RxCe - Collaborative Care in COPD: Evidence-Based S Materials

COLLABORATIVE CARE IN COPD: EVIDENCE-BASED STRATEGIES FOR THE HEALTHCARE TEAM

Faculty:

L. Austin Fredrickson, MD, FACP

L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 

Liz Fredrickson, PharmD, BCPS

Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy, where she is course director of the Parenteral Products and Basic Pharmaceutics Lab courses.

Pamela Sardo, PharmD, BS

Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable public health challenge that is now one of the top three causes of death worldwide. COPD is characterized by chronic respiratory symptoms, which cause airflow obstruction that is persistent and often progressive. The early and appropriate diagnosis of COPD can help guide treatment and improve the quality of life for those with the condition. Pharmacotherapy reduces symptoms, frequency, and severity of COPD exacerbations. Fortunately, several treatment options are available for COPD, and treatment regimens should be individualized for each patient.

Accreditation Statements

In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation Council^TM for Continuing Medical Education (ACCME^®), the Accreditation Council for Pharmacy Education (ACPE^®), and the American Nurses Credentialing Center (ANCC^®), to provide continuing education for the healthcare team.

Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are as follows:

Pharmacists: JA4008424-0000-26-096-H01-P

Pharmacy Technicians: JA4008424-0000-26-096-H01-T

Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit.

Credit Types:

Pharmacy - 2 Credits

Type of Activity: Application

Media: Computer-Based Training (i.e., online courses)

Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Activity Pre-Test, Post-Test, and Activity Evaluation.

Release Date: June 22, 2026 Expiration Date: October 20, 2028

Target Audience: This educational activity is for Pharmacists and Pharmacy Technicians

How to Earn Credit: From June 22, 2026, through October 20, 2028, participants must:

Read the “learning objectives” and “author and planning team disclosures;”

Take the “Educational Activity Pre-Test;”

Study the section entitled “Educational Activity;” and

Complete the Educational Activity Post-Test and Activity Evaluation. The Educational Activity Post-Test will be graded automatically. Following successful completion of the Educational Activity Post-Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)

CE Credits: Credits for this course will be uploaded to CPE Monitor^® for pharmacists and pharmacy technicians.

Statement of Need

Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable public health challenge that is now one of the top three causes of death worldwide. The appropriate and early diagnosis of COPD is a necessary skill. Applying these skills can help guide treatment and improve the quality of life for those with COPD. Pharmacotherapy reduces symptoms, frequency, and severity of COPD exacerbations.

Learning Objectives: Upon completion of this educational activity, participants should be able to:

List the diagnostic criteria and common clinical presentation of COPD

Identify risk factors that can increase the risk of developing COPD or exacerbations

Discuss pharmacotherapy options for COPD exacerbations

Outline treatment options for the management of stable COPD

Disclosures

The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; Liz Fredrickson, PharmD, BCPS; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity.

Educational Activity Pre-Test

Which of the following is a hallmark symptom of COPD?

Nocturnal wheezing only

Sudden chest pain

Progressive dyspnea

Frequent hemoptysis

In what scenario are antibiotics typically recommended during a COPD exacerbation?

In all exacerbations

Only if a chest X-ray shows pneumonia

When sputum is purulent and increased in volume

Only for patients on chronic oxygen

Treatment options for stable COPD include

phosphodiesterase-4 (PDE4) inhibitors.

prescribing CSN depressants.

prescribing benzodiazepines as a first-line treatment.

recommending the regular use of aspirin.

Educational Activity

Collaborative Care in COPD: Evidence-Based Strategies for the Healthcare Team

Introduction

Chronic obstructive pulmonary disease is a chronic respiratory lung condition. It results from a combination of genetic and environmental factors that can lead to lung damage over time. Symptoms include dyspnea, cough, and sputum production, which may result from abnormalities in the airways or alveoli, leading to progressive airflow obstruction. Pharmacologic therapy and lifestyle changes can help manage chronic obstructive pulmonary disease. Choosing medications for a patient should be individualized, taking into account availability, cost, side effects, and clinical response.

The Prevalence and Burden of COPD

Chronic Obstructive Pulmonary Disease (COPD) is a significant public health challenge that remains one of the top four causes of death worldwide despite being preventable and treatable.¹ In 2021, over 3 million deaths occurred due to COPD, which accounted for 6% of all deaths globally.¹ In the United States, almost 15.7 million Americans (6.4%) reported having a COPD diagnosis, with some adults unaware that they have COPD.² The prevalence of COPD varies across countries; however, it has been found that COPD prevalence is directly related to the prevalence of tobacco smoking.³ Continued exposure to COPD risk factors and the aging of the world population are expected to increase the prevalence and burden of COPD over the coming decades.^4,5

The current GOLD Report provides an unbiased review of evidence on the assessment, diagnosis, and treatment of people with COPD.⁶ Treatment for COPD can be broken into objectives directed toward relieving and reducing the impact of symptoms and objectives that reduce the risk of adverse health events that may affect the patient at some point in the future.⁶

