COPD (โรคปอดอุดกั้นเรื้อรัง, ถุงลมโป่งพอง)

ICD10:
- J44.0 – Chronic obstructive pulmonary disease with acute lower respiratory infection
- J44.1 – Chronic obstructive pulmonary disease with acute exacerbation, unspecified
- J44.9 – Chronic obstructive pulmonary disease, unspecified
- J43.9 – Emphysema, unspecified
ICD11:
- CA22 – Chronic obstructive pulmonary disease
- CA22.0 – Predominantly chronic bronchitic pattern
- CA22.1 – Predominantly emphysematous pattern
- CA22.Y – Other specified chronic obstructive pulmonary disease

⚠️ This article is intended for medical professionals – ฉบับภาษาไทย คลิก →

Key points

COPD is a progressive, preventable lung disease characterised by persistent airflow limitation.
Main causes include long-term exposure to cigarette smoke, biomass fuel, and air pollution.
Two major clinical phenotypes: chronic bronchitis and emphysema.
Diagnosis is confirmed by spirometry showing FEV1/FVC < 0.70 post-bronchodilator.
Management focuses on smoking cessation, inhaled bronchodilators, and pulmonary rehabilitation.

Overview

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable, and treatable respiratory condition characterised by chronic airflow limitation that is not fully reversible. It encompasses two main pathophysiological components — chronic bronchitis, defined by productive cough lasting at least three months for two consecutive years, and emphysema, defined by alveolar wall destruction leading to hyperinflation and gas exchange impairment.

The disease results from a complex interaction between genetic susceptibility and environmental exposures, primarily tobacco smoke. Persistent airway inflammation leads to structural changes, mucus hypersecretion, and loss of elastic recoil. COPD is associated with systemic effects, including skeletal muscle dysfunction and cardiovascular comorbidities. It remains one of the leading causes of morbidity and mortality worldwide.

Current management focuses on symptom relief, reducing exacerbations, and improving quality of life. Interventions include smoking cessation, pharmacologic bronchodilation, vaccination, pulmonary rehabilitation, and, in advanced cases, oxygen therapy or surgical intervention. Despite its chronic progressive nature, early diagnosis and aggressive management can significantly slow disease progression.

Epidemiology

COPD affects approximately 10% of adults over the age of 40 years globally, making it one of the most prevalent chronic diseases. According to the World Health Organization (WHO), COPD was the third leading cause of death worldwide in 2019, responsible for over 3.2 million deaths annually. Its prevalence continues to rise, particularly in low- and middle-income countries, where tobacco use and biomass fuel exposure are widespread.

The disease shows a higher prevalence among males, although this gender gap is narrowing due to increased smoking rates among women. The incidence of COPD also correlates strongly with advancing age and cumulative exposure to risk factors. Genetic predisposition, such as alpha-1 antitrypsin deficiency, accounts for a small proportion of cases but significantly increases risk when present.

Socioeconomic factors, occupational exposure to dust and chemicals, and indoor air pollution play substantial roles in disease burden, especially in developing countries. Smoking remains the dominant modifiable risk factor, with approximately 80–90% of COPD cases attributed to tobacco use. Preventive efforts, including public health campaigns and smoking cessation programs, have proven to reduce incidence and mortality.

Microbiology

Although COPD is not primarily an infectious disease, respiratory infections play a crucial role in acute exacerbations, which accelerate lung function decline. The most common bacterial pathogens implicated in exacerbations include Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis. In severe or hospitalised cases, Pseudomonas aeruginosa may be isolated, particularly in patients with advanced disease or frequent antibiotic exposure.

Viral pathogens are also major contributors, accounting for 30–50% of exacerbations. Common viruses include rhinovirus, influenza virus, respiratory syncytial virus (RSV), and coronavirus. Co-infection with bacteria and viruses is common and is associated with more severe and prolonged exacerbations.

Chronic bacterial colonisation of the lower airways contributes to ongoing inflammation and progression of the disease even in stable COPD. The presence of pathogenic bacteria in the bronchial mucosa can stimulate neutrophilic inflammation, perpetuating airway injury. Preventive measures such as annual influenza vaccination and pneumococcal vaccination significantly reduce exacerbation frequency and mortality.

