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Pulmonology

COPD: Spirometry, GOLD Classification, and Stepwise Therapy

WhiteCoat Pro Editorial BoardApril 11, 2026Updated April 19, 20264 min read
Table of Contents · 11 sections
  1. 1. Definition and epidemiology
  2. 2. Etiology and Risk Factors
  3. 3. Pathophysiology
  4. 4. Clinical presentation
  5. 5. Diagnostics
  6. 6. GOLD 2023 Classification — Groups A/B/E
  7. 7. Treatment: Initial Therapy per GOLD 2023
  8. 8. Non-Pharmacological Interventions
  9. 9. COPD Exacerbation
  10. 10. Complications
  11. 11. FAQ

In a nutshell. COPD is a chronic, partially reversible airflow limitation resulting from an inflammatory response to noxious particles (most commonly smoking). The diagnosis is confirmed by spirometry (post-bronchodilator FEV1/FVC < 0.7). The GOLD 2023 classification takes into account the degree of limitation (1–4) and clinical features (groups A/B/E). The mainstay of treatment is long-acting bronchodilators (LAMA ± LABA), with ICS indicated for the exacerbation/eosinophilia phenotype.

1. Definition and epidemiology

COPD is a heterogeneous lung disease characterized by chronic respiratory symptoms (dyspnea, cough, sputum production) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, progressive airflow limitation.

It is the 3rd leading cause of death worldwide. In Russia, the prevalence is 15% in individuals > 40 years of age. The main risk factor is smoking (80–90% of cases).

2. Etiology and Risk Factors

  • Smoking (active and passive) is the key factor.
  • Occupational hazards: dusts, chemical fumes.
  • Air pollution, biomass smoke (in developing countries).
  • Alpha-1 antitrypsin deficiency is a hereditary cause, especially in young individuals.
  • Chronic lower respiratory tract infections in childhood.
  • Prematurity, bronchopulmonary dysplasia.

3. Pathophysiology

Chronic exposure to irritants → inflammation (CD8+ lymphocytes, macrophages, neutrophils) → protease/antiprotease imbalance → destruction of alveolar elastin (emphysema) and remodeling of small airways (bronchiolitis obliterans) → expiratory flow limitation and air trapping → lung hyperinflation → dyspnea.

4. Clinical presentation

  • Chronic cough (for years).
  • Sputum production, predominantly in the morning.
  • Progressive dyspnea (mMRC 0–4).
  • Frequent respiratory infections.
  • In late stages: weight loss, muscle weakness, cyanosis, pulmonary hypertension, and chronic cor pulmonale.

Classic phenotypes: "blue bloater" (cyanotic, edematous bronchitic) and "pink puffer" (panting, cachectic emphysematous). In practice, mixed forms are more common.

5. Diagnostics

Spirometry is mandatory

  • Post-bronchodilator FEV1/FVC < 0.7 confirms persistent obstruction.
  • Severity assessment by FEV1:
    • GOLD 1 (mild): FEV1 ≥ 80%.
    • GOLD 2 (moderate): 50–79%.
    • GOLD 3 (severe): 30–49%.
    • GOLD 4 (very severe): < 30%.

Additional Methods

  • Chest X-ray — to rule out other conditions and check for complications.
  • High-resolution CT (HRCT) — to assess emphysema and bronchiectasis, indicated in smokers > 50 years with lung cancer risk.
  • Arterial blood gases — if FEV1 < 50%.
  • 6-minute walk test — to assess functional status.
  • Alpha-1 antitrypsin — in young, non-smoking patients with a positive family history.

6. GOLD 2023 Classification — Groups A/B/E

GroupSymptoms (mMRC/CAT)Exacerbations in the past year
ALow symptom burden (mMRC 0–1, CAT < 10)0–1 without hospitalization
BHigh symptom burden (mMRC ≥ 2, CAT ≥ 10)0–1 without hospitalization
EAny symptom level≥ 2 outpatient exacerbations or ≥ 1 resulting in hospitalization

Letter groups A/B/E guide initial therapy, while numeric grades 1–4 (based on spirometry) guide prognosis.