What is COPD

Chronic obstructive pulmonary disease is a lung condition characterized by chronic respiratory symptoms such as dyspnea, cough, sputum production, and/or exacerbations. Chronic obstructive pulmonary disease may result from abnormalities in the airways (bronchitis, bronchiolitis) and/or the alveoli (emphysema), leading to persistent, often progressive airflow obstruction.⁷ Chronic obstructive pulmonary disease results from gene(G)-environment(E) interactions that occur over the lifetime(T) of an individual (GETomics), which can damage the lungs. These GETomics can damage the lungs and/or alter their normal development and aging processes.⁸

Tobacco smoking and the inhalation of toxic particles and gases from household and outdoor air pollution are the main environmental exposures that can lead to COPD.⁹ Individuals who smoke cigarettes have a higher prevalence of respiratory symptoms and lung function abnormalities. Smokers have a greater annual rate of decline in FEV₁ (forced expiratory volume over 1 second) and a greater COPD mortality rate than non-smokers.¹⁰ Smoking during pregnancy may increase the risk of altered lung growth in the fetus.¹¹ Tobacco use is the leading risk for COPD in high-income countries; however, in low to middle-income countries, the risk of developing COPD is sometimes attributed more to environmental exposures.⁹ Examples of outdoor, occupational, and household air pollution include the burning of wood and other biomass fuels.¹² Genetic risk factors can also lead to COPD - the most relevant being a mutation in the SERPINA1 gene, which is epidemiologically rare.⁶

The current GOLD report has proposed taxonomy (etiotypes) for COPD that extend past the traditionally known smoking causation. These proposed etiotypes have little impact on clinical practice but highlight the need to explore current and future therapies based on the causes of COPD. These include the following:^6,13

Genetically determined COPD (COPD-G): Alpha-1 antitrypsin deficiency and other genetic variants with minor effects acting in combination

COPD due to abnormal lung development (COPD-D): early life events, including premature birth and low birth weight

Cigarette smoking COPD (COPD-C): exposure to tobacco smoke, including in utero or via passive smoking, vaping or e-cigarette use, and cannabis

Biomass and pollution exposure COPD (COPD-P): household pollution, ambient air pollution, wildfire smoke, occupational hazards

COPD due to infections (COPD-I): childhood infections, tuberculosis-associated COPD, HIV-associated COPD

COPD and asthma (COPD-A): particularly childhood asthma

COPD of unknown cause (COPD-U)

Diagnosis and Clinical Presentation

A combination of small-airway disease and parenchymal destruction can cause airflow obstruction.⁶ Small airway disease increases airway resistance and parenchymal destruction, also known as emphysema, which can reduce the normal elastic recoil of the lung parenchyma.⁶ The reduction of normal elastic recoil of the lung parenchyma can also be caused by chronic inflammation of the lungs, which may cause structural changes. These changes reduce the airways' ability to remain open during expiration. They can limit lung emptying during forced expiration, thereby decreasing FEV1 and the FEV₁/FVC ratio (forced expiratory volume/forced vital capacity), and contribute to gas trapping and lung hyperinflation.⁶ The outcomes of these various airflow obstruction causes may be measured by spirometry, a widely available and reproducible lung function test.⁶

The presence of non-fully reversible airflow limitation (a post-bronchodilator spirometric FEV1/FVC <0.7) is required to diagnose COPD.⁶ Patients with dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors should be considered for testing.⁶ Some individuals are labeled as ‘Pre-COPD’, which includes the presence of structural lung lesions such as emphysema and/or physiological abnormalities without airflow obstruction. These physiological abnormalities may include low-normal FEV₁, gas trapping, hyperinflation, reduced lung diffusing capacity, and/or rapid decline in FEV₁. Individuals with a normal FEV₁/FVC ratio but abnormal spirometry may be termed with ‘PRISm,’ meaning Preserved Ratio Impaired Spirometry.⁶ Individuals with Pre-COPD or PRISm may be at risk of developing airflow obstruction over time; however, not all patients do. Underdiagnosis and misdiagnosis of COPD can cause individuals to receive no treatment or incorrect treatment.⁶

Once COPD has been diagnosed and confirmed by spirometry, four fundamental aspects guide therapy: the severity of airflow limitation, the nature and magnitude of current symptoms, the previous history of moderate and severe exacerbations, and the presence and type of other diseases.⁶ The GOLD grades and severity of airflow obstruction based on post-bronchodilator FEV₁ (% reference) in COPD are as follows:⁶

Gold 1: Mild - FEV1 ≥ 80% predicted

Gold 2: Moderate - 50% ≤ FEV1 < 80% predicted

Gold 3: Severe - 30% ≤ FEV1 < 50% predicted

Gold 4: Very Severe - FEV1 <30% predicted

If a patient is suspected of having COPD, a thorough medical history should be collected.⁶ An important aspect of medical history collection is a patient’s exposure to risk factors, past medical history, and family history. The pattern of symptom development can help differentiate COPD from other lung conditions.⁶