Pathophysiology

Key points

COPD results from chronic airway inflammation due to exposure to noxious particles, mainly cigarette smoke.
Pathophysiological hallmarks include airway narrowing, mucus hypersecretion, alveolar destruction, and loss of elastic recoil.
Persistent inflammation involves neutrophils, macrophages, and CD8+ T lymphocytes, leading to structural lung damage.
Emphysema causes air trapping and reduced gas exchange due to alveolar wall destruction.
Systemic inflammation contributes to muscle wasting, cardiovascular disease, and metabolic abnormalities.
Oxidative stress and protease-antiprotease imbalance are central mechanisms driving tissue injury.

Chronic Obstructive Pulmonary Disease (COPD) is characterised by persistent, progressive airflow limitation caused by abnormal inflammatory responses of the lungs to inhaled toxic substances — most notably cigarette smoke, air pollution, and occupational irritants. The pathophysiology involves both the airways and the lung parenchyma, leading to airflow obstruction that is not fully reversible.

1. Airway inflammation and remodelling

Inhaled irritants activate epithelial cells and alveolar macrophages, releasing inflammatory mediators such as tumour necrosis factor-α (TNF-α), interleukin (IL)-8, and leukotriene B4. These attract neutrophils, macrophages, and CD8+ cytotoxic T cells into the airways. The persistent presence of these immune cells results in chronic inflammation, tissue destruction, and airway wall thickening.

Over time, repeated epithelial injury promotes goblet cell hyperplasia and submucosal gland hypertrophy, leading to excessive mucus production and impaired mucociliary clearance. The small airways (bronchioles <2 mm) are the primary site of increased resistance in COPD, becoming narrowed due to inflammation, fibrosis, and luminal obstruction by mucus plugs.

2. Protease–antiprotease imbalance

Under normal conditions, proteolytic enzymes such as neutrophil elastase and matrix metalloproteinases (MMPs) are counterbalanced by antiproteases including α1-antitrypsin and tissue inhibitors of metalloproteinases (TIMPs). In COPD, chronic inflammation disrupts this balance, resulting in excessive protease activity and destruction of connective tissue components such as elastin and collagen. This imbalance is particularly evident in emphysema, where alveolar septal walls are destroyed, leading to enlarged airspaces and loss of elastic recoil.

Patients with α1-antitrypsin deficiency represent a classic genetic model of COPD, as the absence of adequate antiprotease protection accelerates emphysematous destruction even in non-smokers.

3. Oxidative stress

Cigarette smoke and activated inflammatory cells generate large amounts of reactive oxygen species (ROS), leading to oxidative stress that damages lipids, proteins, and DNA. ROS also inactivate antiproteases, amplify inflammatory signalling (e.g., through NF-κB activation), and impair ciliary motility, thereby perpetuating airway inflammation. Oxidative stress contributes to steroid resistance in COPD by reducing histone deacetylase-2 (HDAC2) activity, which normally suppresses inflammatory gene expression.

4. Air trapping and dynamic hyperinflation

In emphysematous lungs, destruction of alveolar walls and loss of elastic recoil impair expiratory flow, causing air to remain trapped within distal airspaces. This leads to increased residual volume (RV) and total lung capacity (TLC), resulting in hyperinflation. During exercise or acute exacerbations, incomplete exhalation causes dynamic hyperinflation, which increases the work of breathing and contributes to dyspnoea and exercise intolerance.

The collapse of small airways during expiration also causes ventilation-perfusion (V/Q) mismatch, leading to hypoxaemia. Chronic hypoxaemia and hypercapnia may subsequently lead to pulmonary hypertension and cor pulmonale (right heart failure).

5. Mucus hypersecretion

Chronic bronchitis, one of the phenotypes of COPD, is defined clinically by chronic productive cough. Pathologically, there is hypertrophy of mucus-secreting glands and goblet cell hyperplasia, resulting in excessive mucus production. Mucus stasis further predisposes to bacterial colonisation and recurrent infections, leading to exacerbations and acceleration of disease progression.

6. Small airway disease and emphysema interaction

Airflow obstruction in COPD is due to both small airway narrowing and loss of alveolar attachments from emphysema. In early disease, inflammation and fibrosis of small airways predominate; in advanced disease, alveolar destruction and decreased tethering exacerbate airway collapse. These two processes act synergistically to produce fixed airflow limitation.

