Chronic Obstructive Pulmonary Disease (COPD)

Page Summary

• Chronic obstructive pulmonary disease (COPD) is diagnosed when post-bronchodilator spirometry shows a forced expiratory volume in one second to forced vital capacity (FEV₁/FVC) ratio below 0.70.
• COPD is a heterogeneous, preventable and treatable condition in which airway and alveolar damage causes air trapping, hyperinflation, breathlessness and carbon dioxide retention, and cigarette smoking is the most common cause.
• Physiotherapists treating hospitalised patients with COPD exacerbation assess first, mobilise early at a Borg dyspnoea rating of 4–6/10, and use airway clearance only when sputum retention is present.
• Patients with COPD or at risk of hypercapnia have a target oxygen saturation (SpO₂) of 88–92%, and exercise stops or is modified if SpO₂ stays below target.

Original Editor - Rachael Lowe

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Introduction

Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease. Two processes drive the disease. In chronic bronchitis, inflamed, mucus-filled airways cause chronic cough and sputum. In emphysema, oxidative stress and a protease–antiprotease imbalance destroy alveolar walls and elastin, so the lung loses its recoil. The result is that small airways collapse on exhalation, air is trapped, and the lungs hyperinflate. The diaphragm flattens and works at a mechanical disadvantage. Ventilation–perfusion mismatch causes hypoxemia, while increased dead space and tired respiratory muscles can lead to CO₂ retention.

COPD Definition

COPD is a heterogeneous lung condition characterised by chronic respiratory symptoms (dyspnea, cough, expectoration) due to persistent abnormalities of the airways (bronchitis, bronchiolitis), and/or alveoli (emphysema), that often results in progressive airflow limitation.

COPD Pathological Process

COPD is characterised by persistent, non-fully reversible airflow limitation due to airway narrowing, chronic inflammation, airway remodelling (including small airway fibrosis, goblet cell hyperplasia, and smooth muscle thickening), and destruction of alveolar walls with loss of elastic recoil (emphysema). Airway obstruction and loss of recoil make expiration inefficient, trapping air in the lungs at the end of exhalation. This leads to static and dynamic hyperinflation, which places the diaphragm at a mechanical disadvantage by flattening it, increasing the work of breathing and causing severe dyspnea and exercise intolerance.

Driven by ongoing inflammation, structural airway changes, excessive mucus secretions, and parenchymal destruction, impaired gas exchange reduces overall ventilatory reserve and capacity to tolerate physical exertion.

With disease progression, the reduction in ventilation or increase in physiologic dead space leads to CO2 retention.

Etiology/Epidemiology

Cigarette smoking is the most common cause, but second-hand smoke, occupational and indoor air pollution, alpha-1 antitrypsin deficiency, early-life lung injury and ageing also contribute. Many people with COPD have never smoked, but they may have been exposed to tobacco smoke.

COPD is the third leading cause of death worldwide, with an estimated 3.5 million deaths in 2021, and it remains under-diagnosed.

COPD Diagnosting Tests

Pulmonary function tests (PFTs) offer notable strengths and key limitations in the diagnosis and management of COPD, as expert consensus remains elusive on several topics, including the fundamental criteria for defining airflow obstruction.

PFTs include spirometry, lung volume measurement (LVM) and diffusing capacity (DLCO).

Spirometry

According to Bailey,  “Spirometry is the gold standard for making the diagnosis of COPD. It should be performed in every case of suspected COPD.“

Spirometry measures airflow by having the patient exhale forcefully following maximum inhalation. FEV₁ is the air blown out in the first second (airflow); FVC is the total air blown out (lung size). The Global Initiative for Chronic Obstructive Lung Disease (GOLD) strategy reports that a diagnosis of COPD is confirmed when post-bronchodilator spirometry demonstrates an FEV₁/FVC ratio of less than 0.70.

Clinical note: FEV₁ alone does not predict function. A person with a modest FEV₁ can be profoundly limited. It is best to combine PFTs with symptoms and functional testing.