The impact of disease on a patient’s life should also be evaluated. This assessment should determine the patient's economic impact and general well-being. More specifically, the limitation of activities, missed work, implications for family routines, depression or anxiety, and sexual activity should all be considered. Collecting medical history, inquiring about available social and family support, and considering ways to reduce risk factors may help guide treatment.⁶

Chronic obstructive pulmonary disease may present with dyspnea, wheezing, chest tightness, fatigue, activity limitation, and cough (with or without sputum production).⁶ Some or all of these symptoms may be present, and symptoms may vary daily. It may be helpful to use the Dyspnea questionnaire or other multidimensional assessment tools to help gauge a patient's symptoms.^6,14 Other tools may include the Medical Research Council dyspnea scale (MRC; or modified MRC [mMRC], which is more widely used), Dyspnea Exertion Scale (DES), Oxygen Cost Diagram (OCD), and the Baseline Dyspnea Index (BDI).¹⁴

Dyspnea may be progressive over time, worse with exercise, and/or persistent.^6,14 Patients may describe dyspnea as increased breathing effort, chest tightness, air hunger, or mental effort to breathe.¹⁴ Chronic cough can often be an overlooked symptom of COPD, as it is an expected consequence of smoking and/or environmental exposure.⁶ Other causes of chronic cough may include asthma, lung cancer, tuberculosis, bronchiectasis, left heart failure, interstitial lung disease, cystic fibrosis, idiopathic cough, chronic allergic rhinitis, post-nasal drip syndrome, upper airway cough syndrome, gastroesophageal reflux, and due to medication. The cough (productive or unproductive) may be intermittent and, over time, more prevalent.⁶

Individuals with COPD may experience exacerbations, which are acute events characterized by an increase in respiratory symptoms.⁶ Patients with COPD may have other comorbidities that can mimic or aggravate an acute exacerbation. Individuals with asthma have been found to have an increased risk of developing chronic airflow obstruction and COPD. Differentiating the symptoms of asthma and COPD in adults can be clinically complex because they share many symptoms.⁶ When comparing the symptoms of COPD and asthma, the following suggestive features might help. Chronic obstructive pulmonary disease symptoms are slowly progressive, with a history of tobacco smoking or other risk factors.⁶ Suggestive features of asthma include variable airflow obstruction, symptoms that vary widely from day to day, symptoms that are worse at night/early morning, allergy, rhinitis, and/or eczema are also present, often occurring in children. The patient’s family history of asthma is also reviewed and considered.¹⁵

Patients with COPD may also present with chronic bronchitis.⁶ Chronic bronchitis is defined as the presence of cough with expectorated sputum for at least 3 months per year for two consecutive years. A caveat to the definition of chronic bronchitis is that symptoms are present in the absence of other conditions that could explain them.⁶

Two commonly used scales to help assess COPD in a patient include the modified Medical Research Council dyspnea scale (mMRC) (Table 1) and the COPD Assessment Test (CAT^TM) (Table 2).⁶ The mMRC is a scale that helps to measure breathlessness and grades a patient from 0 to 4. The CAT^TM is an 8-item, more multidimensional questionnaire designed to assess the health status of patients with COPD. The CAT^TM has scores that can range from 0 to 40.⁶

Table 1

mMRC Dyspnea Scale⁶

mMRC Dyspnea Scale - Patient must choose one of the following
Grade 0	I only get breathless with strenuous exercise
Grade 1	I get short of breath when hurrying on the level or walking up a slight hill
Grade 2	I walk slower than people of the same age on the level because of breathlessness, or I have to stop for breath when walking at my own pace on the level
Grade 3	I stop for breath after walking about 100 meters or after a few minutes on the level
Grade 4	I am too breathless to leave the house, or I am breathless when dressing or undressing.

Table 2

CAT^TM Assessment^6,17

CAT^TM Assessment: patients are to rate each of the following items from 0 to 5. Score of 0 being closer to “I have no limitation” with the examples on the left, and score of 5 being limitations and closer to the statements on the right.
I never cough	I cough all the time
I have no phlegm (mucus) in my chest at all	My chest is completely full of phlegm (mucus)
My chest does not feel tight at all	My chest feels very tight
When I walk up a hill or one flight of stairs, I am not breathless	When I walk up a hill or one flight of stairs, I am very breathless
I am not limited to doing any activities at home	I am very limited in doing activities at home
I am confident about leaving my home despite my lung condition	I am not at all confident leaving my home because of my lung condition
I sleep soundly	I don’t sleep soundly because of my lung condition
I have lots of energy	I have no energy at all
Patients with a total score of 10 or more should be considered for regular symptom treatment.