7. Pulmonary vascular changes

Chronic hypoxia induces vasoconstriction of pulmonary arterioles, leading to vascular remodelling characterised by smooth muscle hypertrophy and intimal fibrosis. Over time, these changes cause pulmonary hypertension, which can progress to right ventricular hypertrophy and eventual right heart failure (cor pulmonale).

Additionally, endothelial dysfunction from oxidative stress contributes to impaired vasodilatory capacity, promoting thrombosis and worsening V/Q mismatch.

8. Systemic inflammation and extrapulmonary effects

COPD is increasingly recognised as a systemic inflammatory disorder rather than a disease confined to the lungs. Circulating cytokines such as IL-6, TNF-α, and C-reactive protein (CRP) contribute to muscle wasting, weight loss (cachexia), insulin resistance, and osteoporosis. Systemic inflammation also increases the risk of comorbidities including cardiovascular disease, metabolic syndrome, and depression.

9. Neural mechanisms and dyspnoea

Sensory nerve activation within inflamed airways contributes to the sensation of breathlessness. Vagal nerve reflexes induce bronchoconstriction, mucus secretion, and cough. Central perception of dyspnoea results from complex integration of mechanoreceptor and chemoreceptor input, explaining why dyspnoea severity may not always correlate with spirometric findings.

10. Acute exacerbations and disease progression

Acute exacerbations of COPD (AECOPD) are typically triggered by respiratory infections or environmental irritants. Exacerbations accelerate lung function decline, increase systemic inflammation, and worsen prognosis. Each exacerbation episode is associated with further loss of FEV1 and may result in long-term disability or death in severe cases.

Overall, COPD pathophysiology represents a complex interplay of inflammatory, proteolytic, and oxidative mechanisms affecting both central and peripheral airways as well as the pulmonary vasculature. The progressive destruction of lung parenchyma, airway remodelling, and systemic consequences explain the chronic and debilitating nature of this disease.

Diagram showing airway inflammation, mucus hypersecretion, and alveolar destruction in COPD pathophysiology.

Clinical Presentation

The clinical presentation of Chronic Obstructive Pulmonary Disease (COPD) varies depending on disease severity and phenotype (chronic bronchitis vs. emphysema). Symptoms develop gradually over many years and are often under-recognised until moderate airflow limitation occurs. The hallmark features include dyspnoea, chronic cough, sputum production, and a history of exposure to risk factors such as cigarette smoking or biomass fuels.

Sign & Symptom	Pathogenesis	Frequency	Specificity
Chronic cough	Airway inflammation and mucus gland hypertrophy	+++	++
Sputum production	Goblet cell hyperplasia and mucus hypersecretion	+++	++
Dyspnoea (exertional)	Airflow limitation and dynamic hyperinflation	++++	+++
Wheezing	Airway narrowing and bronchospasm	++	+
Prolonged expiratory phase	Reduced elastic recoil and air trapping	+++	+++
Barrel-shaped chest	Chronic hyperinflation	++	+++
Use of accessory muscles	Increased work of breathing	+++	+++
Cyanosis (“Blue bloater” phenotype)	Chronic hypoxaemia in bronchitic patients	++	+++
Cachexia (“Pink puffer” phenotype)	Increased energy expenditure and systemic inflammation	+	+++

Physical examination may reveal hyperresonant percussion, decreased breath sounds, and prolonged expiratory phase. In severe disease, signs of right heart failure (cor pulmonale), including peripheral oedema, elevated jugular venous pressure, and hepatomegaly, may appear. Clubbing is uncommon and should prompt evaluation for alternative diagnoses such as bronchiectasis or lung cancer.

Investigation

The diagnosis of COPD is confirmed by spirometry demonstrating irreversible airflow limitation. Investigations aim to assess severity, rule out alternative diagnoses, and identify complications or comorbidities.

Specific test

Spirometry: Post-bronchodilator FEV1/FVC < 0.70 confirms persistent airflow limitation.
Bronchodilator reversibility test: Limited reversibility (<12% or <200 mL increase in FEV1) supports COPD over asthma.
Arterial Blood Gas (ABG): Used in severe disease to assess hypoxaemia or hypercapnia.
Diffusing capacity for CO (DLCO): Decreased in emphysema due to alveolar destruction.
Alpha-1 antitrypsin level: Measured in young non-smokers with basal emphysema.