7. Treatment: Initial Therapy per GOLD 2023

GroupStart
ABronchodilator (SAMA/SABA as needed or LAMA/LABA)
BLAMA + LABA
ELAMA + LABA; + ICS if eosinophils ≥ 300/µL

Drug Classes

  • SABA (salbutamol), SAMA (ipratropium) — short-acting, "as needed".
  • LABA (formoterol, indacaterol) — long-acting β₂-agonists.
  • LAMA (tiotropium, umeclidinium) — long-acting muscarinic antagonists; preferred when there is a risk of exacerbations.
  • ICS (budesonide, fluticasone) — combined with LABA/LAMA in case of eosinophilia and frequent exacerbations. Risks: pneumonia, systemic side effects.
  • Roflumilast, low-dose azithromycin — for severe exacerbations despite triple therapy.

8. Non-Pharmacological Interventions

  • Smoking cessation is the only intervention that slows disease progression.
  • Vaccination: annual influenza, pneumococcal vaccines, COVID-19, RSV (> 60 years).
  • Pulmonary rehabilitation — exercise training programs, patient education, nutritional support: ↓ exacerbations, ↑ quality of life.
  • Long-term oxygen therapy (> 15 h/day): indicated for PaO₂ ≤ 55 mmHg or SpO₂ ≤ 88 %; reduces mortality.
  • Non-invasive ventilation: indicated for chronic hypercapnia.
  • Surgery: bullectomy, lung volume reduction surgery, lung transplantation in selected patients.

9. COPD exacerbation

Definition: an acute worsening of respiratory symptoms that requires a change in medication. Severity classification: outpatient treatment, hospitalization, ICU.

Exacerbation management

  • Increased doses of bronchodilators (SABA ± SAMA via nebulizer).
  • Systemic corticosteroids — prednisolone 40 mg/day for 5 days.
  • Antibiotics for purulent sputum or CRP > 20 mg/L: amoxicillin/clavulanate, macrolide.
  • Oxygen therapy — target SpO₂ 88–92 % (in CO₂-retainers).
  • Non-invasive ventilation (BiPAP) for acidosis, pH < 7.35 — ↓ mortality and intubation rate.

10. Complications

  • Pulmonary hypertension, chronic cor pulmonale.
  • Secondary polycythemia.
  • Cardiovascular events (myocardial infarction, stroke) — a leading cause of death in some patients.
  • Lung cancer (especially in smokers).
  • Depression, anxiety disorders.
  • Cachexia, sarcopenia.

11. FAQ

How does COPD differ from asthma?
Asthma features variable, often reversible obstruction, atopy, childhood onset, and eosinophil predominance. COPD is progressive, partially reversible, occurs in smokers, and features neutrophil predominance. A combination is possible (ACO).

Is COPD curable?
No. Therapy relieves symptoms, reduces exacerbation frequency, and improves quality of life. Disease progression is slowed only by smoking cessation and long-term oxygen therapy (in hypoxemia).

When are ICS indicated?
When blood eosinophils are ≥ 300/µL or ≥ 100/µL with frequent exacerbations; in asthma-COPD overlap. Use with caution in patients with a history of pneumonia.

What is mMRC?
Dyspnea scale (0–4): 0 — breathless only with strenuous exercise; 4 — too breathless to leave the house or breathless when dressing. Used for A/B/E classification.

What is the role of CT?
Not for diagnosing COPD (which is clinical and functional), but for assessing emphysema, ruling out bronchiectasis, and screening for lung cancer in smokers.

See also: Pneumonia · Pneumothorax · Pediatric asthma · Glucocorticoids · CURB-65 · Pulmonology catalog

This material is educational in nature and does not replace a doctor's consultation. Verify treatment regimens and dosages with current clinical guidelines.

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