Smoking Cessation

Despite smoking cessation being a key to decreasing the risks and progression of COPD, approximately 40% of those with COPD are current smokers.¹⁸ There are several pharmacotherapies for smoking cessation, including nicotine replacement products (nicotine gum, inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge), bupropion, varenicline, naltrexone, nortriptyline, and clonidine.⁶ Patients must be willing to stop smoking, and healthcare providers should recognize that relapse is common and reflects the chronic nature of dependence and addiction to tobacco products.⁶

The five-step program (also called the 5A’s) for intervention to help the patient who is willing to quit includes the “ask, advise, assess, assist, and arrange.”¹⁹ All patients should be asked about tobacco use at every visit. Patients who use tobacco, with or without a diagnosis of COPD, should be strongly urged to quit. If the patient uses tobacco, the provider should assess the willingness and rationale of the patient’s desire to make a quit attempt. Providers should assist patients in quitting and in developing a plan that includes support and pharmacotherapy. Follow-up contact should be arranged to support the patient's success.¹⁹

Pharmacotherapy

Reducing symptoms, exacerbation frequency and severity, while improving exercise tolerance and health status, are the goals of pharmacologic therapy for COPD.⁶ While no trials have been sufficiently conclusive showing that pharmacotherapy can reduce the rate of FEV₁ decline, maintenance therapy can help to manage COPD.⁶ Choosing medications for a patient should be individualized, and the availability, cost, side effects, and clinical response should all be considered. The availability of agents is constantly changing, and the patient’s ability to use a metered-dose inhaler (MDI), a dry powder inhaler (DPI), a soft mist inhaler (SMI), or a nebulizer should be considered. Combination products are available and should be considered when appropriate. Package insert material should be referenced for all dosing-related questions.⁶

Many medications used for COPD are delivered via inhalation devices such as nebulizers, MDIs, DPIs, and SMI devices.⁶ The proper education and training on the use of these devices is key to treatment success. Instructions vary by device type, and pharmacy staff should familiarize themselves with each device carried.⁶ Errors in device use often lead to problems with inspiratory flow, coordination, inhalation duration, preparation of dose, exhalation maneuver before inhalation, and breath-holding following dose inhalation.²⁰ Dry powder inhalers are only appropriate if the patient can make forceful and deep inhalations.⁶ The ‘teach-back’ method can be used to help gauge a patient's understanding of inhaler use. Patients should be prescribed a spacer/valved holding chamber if there is doubt that they will be able to use a pressurized metered dose inhaler correctly.⁶ Spacers help to reduce difficulties that can be caused by poor coordination, increase pulmonary function, reduce oropharyngeal deposition, and minimize the risk of oropharyngeal candidiasis with ICS.²¹

Medication adherence can be a challenge with COPD, and along with other factors, medication delivery device consideration can be a key part of increasing adherence.⁶ Non-adherence is associated with poor symptom control, increased risk of exacerbation, increased healthcare costs and utilization, increased mortality risk, and decreased quality of life. Proper inhaler technique and medication adherence should be assessed before determining that current therapy is insufficient.⁶

Bronchodilators

Bronchodilators include beta₂-agonists and antimuscarinic agents. Bronchodilators are commonly used as maintenance therapy; however, they may also be used for some occasional symptoms or immediate symptom relief.⁶

Beta₂-agonists

Beta₂-agonists help relax airway smooth muscle by stimulating beta2-adrenergic receptors, increasing cyclic AMP, and antagonizing bronchoconstriction, helping to prevent or reduce symptoms of COPD.⁶ The improvements in expiratory flow and potential increase in FEV₁ reflect a widening of the airways rather than changes in elastic lung recoil.⁶ Short-acting beta₂-agonists (SABA) have an effect that lasts 4 to 6 hours and can be used on a regular or as-needed basis to help improve FEV₁ and symptoms.^22-24 SABA include fenoterol, levalbuterol, albuterol, and terbutaline.⁶ Although concerns of loss of lung function or increased mortality have been reported with the use of SABAs in asthma treatment, no association between SABAs and these outcomes has been reported in COPD.⁶ Long-acting beta₂-agonists (LABA) have a duration of action of 12 or more hours. LABAs include arformoterol, formoterol, indacaterol, olodaterol, and salmeterol. Resting sinus tachycardia, which can precipitate cardiac rhythm disturbances in susceptible patients, is an adverse effect to monitor when stimulating beta₂-adrenergic receptors.⁶

Antimuscarinic Drugs

Antimuscarinic drugs, also known as anticholinergics, work by blocking the bronchoconstrictor effects of acetylcholine on M3 muscarinic receptors expressed in airway smooth muscle.²⁵ Some antimuscarinic agents also bind to M2 receptors that can potentially cause vagally induced bronchoconstriction. Short-acting antimuscarinics include ipratropium bromide and oxitropium bromide, which have a duration of action lasting 6 to 9 hours.⁶ SAMAs have been shown to provide small benefits over SABAs for lung function, health status, and requirement for oral steroids.²⁶ Long-acting antimuscarinic (LAMA) agents that can help improve symptoms such as cough, sputum, and health status include aclidinium bromide, glycopyrronium bromide, tiotropium, umeclidinium, glycopyrrolate, and revefenacin.⁶ Dosing schedules for LAMAs should be confirmed, as some may be administered once a day and others require twice daily dosing. LAMAs can help to reduce exacerbations and related hospitalizations. Systemic adverse effects are limited as inhaled anticholinergic drugs are poorly absorbed. One of the main side effects is mouth dryness, and some patients who have taken ipratropium report a bitter, metallic taste.⁶ Cardiovascular function should be monitored, as there has been a small increase in cardiovascular events in patients regularly treated with ipratropium bromide.^27,28