General finding

Chest X-ray: Shows hyperinflated lungs, flattened diaphragm, and increased retrosternal airspace.
High-resolution CT (HRCT): Confirms emphysematous changes or bronchial wall thickening.
Complete blood count (CBC): May show polycythaemia in chronic hypoxaemia.
Electrocardiogram (ECG): Detects right ventricular strain or cor pulmonale.
Echocardiogram: Assesses pulmonary hypertension and right heart function.

Diagnosis Criteria (Dx)

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines COPD based on symptoms, risk factors, and spirometric confirmation. Diagnosis requires evidence of chronic airflow limitation that is not fully reversible.

1. Clinical criteria: Chronic cough, sputum production, and dyspnoea, especially with history of smoking or exposure to pollutants.
2. Spirometric confirmation:
- FEV1/FVC ratio < 0.70 post-bronchodilator.
- Severity grading based on post-bronchodilator FEV1:
  - GOLD 1: Mild (FEV1 ≥ 80% predicted)
  - GOLD 2: Moderate (50–79%)
  - GOLD 3: Severe (30–49%)
  - GOLD 4: Very severe (<30%)
3. Symptom assessment: Use validated tools such as the COPD Assessment Test (CAT) or mMRC Dyspnoea Scale to evaluate symptom burden.
4. Exclusion of other causes: Asthma, bronchiectasis, and heart failure must be ruled out by history, examination, and appropriate investigations.

COPD is thus diagnosed by combining clinical suspicion with objective demonstration of airflow obstruction, supported by risk factor exposure and absence of full reversibility.

Diffential Diagnosis (DDx)

COPD shares overlapping symptoms with several respiratory and cardiac disorders. Accurate differentiation is essential for proper management.

Disease	Distinguishing Features	Lab / Imaging Findings	Specific Test for Rule-out
Asthma	Onset at younger age; intermittent symptoms; strong atopy history; significant reversibility	Normal or hyperinflated lungs	Bronchodilator reversibility ≥12% or ≥200 mL in FEV1
Bronchiectasis	Chronic productive cough with purulent sputum and frequent infections	“Tram-track” lines and ring shadows on imaging	High-resolution CT scan
Congestive Heart Failure (CHF)	Orthopnoea, paroxysmal nocturnal dyspnoea, basal crackles, pedal oedema	CXR: cardiomegaly, pulmonary congestion	Echocardiography showing reduced ejection fraction
Tuberculosis (TB)	Chronic cough, haemoptysis, weight loss, fever, night sweats	Upper lobe cavitation on CXR	Sputum AFB smear or GeneXpert MTB/RIF
Lung Cancer	Persistent cough, haemoptysis, unexplained weight loss, unilateral wheeze	Mass or nodule on imaging	CT chest with biopsy confirmation

Careful clinical correlation, pulmonary function testing, and imaging help differentiate COPD from these mimicking conditions. Asthma-COPD overlap (ACO) should also be considered in patients showing features of both conditions.

Treatment

The treatment of Chronic Obstructive Pulmonary Disease (COPD) focuses on symptom control, prevention of exacerbations, and improvement of quality of life. While the damage to lung tissue is irreversible, appropriate therapy can significantly slow disease progression. Management follows a stepwise approach based on disease severity as defined by the GOLD (Global Initiative for Chronic Obstructive Lung Disease) guidelines.

The cornerstone of treatment is smoking cessation, which is the only intervention proven to reduce disease progression. All patients should receive smoking cessation counselling and pharmacotherapy when appropriate (e.g., nicotine replacement, varenicline, or bupropion).

Pharmacologic treatment includes bronchodilators as the mainstay of therapy. Short-acting bronchodilators (SABA or SAMA) provide rapid relief of symptoms, while long-acting agents (LABA and LAMA) are used for maintenance therapy. Inhaled corticosteroids (ICS) are added for patients with frequent exacerbations or eosinophilic inflammation. Combination therapy (ICS/LABA or LABA/LAMA) is preferred for moderate to severe disease.

Non-pharmacologic strategies include pulmonary rehabilitation, vaccination (influenza and pneumococcal), and management of comorbidities. In advanced cases, long-term oxygen therapy (LTOT) is indicated for patients with chronic hypoxaemia (PaO₂ ≤ 55 mmHg). Surgical options such as lung volume reduction surgery or lung transplantation are considered in highly selected individuals.