Clinical tip: Certain patients struggle to execute spirometry correctly. Failing to meet the end-of-forced-expiration criteria represents a frequent error during these evaluations. In such cases, pulmonary function technologists should avoid immediately deeming the session a failure or withholding results, as lower-quality tests may still yield valuable clinical insight.

Lung Volume Measurement (LVM)

Lung volume measurement evaluates total lung capacity (TLC) using methods such as helium dilution and plethysmography. It can give insight into physiological consequences of COPD such as hyperinflation.

Lung Diffusion Testing (DLCO)

DLCO assesses total lung carbon monoxide diffusion to determine gas exchange effectiveness at the alveolar level. As a physiologically and technically intricate assessment, DLCO evaluates several facets of pulmonary function, such as lung volume, alveolar-capillary membrane diffusion, pulmonary vascular volume, and ventilation-perfusion distribution.

Because the pathophysiological mechanisms of COPD can impact each of these functional areas, DLCO serves as a valuable diagnostic modality for evaluating individuals suspected of having COPD.

PFT sample report. These parameters indicate severe obstruction with hyperinflation, air trapping and reduced gas transfer, consistent with emphysema:

• Post-bronchodilator FEV₁ 1.1 L (38% predicted),
• FVC 2.4 L (68%)
• FEV₁/FVC 0.46
• TLC 128%
• DLCO 42%.

COPD Classification System

The 2025 GOLD report proposed a new classification system for COPD. This classification includes six etiotypes of COPD:

1. Genetically determined COPD (COPD-G) due to Alpha-1 antitrypsin deficiency and other genetic variants
2. COPD due to abnormal lung development as a result of premature birth and low birthweight
3. Environmental COPD
   • Cigarette smoking COPD (COPD-C): exposure to tobacco smoke, vaping, e-cigarette use, or cannabis.
   • Biomass and pollution exposure COPD (COPD-P): exposure to household pollution and occupational hazards
4. COPD due to infections (COPD-I): childhood infections, Tuberculosis, HIV
5. COPD and Asthma (COPD-A)
6. COPD of Unknown cause (COPD-U)

COPD Severity Assessment

To effectively guide treatment decisions and capture disease heterogeneity, COPD management relies on comprehensive patient profiling. The Global Initiative for Chronic Obstructive Lung Disease establishes a multidimensional evaluation framework for this purpose, integrating spirometric staging (grades 1–4), symptom assessment (mMRC/CAT), and exacerbation risk (ABE groups).

Spirometry Staging

To grade the severity of airflow obstruction in COPD, the GOLD evaluates FEV₁ % predicted using post-bronchodilator spirometry (FEV₁/FVC < 0.70):

Table 1. Spirometry staging

GOLD grade	Severity	Post-bronchodilator FEV₁ (% predicted)
1	Mild	≥80%
2	Moderate	50–79%
3	Severe	30–49%
4	Very severe	<30%

COPD Symptoms Assessment and Exacerbation Risk

Initial pharmacological treatment in patients with COPD is guided by the GOLD ABE classification, a clinical assessment tool that categorises individuals according to their exacerbation history and symptom burden:

• Group A with low symptoms and low risk. Includes patients with 0–1 moderate exacerbations in the previous year and modified Medical Research Council (mMRC) dyspnea scale 0–1, Chronic Airways Assessment Test (CAAT) <10
• Group B with high symptoms and low risk. Includes patients with 0–1 moderate exacerbations in the previous year and mMRC ≥2 and/or CAAT ≥10
• Group E with high exacerbation risk. It has two or more moderate exacerbations, or at least one leading to hospitalisation, regardless of symptoms.

COPD Clinical Presentation

At the bedside, clinician must look for a barrel chest, pursed-lip breathing, tripod positioning ( a person's forward-leaning posture with bracing their hands or elbows on their knees, a table, or the back of a chair), accessory muscle use and prolonged expiration. Hoover's sign suggests severe hyperinflation. Other symptoms include cough with sputum production, which can be present in up to 30% of patients.

The typical course is a gradual decline in lung function punctuated by exacerbations. Each severe exacerbation speeds up decline, adds deconditioning and raises the risk of readmission and death.