Methylxanthines

Methylxanthines, such as aminophylline and sustained-release theophylline, are systemic oral medications whose exact effects on COPD are unknown. It is thought that they may act as non-selective phosphodiesterase inhibitors. Although the significance has been disputed, methylxanthines have been reported to have a range of non-bronchodilator actions.^29,30 Theophylline does exert a small bronchodilator effect in patients with stable COPD.⁶ Methylxanthines cause more side effects (insomnia, headache, nausea, heartburn) and have significant interactions with commonly used medications (erythromycin, ciprofloxacin, allopurinol, cimetidine, fluvoxamine) than medications previously discussed. Atrial and ventricular arrhythmias and grand mal convulsions are side effects that may steer a provider away from choosing a methylxanthine over other options for COPD. Toxicity is dose-related, and clearance of the drug declines with age.⁶

Combination Bronchodilator Therapy

Combination products of LABA+LAMA, SABA+SAMA, and LABA+ICS (inhaled corticosteroids), and LABA+LAMA+ICS, exist and may be considered.⁶ Combining bronchodilators with different mechanisms and durations of action can help to increase the degree of bronchodilation and lower the side effects of having a high dose of a single bronchodilator. The combination of SABA+SAMA has been shown to be superior to either medication alone.⁶ Combining LABAs and LAMAs helps to improve lung function significantly, as well as health status. It also improves dyspnea, reduces exacerbations, increases FEV1, and reduces symptoms compared with monotherapy. Also, in patients with moderate to very severe COPD, LABA+ICS therapy is more effective at improving health status by improving lung function and reducing exacerbations compared with either LABA or ICS alone. Combination therapy can be helpful because single-inhaler therapy is more convenient than using multiple inhalers.⁶

Table 3

Current Combinations Available Per GOLD Guidelines⁶

SABA+SAMA

Fenoterol/ipratropium

Albuterol/ipratropium

LABA+LAMA

Formoterol/aclidinium Formoterol/glycopyrronium Indacaterol/glycopyrronium Vilanterol/umeclidinium Olodaterol/tiotropium

LABA+ICS

Formoterol/beclometasone

Formoterol/budesonide

Formoterol/mometasone

Salmeterol/fluticasone propionate

Vilanterol/fluticasone furoate

LABA+LAMA+ICS

Fluticasone/umeclidinium/vilanterol

Beclometasone/formoterol/glycopyrronium

Budesonide/formoterol/glycopyrrolate

Anti-inflammatory agents

The main clinically relevant endpoint to assess the efficacy of anti-inflammatory drugs is the exacerbation rate. Anti-inflammatory therapy recommended in stable COPD includes inhaled corticosteroids, PDE4 inhibitors, and antibiotics.⁶

Inhaled Corticosteroids

Inhaled corticosteroids that can be used for COPD include beclomethasone, budesonide, fluticasone, and mometasone.⁶ Inhaled respiratory corticosteroids help to reduce bronchial inflammation by binding to glucocorticoid cytoplasmic receptors. This action leads to either the induction of potent anti-inflammatory mediators or the repression of transcription of proinflammatory mediators.^31,32 Regular ICS treatment may be of concern, as it may increase the risk of pneumonia, especially in patients with severe disease.⁶ A higher risk of pneumonia in patients taking ICS is seen in patients who are 55 or older, with a history of prior pneumonia or exacerbations, BMI < 25 kt/m², a poor dyspnea grade, and/or severe airflow obstruction.⁶ Evidence has shown that ICS use can modify the airway microbiome and is associated with a higher prevalence of oral candidiasis, hoarse voice, skin bruising, and pneumonia.⁶ Patients should always rinse their mouths after using an inhaler containing ICS. Most studies have found that treatment with an ICS alone does not modify the long-term decline of FEV₁ or mortality in patients with COPD, and long-term monotherapy is not recommended.⁶

The GOLD Report strongly favors adding ICS to long-acting treatment when there is a history of hospitalization for COPD exacerbation, 2 or more moderate exacerbations of COPD per year, blood eosinophils ≥ 300 cells/µL, and a history of or concomitant asthma.⁶ Use of an add-on ICS is favorable when there is 1 moderate exacerbation of COPD per year and blood eosinophils range from 100 to <300 cells/µL. Use of ICS as an add-on treatment should not be used if a patient has had recurrent pneumonia, blood eosinophils <100 cells/µL, or a history of mycobacterial infection.⁶