Exacerbations are treated with short-acting bronchodilators, systemic corticosteroids (prednisolone 40 mg daily for 5 days), and antibiotics if infection is suspected. Early recognition and prompt treatment of exacerbations are crucial to prevent decline in lung function and reduce hospitalisation rates.

Pharmacology

Pharmacologic therapy in COPD aims to relieve symptoms, improve exercise tolerance, and prevent exacerbations. Drug selection is guided by the GOLD classification and individual patient phenotype. The main classes of drugs include bronchodilators, corticosteroids, phosphodiesterase inhibitors, and biologics for selected cases.

Drug Class	Example	Mechanism of Action	Typical Adult Dose	Clinical Notes
Short-acting β₂-agonists (SABA)	Salbutamol, Terbutaline	Stimulate β₂ receptors → bronchodilation via smooth muscle relaxation	Salbutamol 100–200 µg inhaled PRN	Used for quick symptom relief in mild COPD and acute exacerbations
Short-acting muscarinic antagonists (SAMA)	Ipratropium bromide	Block M3 receptors → prevent bronchoconstriction and mucus secretion	20 µg (2 puffs) inhaled q6h PRN	Often combined with SABA for additive bronchodilatory effect
Long-acting β₂-agonists (LABA)	Formoterol, Salmeterol, Indacaterol	Prolonged activation of β₂ receptors → sustained bronchodilation	Formoterol 12 µg BID or Indacaterol 150 µg daily	Maintenance therapy to reduce daily symptoms and improve exercise tolerance
Long-acting muscarinic antagonists (LAMA)	Tiotropium, Glycopyrronium	Inhibit M3 receptors → prevent bronchospasm and reduce air trapping	Tiotropium 18 µg inhaled daily	First-line maintenance therapy; reduces exacerbations and hospitalisations
Inhaled corticosteroids (ICS)	Budesonide, Fluticasone	Suppress airway inflammation and reduce eosinophilic activity	Budesonide 400–800 µg/day divided BID	Used in combination with LABA for patients with frequent exacerbations
Combination inhalers (LABA/LAMA or LABA/ICS)	Budesonide/Formoterol, Tiotropium/Olodaterol	Dual bronchodilation or anti-inflammatory and bronchodilation synergy	1 puff BID (formulation-specific)	Improves symptom control and reduces exacerbations more effectively than monotherapy
Phosphodiesterase-4 (PDE4) inhibitors	Roflumilast	Inhibits PDE4 enzyme → reduces inflammation and cytokine release	500 µg PO daily	Adjunct in severe COPD with chronic bronchitis and frequent exacerbations
Methylxanthines	Theophylline	Inhibits phosphodiesterase → mild bronchodilation and central respiratory stimulation	200–400 mg PO BID (monitor levels)	Limited by narrow therapeutic index and side effects; reserved for refractory cases
Systemic corticosteroids	Prednisolone	Broad anti-inflammatory action during acute exacerbations	40 mg PO daily for 5–7 days	Short-term use only to prevent steroid-related complications
Antibiotics (for exacerbation)	Amoxicillin-clavulanate, Azithromycin	Treat bacterial infections triggering exacerbations	Amoxicillin-clavulanate 625 mg PO q8h × 5–7 days	Indicated when sputum purulence or fever is present

Long-term therapy should be individualised according to GOLD category (A–E). Dual or triple therapy (LABA/LAMA/ICS) is recommended for patients with persistent symptoms or frequent exacerbations despite monotherapy. Non-adherence and incorrect inhaler technique are major causes of treatment failure, so patient education and inhaler training are essential.

Guideline

The management of Chronic Obstructive Pulmonary Disease (COPD) is guided by international standards such as the Global Initiative for Chronic Obstructive Lung Disease (GOLD 2024) and national respiratory societies. The primary goals of treatment are to reduce symptoms, prevent exacerbations, improve quality of life, and slow disease progression. COPD management should be individualised based on the severity of airflow limitation, symptom burden, and risk of exacerbation.

1. Initial Assessment and Classification

All patients should undergo a comprehensive assessment that includes:

Symptom evaluation using mMRC Dyspnoea Scale or COPD Assessment Test (CAT).
Spirometric confirmation of diagnosis (post-bronchodilator FEV₁/FVC < 0.70).
Exacerbation history (number and severity in the past 12 months).
Identification of comorbidities such as cardiovascular disease, diabetes, and anxiety.