COPD Exacerbation

An exacerbation is an acute worsening of respiratory symptoms beyond normal day-to-day variation that leads to a change in treatment. The cardinal symptoms are increased dyspnea, increased sputum volume and increased sputum purulence. Common triggers are viral and bacterial infection, air pollution and non-adherence to treatment, although often no cause is found.

The medical team must rule out look-alikes such as pneumonia, pulmonary embolism, heart failure, arrhythmia or pneumothorax. Physiotherapists working with a patient should report new chest pain, unilateral leg swelling or signs of fluid overload.

Red flags for acute respiratory failure include respiratory rate (RR) >30, severe accessory muscle use, new confusion or drowsiness, oxygen saturation (SpO₂) <88% despite use of oxygen, and a pH <7.35 with rising PaCO₂ (partial pressure of carbon dioxide in arterial blood). These symptoms require immediate medical attention.

Common COPD Medications

Table 2 lists common medications for COPD and their relevance to physiotherapy treatment.

Table 2. Common COPD Medications

Medication	Role	Relevance to phyisotherapy
SABA (salbutamol) ± SAMA (ipratropium)	First-line rescue in exacerbation	Fast relief. Can cause tremor, tachycardia and low potassium. Time sessions about 20–30 min after a dose.
LABA / LAMA(formoterol, tiotropium)	Daily maintenance. Dual LABA/LAMA is preferred in most patients with significant symptoms.	Confirm the patient has taken their maintenance dose.
ICS (in LABA/LAMA/ICS combinations)	Added for frequent exacerbations or higher blood eosinophils (white blood cells produced in the bone marrow that help manage inflammatory responses).	Raises pneumonia risk. Check mouth rinsing and inhaler technique.
Systemic corticosteroids	Typically prednisolone 40 mg daily for 5 days	Hyperglycemia, fluid retention, mood changes, and steroid myopathy with repeated courses.
Antibiotics	When sputum purulence increases with another cardinal symptom, or if ventilated. Usually 5–7 days.	Watch for diarrhea, dehydration, and tendon problems with fluoroquinolones.
Newer options	Roflumilast, azithromycin, ensifentrine and biologics (e.g., dupilumab, mepolizumab) for selected phenotypes	Added by specialists for frequent exacerbators. Know they exist.

Clinical tip: Poor inhaler technique is common and treatable. Watching a patient use their inhaler is within a physiotherapists' scope and can help prevent readmission.

Oxygen Therapy in COPD

For patients with COPD or at risk of hypercapnia, the target is SpO₂ 88–92%. Over-oxygenation can worsen CO₂ retention, so medical team must treat hypoxemia, but avoid pushing saturations above target. Exertion often drops SpO₂, so clinician must titrate oxygen to stay within target during activity and return to baseline settings at rest.

Physiotherapists must follow their local policy, physiotherapy practice acts or the APTA Acute Care oxygen therapy guidance during patient's treatment. Supplemental oxygen may be administered or adjusted by physiotherapists, provided that institutional protocols and physician prescriptions are followed. Advanced practice physiotherapists can be eligible to initiate and adjust the oxygen prescription, however clinical experience, advanced training, and passing a written exam is often required.

The following are oxygen delivery devices:

• Nasal cannula: Delivers 1–4 L/min (about 24–36% fraction of inspired oxygen (FiO₂). Comfortable to use and allows talking and eating.
• Venturi mask: Provides fixed FiO₂ (24–35%). It is preferred when precise, controlled oxygen delivery is required.
• Simple face mask: Delivers 5–10 L/min. Less precise and requires a minimum flow to prevent CO₂ rebreathing.
• High-flow nasal cannula (HFNC): Supplies up to 60 L/min of heated and humidified oxygen. This device is an option for hypoxemic or mildly hypercapnic patients that improves comfort and secretion clearance.
• Non-invasive ventilation (NIV / BiPAP): Provides pressure support and serves as a first-line treatment for acute hypercapnic respiratory failure. Physiotherapists must know the patient's NIV settings and whether the team allows time off the ventilator for mobilisation. Intubation is considered if NIV fails. During therapy, clinicians assure safety by preventing tripping on tubing and secure cannulas during mobilisation.