Phosphodiesterase-4 (PDE4) Inhibitors

Phosphodiesterase-4 inhibitors, such as roflumilast, reduce inflammation by inhibiting the breakdown of intracellular cyclic AMP (cAMP).³³ Roflumilast does not have direct bronchodilator activity and is taken as a once-daily oral medication.⁶ Roflumilast helps patients with moderate to severe COPD exacerbations with chronic bronchitis treated with systemic corticosteroids, severe to very severe COPD, and patients with a history of exacerbations. Roflumilast is an option for patients not controlled on fixed-dose LABA+ICS combinations, and it can improve lung function when added to long-acting bronchodilators.⁶ Side effects commonly seen with PDE4 inhibitors are diarrhea, nausea, reduced appetite, abdominal pain, weight loss, headaches, and sleep disturbances. These side effects seem to occur early in treatment and diminish over time with continued treatment.⁶

Combination PDE3 and PDE4

Inhibiting PDE3 increases cAMP, leading to bronchodilation. Ensifentrine blocks PDE3 and PDE4 enzymes, increasing cAMP levels in the lung cells.³⁴ It is indicated for the maintenance treatment of chronic obstructive pulmonary disease (COPD) in adult patients.³⁴ It is dosed as 3 mg (one ampule) twice daily, administered by oral inhalation using a standard jet nebulizer with a mouthpiece.³⁴ Results from the ENHANCE-1 and ENHANCE-2 trials demonstrated a statistically significant improvement in FEV₁ AUC_0-12h compared to placebo.³⁴ Ensifentrine should not be physically mixed with other drugs or added to solutions containing other drugs and should not be used to treat acute symptoms of bronchospasm. Commonly reported adverse effects include back pain, hypertension, urinary tract infection, and diarrhea.³⁴

Interleukin-4 Receptor Alpha Antagonist

Dupilumab is indicated for multiple indications, including a recent approval for COPD as an add-on maintenance treatment of adult patients with inadequately controlled COPD and an eosinophilic phenotype.³⁵ It is an interleukin-4 receptor alpha antagonist, a human monoclonal antibody of the IgG4 subclass that binds to the IL-4R subunit and inhibits IL-4 and IL-13 signaling.³⁵ The results of the BOREAS and NOTUS trials were the annualized rate of moderate or severe COPD exacerbations during the 52-week treatment period.³⁵ In both trials, dupilumab demonstrated a significant reduction in the annualized rate of moderate or severe COPD exacerbations compared to placebo when added to background maintenance therapy.³⁵ The recommended dosage for adult patients is 300 mg given every 2 weeks as a subcutaneous injection.³⁵ It is not for the relief of acute bronchospasm. Common adverse effects include viral infection, headache, nasopharyngitis, back pain, diarrhea, arthralgia, urinary tract infection, local administration reactions, rhinitis, eosinophilia, toothache, and gastritis.³⁵

Antibiotics

There is controversy over the efficacy of reducing exacerbations through the prophylactic continuous use of antibiotics.⁶ Older studies show no effect, while some later studies show they may help reduce the exacerbation rate. The two antibiotics most frequently used are azithromycin, administered at 250 mg once daily or 500 mg three times weekly, and erythromycin, given at 250 mg twice daily for 1 year. These medications can be used for patients prone to exacerbation; however, the risk of increased bacterial resistance, prolonged QTc interval, and impaired hearing tests limits their use.⁶

Treatment and Management of Stable COPD

Initial treatment of COPD should be based on the patient’s GOLD group.⁶ The severity of airflow obstruction, symptoms, history of exacerbations, exposure to risk factors, and comorbidities guide the treatment of COPD.⁶ Treatable traits of COPD include breathlessness and exercise limitation as well as exacerbation frequency while on maintenance therapy, which helps guide escalation and de-escalation. Although asthma and COPD may coexist in an individual patient, pharmacotherapy should primarily follow asthma guidelines while also considering pharmacologic and nonpharmacologic approaches that may be needed for COPD. Treatment goals for stable COPD include reducing and relieving symptoms, improving exercise tolerance, and improving health status. This involves reducing risk by preventing disease progression, preventing and treating exacerbations, and reducing mortality.⁶

In 2020, the American Thoracic Society published guidelines for the management of COPD.³⁶ They included an observed benefit in advanced refractory dyspnea with opioids, despite otherwise optimal treatment that outweighed uncertain risks. Historical studies were undertaken when only minimal maintenance medications were available to treat COPD. Given the very low certainty of evidence, the use of opioids must be evaluated by clinicians and patients in a shared decision-making process.^36,37

Among bronchodilators, long-acting agents are preferred over short-acting agents, except in patients with only occasional dyspnea.⁶ Rescue short-acting bronchodilators should be provided for patients who need immediate symptom relief and may also be used in patients who are already on long-acting bronchodilators for maintenance therapy. Initial therapy should include a LAMA+LABA combination. When an ICS is indicated, the combination of LABA+LAMA+ICS has been shown to be superior to LABA+ICS therapy. If a patient has COPD and asthma, treatment should contain an ICS.⁶

Initial therapy can be discontinued based on mMRC and CATTM scores as follows:⁶

Group A patients have zero to one moderate exacerbations that do not lead to hospital admission.

mMRC score of 0-1 or a CAT^TM score of less than 10.