Patients are categorised into GOLD Groups A, B, or E according to symptom burden and exacerbation risk:

Group A: Low symptoms (CAT <10 or mMRC 0–1), 0–1 exacerbation per year.
Group B: High symptoms (CAT ≥10 or mMRC ≥2), 0–1 exacerbation per year.
Group E: Any patient with ≥2 exacerbations or ≥1 hospitalisation in the past year.

2. Stepwise Pharmacologic Management (GOLD 2024)

Group A – Mild disease:

Start with a single bronchodilator (SABA or SAMA) as needed for symptom relief.
If symptoms persist, switch to a long-acting bronchodilator (LABA or LAMA).

Group B – Symptomatic disease (no frequent exacerbations):

Initial therapy: Dual bronchodilator (LABA + LAMA) combination for better symptom control.
If dual therapy not tolerated, use either LABA or LAMA monotherapy.
ICS monotherapy is not recommended due to increased pneumonia risk.

Group E – Frequent exacerbations:

Start with LABA + LAMA combination.
If eosinophil count ≥300 cells/µL or evidence of asthma overlap, consider adding ICS (triple therapy: LABA + LAMA + ICS).
Roflumilast or Azithromycin may be used as add-on therapy in chronic bronchitis phenotype or in frequent exacerbators.

3. Management of Acute Exacerbations

Administer short-acting bronchodilators (SABA ± SAMA) every 4–6 hours.
Give systemic corticosteroids: Prednisolone 40 mg orally daily for 5 days.
Start antibiotics (e.g., Amoxicillin-clavulanate 625 mg q8h for 5–7 days) if there is increased sputum purulence or fever.
Provide oxygen therapy to maintain SpO₂ 88–92%.
In severe exacerbations, hospitalisation may be required for nebulised bronchodilators, IV corticosteroids, or non-invasive ventilation (NIV).

4. Long-term Oxygen Therapy (LTOT)

Indicated in patients with PaO₂ ≤ 55 mmHg or SpO₂ ≤ 88% at rest on room air.
Also indicated if PaO₂ 56–59 mmHg with evidence of pulmonary hypertension, polycythaemia, or right heart failure.
Should be administered ≥15 hours/day to improve survival.

5. Non-Pharmacologic Interventions

Smoking cessation: The most effective intervention to slow disease progression; offer pharmacologic support such as nicotine replacement or varenicline.
Pulmonary rehabilitation: Structured exercise and education program that improves exercise tolerance, dyspnoea, and quality of life.
Vaccination: Annual influenza and pneumococcal vaccines reduce exacerbations and mortality.
Nutritional support: Address malnutrition and maintain optimal body weight.
Education and inhaler training: Ensure correct technique and adherence to inhaled therapies.

6. Advanced and Surgical Therapies

Lung volume reduction surgery (LVRS): Beneficial in selected patients with predominant upper-lobe emphysema and low exercise capacity.
Bronchoscopic lung volume reduction: Minimally invasive alternative using endobronchial valves or coils.
Lung transplantation: Considered in younger patients with end-stage COPD refractory to medical therapy.

7. Monitoring and Follow-up

Reassess symptoms, inhaler technique, and adherence every 3–6 months.
Repeat spirometry annually to monitor decline in FEV₁.
Monitor for comorbidities such as osteoporosis, depression, and heart disease.
Encourage early recognition of exacerbation symptoms and provide a personalised COPD Action Plan.

* Important note: Inhaled bronchodilators (LABA, LAMA) remain the foundation of COPD treatment. The addition of inhaled corticosteroids should be reserved for patients with frequent exacerbations or high blood eosinophil counts. Overuse of ICS may increase the risk of pneumonia. Management must always include smoking cessation, pulmonary rehabilitation, and vaccination as integral components of care.

In summary, effective COPD management requires a comprehensive, multidimensional approach integrating pharmacologic therapy, lifestyle modification, and patient education. Adherence to GOLD guideline principles allows clinicians to tailor therapy, prevent exacerbations, and significantly improve long-term outcomes for patients living with COPD.

