterol (symptomatic benefit)
- Theophylline (improvements in expiratory flow rates and vital capacity and a slight improvement in arterial oxygen and carbon dioxide levels in patients with moderate to severe COPD)
- N-acetyl cysteine (mucolytic and antioxidant)



Summary:

One reply on “Chronic obstructive pulmonary disease (COPD)”
[…] Chronic obstructive pulmonary disease (COPD), asthma, α1-antitrypsin deficiency […]