Initial treatment with a bronchodilator (long- or short-acting) may be appropriate.

Group B patients have zero to one moderate exacerbations that do not lead to hospital admission.

mMRC score of 2 or more, or a CAT^TM score of more than 10.

LABA+LAMA initial treatment is preferred.

Group E patients have two or more moderate exacerbations or one or more exacerbations leading to hospitalization.

Initial treatment should be LABA+LAMA therapy, with the consideration of LABA+LAMA+ICS or dupilumab, if blood eosinophils are >300.

This therapy may be more convenient and effective if delivered in a single inhaler rather than multiple inhalers.

After initial treatment, a review of management includes symptoms such as dyspnea and exacerbations.⁶ Inhaler technique and adherence should be assessed, as well as non-pharmacological approaches such as pulmonary rehabilitation and self-management education in all patients. After review and assessment, the therapy may be adjusted, including escalating, switching the inhaler device or medication type, or de-escalating. The cycle of review, assessment, and adjustment should be done frequently to help ensure optimal treatment.⁶ If the response to initial treatment is appropriate, it is advised to maintain that treatment option. If the response to initial treatment is not as expected, therapy should be evaluated.⁶

If dyspnea remains uncontrolled:

The first step is to introduce a LABA or LAMA.

If there is still no symptom control, the next step is a LABA+LAMA.

If there is still no control, consider switching to a different inhaler device or molecule, implementing or escalating non-pharmacologic treatments, and investigating and treating other causes of dyspnea.

If exacerbation control is being targeted, there are two routes to take, depending on blood eosinophil count.

The 2025 GOLD report recommends dupilumab as an add-on treatment for COPD in patients with high eosinophil count (≥300 cells/µL) and chronic bronchitis with continuing symptoms despite LABA+LAMA+ICS.⁶

Blood eosinophils help determine whether patients are more likely to benefit from ICS. Both routes start with LABA or LAMA therapy.

If blood eosinophils are <300, the next step is LABA+LAMA therapy.

If blood eosinophils remain below 100 but the patient is still having exacerbations, roflumilast (if the patient has an FEV₁ <50% with chronic bronchitis) or azithromycin (if the patient is a former smoker).

If a patient with blood eosinophils <300 who is started on LABA+LAMA needs further treatment.

If blood eosinophils are >100, the next step would be LABA+LAMA+ICS

If that is unsuccessful, roflumilast and azithromycin may be an option.

Patients with uncontrolled exacerbations who have started the first step of LABA or LAMA without success will go straight to LABA+LAMA+ICS if their blood eosinophils are >300.

If treatment is unsuccessful, patients can be considered for roflumilast (or ensifentrine) or azithromycin.

ICS can be withdrawn from therapy if pneumonia or other considerable side effects develop.

Smoking cessation and pulmonary rehabilitation are essential parts of nonpharmacologic COPD management.⁶ Physical activity is also recommended, and depending on local guidelines, vaccinations including influenza, pneumococcal, pertussis, COVID-19, and shingles may be recommended. Education and self-management interventions, including a written action plan, should be ongoing in treatment.⁶

Treatment of Co-Occurring Depression or Anxiety

Depression and anxiety are comorbidities that are often associated with COPD.^38-40 An interdisciplinary care model is important for treating behavioral and psychosocial conditions, as well as anxiety due to concerns about shortness of breath in individuals presenting with COPD. Breathlessness can trigger a stress response in the brain, further restricting breathing and worsening symptoms.⁴¹ Shared decision-making can unravel whether antidepressants may exacerbate COPD, or if modifying the COPD regimen is needed to improve patient care.^38-40

Management of Exacerbations

COPD exacerbations are events characterized by increased dyspnea and/or cough and sputum that worsen in <14 days.⁶ These exacerbations may be accompanied by tachypnea and/or tachycardia. Exacerbations are often associated with increased local and systemic inflammation. COPD exacerbations may be triggered by several different factors that include respiratory infections (bacterial, viral, or a combination of both), environmental pollutants, or unknown factors. When a patient is experiencing an exacerbation, there is evidence of increased airway and systemic inflammation, increased gas trapping and hyperinflation with reduced expiratory flow, dyspnea, and worsening of ventilation-perfusion distribution abnormalities that can result in arterial hypoxemia.⁶ A key symptom of exacerbations is dyspnea, and other symptoms may include increased sputum, cough, and wheezing.⁶ Classification of exacerbations is typically retrospective, based on the treatment used. Mild exacerbations can be treated with short-acting bronchodilators only. Moderate exacerbations are treated with short-acting bronchodilators and oral corticosteroids ± antibiotics. Severe exacerbations require hospitalization or emergency room visits.⁶ A differential diagnosis of heart failure, pneumonia, or pulmonary embolism should be ruled out when a patient is being diagnosed with a COPD exacerbation.⁶