Example Doctor’s Orders

Case 1: Moderate COPD (GOLD 2), 60-year-old male, ex-smoker

Dx: Moderate COPD, stable phase

Rx:

Tiotropium 18 µg inhalation once daily
Formoterol 12 µg inhalation BID
Salbutamol 100 µg inhalation PRN for dyspnoea
Influenza vaccine (annual)
Pneumococcal vaccine (every 5 years)
Pulmonary rehabilitation referral
Smoking cessation counselling
Follow-up every 3 months with spirometry

Physician:__________________ License:_________ Date:________ Time:_______

Case 2: Severe COPD (GOLD 3) with acute exacerbation

Dx: Severe COPD with acute exacerbation

Rx:

O₂ therapy to maintain SpO₂ 88–92%
Salbutamol 2.5 mg + Ipratropium 0.5 mg via nebuliser q6h
Prednisolone 40 mg PO daily × 5 days
Amoxicillin-clavulanate 625 mg PO q8h × 7 days
Continue Tiotropium 18 µg inhalation daily
Monitor vital signs and oxygen saturation
Check ABG and repeat CXR after 48 hours
Plan for discharge when clinically stable

Physician:__________________ License:_________ Date:________ Time:_______

Disclaimer: Example for educational purposes only, not for direct patient advice.

Quiz (USMLE OSCE)

What is the GOLD spirometric criterion for diagnosing COPD?

Post-bronchodilator FEV₁/FVC ratio < 0.70 confirms persistent airflow limitation.

What is the primary cause of COPD worldwide?

Long-term exposure to cigarette smoke and air pollutants.

Which two medications form the basis of maintenance therapy in COPD?

Long-acting bronchodilators: LABA and LAMA.

When should inhaled corticosteroids be added in COPD?

In patients with frequent exacerbations or blood eosinophil count ≥300 cells/µL.

Which index predicts mortality and functional decline in COPD?

The BODE index (BMI, Obstruction, Dyspnoea, Exercise capacity).

What is the role of pulmonary rehabilitation in COPD?

It improves exercise capacity, dyspnoea, and quality of life.

What oxygen saturation range should be maintained in COPD patients on O₂ therapy?

Target SpO₂ 88–92% to prevent CO₂ retention.

Which vaccine is essential for preventing COPD exacerbations?

Annual influenza and pneumococcal vaccines.

Which phenotype is associated with chronic cough and sputum production?

The chronic bronchitic phenotype.

What is the main non-reversible component of COPD pathophysiology?

Alveolar destruction and loss of elastic recoil (emphysema).

Frequently Asked Questions (FAQ)

Can COPD be completely cured?

No. COPD cannot be cured because lung tissue damage is irreversible. However, early diagnosis, smoking cessation, and proper treatment can control symptoms and slow disease progression, allowing patients to live active lives.

Is COPD the same as asthma?

No. COPD is characterised by irreversible airflow limitation due to chronic inflammation, while asthma is typically reversible and often related to allergic mechanisms. However, some patients have features of both conditions, known as Asthma-COPD Overlap (ACO).

Why do COPD patients develop cor pulmonale?

Chronic hypoxaemia in COPD leads to pulmonary vasoconstriction and vascular remodelling, causing pulmonary hypertension. This increases the workload on the right ventricle, leading to right-sided heart failure (cor pulmonale).

How does smoking cessation improve COPD outcomes?

Stopping smoking immediately slows the rate of lung function decline and decreases the frequency of exacerbations. It is the most effective intervention for improving prognosis at any disease stage.

What should patients with COPD avoid?

Patients should avoid smoking, air pollution, extreme cold, and respiratory infections. They should also avoid unnecessary sedatives or opioids that may suppress respiratory drive.

Disclaimer: This content is intended for medical professionals for educational purposes only, not for direct patient advice. www.banmor.org

References

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Wouters EFM. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005;2(1):26–33. doi:10.1513/pats.200408-039MS
National Institute for Health and Care Excellence (NICE). Chronic obstructive pulmonary disease in over 16s: diagnosis and management. NICE guideline [NG115]. 2023. Available at: https://www.nice.org.uk/guidance/ng115
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Author & Review

Compiled from peer-reviewed references and clinical guidelines. Adapted and reviewed by:

Teerawat Suwannee MD

Medical Doctor License 44780
นายแพทย์ธีรวัฒน์ สุวรรณี ว.44780

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