Clinical tip: Before mobilising, physiotherapists should check the prescription, alarm limits and tubing length. They should never remove oxygen to "see how will the patient manage" without an order.

Clinical note: NIV is being explored as an adjunct to relieve respiratory muscle burden and increase exercise tolerance. Combining NIV with pulmonary rehabilitation can improve exercise capacity.

Physiotherapist's Role in Treating Patients with COPD Exacerbation in Acute Care

Exercise training is a cornerstone of COPD management, improving health-related quality of life, lowering hospital admission rates, and reducing mortality.

The following principles guide physiotherapists in the treatment of patients with COPD hospitalised in acute care:

Assess first. Review the chart (Arterial blood gas (ABG), SpO₂ and oxygen device, vitals, medications, chest imaging), then the patient (RR, work of breathing, speech, sputum, mental status, strength, mobility). Decide whether the patient is stable enough to treat.

Treat the problem in front of you. For dyspnea, use positions of ease (forward-lean sitting, supported standing), pursed-lip breathing, breathing control and a handheld fan, and teach pacing and energy conservation. Use airway clearance only when sputum retention is present: active cycle of breathing, positive expiratory pressure devices, huffing and good hydration. Avoid routine chest percussion and any technique that provokes bronchospasm.

Mobilise early. Start as soon as the patient is clinically stable, because bed rest quickly worsens weakness and raises the risk of delirium and venous thromboembolism. Progress from bed mobility to sit to stand, marching and hallway walking. Pair this with targeted exercises, such as repeated low-load sit-to-stands, upper and lower limb strengthening and cycling, aiming for a Borg dyspnea rating of 4–6/10. Use short intervals with rests when continuous exercise is too hard. Patients who desaturate can use portable oxygen or HFNC, and some can mobilise with NIV if the team permits.

Stop or modify exercise if SpO₂ falls below target and does not recover with oxygen adjustment, RR is severely elevated, or the patient develops new chest pain, arrhythmia, dizziness, confusion or drowsiness. Report abnormal vitals or suspected deterioration to the team.

Plan discharge from day one. Identify functional status, home setup, falls risk and equipment needs. Physiotherapists are part of the multidisciplinary team and participate in discharge planning by (1) recommending a referral to pulmonary rehabilitation, (2) reviewing the COPD action plan, inhaler technique, and smoking cessation, and (3) flagging high-risk patients that will require a follow-up within 1–4 weeks.

Outcome Measures

Physiotherapists should  choose the outcome measures based on patient stability and time available. These outcome measures may include 2-Minute Walk Test (2MWT), a practical outcome measure tool for acute care and frailer patients, or 6-Minute Walk Test (6MWT), which can be used when patient is stable or near discharge. 6MWT is commonly performed to assess the submaximal functional capacity of a patient. Five Times Sit-to-Stand (5xSTS) test assesses lower limb strength and balance. The test is quick to administer and bedside friendly. Slower times reflect frailty and are linked to readmission risk. Short Physical Performance Battery (SPPB) helps to predict disability and mortality. To assess breathlessness in daily activity, clinicians may use mMRC Dyspnea Scale (0–4). COPD Assessment Test (CAT, 0–40) assesses symptom burden and quality of life. Score ≥10 indicates higher symptom burden. Other tests include Borg Rating of Perceived Exertion (Borg RPE)/dyspnea, grip strength, Incremental Shuttle Walk Test, or Cardiopulmonary exercise testing (CPET).

According to a longitudinal study, changes in patients living with frailty and COPD were associated with significant clinical outcomes related to dyspnea; mobility; physical activity; handgrip and quadriceps strength. It was found that five times sit-to-stand and exacerbations were independent predictors of the improvement in frailty status.

Resources

• British Thoracic Society Guideline for oxygen use in adults in healthcare and emergency settings
• 2026 GOLD Report and Pocket Guide
• Chronic obstructive pulmonary disease (COPD)
• Pulmonary Rehabilitation for Adults with Chronic Respiratory Disease: An Official American Thoracic Society Clinical Practice Guideline