Treatment goals for COPD exacerbations include minimizing the negative impact of the current exacerbation and preventing the development of subsequent events.⁶ Exacerbations can be managed inpatient or outpatient, depending on the severity of the exacerbation and underlying disease.⁶ Potential indications for hospitalization may include severe symptoms, acute respiratory failure, cyanosis, peripheral edema, failure of exacerbation to respond to initial treatment, serious comorbidities, or insufficient support at home. Hospital management of exacerbations consists of respiratory support, which may include oxygen therapy or ventilation.⁶ In severe but not life-threatening exacerbation, the severity of symptoms, blood gases, and a chest radiograph should be assessed. Supplemental oxygen therapy, bronchodilators, oral corticosteroids, oral antibiotics (when signs of bacterial infection are present), and noninvasive mechanical ventilation are treatments that may be considered.⁶

The initial medication regimen recommended to treat an acute exacerbation is SABA±ICS.⁶ These medications may be used as MDI or nebulizers, with nebulizers potentially being an easier delivery method for sicker patients. The GOLD report recommends continuing long-acting bronchodilators during an exacerbation or restarting as soon as possible. Systemic corticosteroids may help improve FEV₁ and oxygenation and shorten recovery time and hospitalization.⁶ Prednisone-equivalent 40 mg per day for 5 days is the current recommendation.^6,34 Some patients may respond well to nebulized budesonide.⁶

Oral glucocorticoids play a role in managing acute exacerbations and should not be used in the daily maintenance of COPD due to the high rate of systemic complications.^6,41 If indicated, antibiotics can help shorten the recovery time, reduce the risk of early relapse or treatment failure, and reduce hospitalization duration. Increased sputum purulence may indicate a bacterial infection, warranting antibiotic treatment. The duration of antibiotics is typically 5 to 7 days, with 5 days or fewer preferred. The choice of antibiotics should be based on local resistance patterns, with initial empirical treatments often including amoxicillin-clavulanic acid, a macrolide, tetracycline, or a quinolone.⁶ If a patient does require ventilation, non-invasive mechanical ventilation should be the first mode used in patients with acute respiratory failure.⁶

Patient Case

A 67-year-old male with a 5-pack-a-week smoking history and chronic cough with sputum production presents with progressive dyspnea. Spirometry reveals an FEV₁/FVC ratio of 0.48, consistent with GOLD Stage 3 (severe) COPD. His CAT score is 18, indicating significant daily symptoms.

What is another laboratory value that may be ordered?

Next, the interprofessional team of a physician, a pharmacist, and a respiratory therapist developed a collaborative plan for medication optimization and re-education on inhaler technique using teach-back.

What is another educational and support opportunity?

The patient begins triple therapy with fluticasone furoate/ umeclidinium/ vilanterol to reduce exacerbation risk and, with shared decision-making, is prescribed a nicotine patch. Influenza and pneumococcal vaccinations are updated.

How often should the patient take this triple combination?

After 6 months, the patient reports improved exercise tolerance and fewer exacerbations, with only 1 mild episode, which was treated with short-term oral prednisone (tapered over 5 days). The patient demonstrates adherence to the treatment. Oxygen saturation remains stable at 94% on room air, and his CAT score improves to 11. Coordinated care, education, and adherence led to improved quality of life, reduced symptoms, and fewer exacerbations, aligning with the goals of the GOLD 2025 guidance.

Patient Case Discussion Points:

What is another laboratory value that may be ordered?

Eosinophils

What is another educational and support opportunity?

Smoking cessation counseling and support, and discussion of vaccinations

How often should the patient take this triple combination?

Once daily

Summary

COPD is a lung condition characterized by chronic respiratory symptoms, including dyspnea, cough, sputum production, and/or exacerbations. COPD may result from abnormalities of the airways (bronchitis, bronchiolitis) and/or the alveoli (emphysema), which can cause persistent, often progressive airflow obstruction. A combination of small-airway disease and parenchymal destruction can cause airflow obstruction. The presence of non-fully reversible airflow limitation is mandatory for the diagnosis of COPD.

Smoking cessation helps to decrease the severity and progression of COPD. Reducing symptoms, exacerbation frequency and severity, and improving exercise tolerance and health status are the goals of pharmacologic therapy for COPD. Choosing medications for a patient should be individualized, considering availability, cost, side effects, and clinical response.

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DISCLAIMER

The information provided in this course is general in nature, and it is designed solely to provide participants with continuing education credit(s). This course and materials are not meant to substitute for the independent, professional judgment of any participant regarding that participant’s professional practice, including but not limited to patient assessment, diagnosis, treatment, and/or health management. Medical and pharmacy practices, rules, and laws vary from state to state, and this course does not cover the laws of each state; therefore, participants must consult the laws of their state as they relate to their professional practice.

Healthcare professionals must consult their employer, healthcare facility, hospital, or other organization for guidelines, protocols, and procedures to follow. The information provided in this course does not replace those guidelines, protocols, and procedures, but is for academic purposes only, and this course’s limited purpose is for the completion of continuing education credits.

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