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The  ATS Clinical Cases are a series of cases devoted to interactive clinical case presentations on all aspects of pulmonary, critical care and sleep medicine. They are designed to provide education to practitioners, faculty, fellows, residents, and medical students in the areas of pulmonary, critical care and sleep medicine.

Currently, we are not accepting new cases for this series, as there are several other venues for publishing cases.  For cases that can be written as brief, image-based quesitons, consider submitting them as to Quick Hits .  For other cases, please contact your assembly web director regarding other opportunities to publish or highlight cases.

ATS Clinical Cases Designated by the Assemblies

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COPD Case Study: Patient Diagnosis and Treatment (2024)

by John Landry, BS, RRT | Updated: May 16, 2024

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that affects millions of people around the world. It is primarily caused by smoking and is characterized by a persistent obstruction of airflow that worsens over time.

COPD can lead to a range of symptoms, including coughing, wheezing, shortness of breath, and chest tightness, which can significantly impact a person’s quality of life.

This case study will review the diagnosis and treatment of an adult patient who presented with signs and symptoms of this condition.

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COPD Clinical Scenario

A 56-year-old male patient is in the ER with increased work of breathing. He felt mildly short of breath after waking this morning but became extremely dyspneic after climbing a few flights of stairs. He is even too short of breath to finish full sentences. His wife is present in the room and revealed that the patient has a history of liver failure, is allergic to penicillin, and has a 15-pack-year smoking history. She also stated that he builds cabinets for a living and is constantly required to work around a lot of fine dust and debris.

Physical Findings

On physical examination, the patient showed the following signs and symptoms:

• His pupils are equal and reactive to light.
• He is alert and oriented.
• He is breathing through pursed lips.
• His trachea is positioned in the midline, and no jugular venous distention is present.

Vital Signs

• Heart rate: 92 beats/min
• Respiratory rate: 22 breaths/min

Chest Assessment

• He has a larger-than-normal anterior-posterior chest diameter.
• He demonstrates bilateral chest expansion.
• He demonstrates a prolonged expiratory phase and diminished breath sounds during auscultation.
• He is showing signs of subcostal retractions.
• Chest palpation reveals no tactile fremitus.
• Chest percussion reveals increased resonance.
• His abdomen is soft and tender.
• No distention is present.

Extremities

• His capillary refill time is two seconds.
• Digital clubbing is present in his fingertips.
• There are no signs of pedal edema.
• His skin appears to have a yellow tint.

Lab and Radiology Results

• ABG results: pH 7.35 mmHg, PaCO2 59 mmHg, HCO3 30 mEq/L, and PaO2 64 mmHg.
• Chest x-ray: Flat diaphragm, increased retrosternal space, dark lung fields, slight hypertrophy of the right ventricle, and a narrow heart.
• Blood work: RBC 6.5 mill/m3, Hb 19 g/100 mL, and Hct 57%.

Based on the information given, the patient likely has chronic obstructive pulmonary disease (COPD) .

The key findings that point to this diagnosis include:

• Barrel chest
• A long expiratory time
• Diminished breath sounds
• Use of accessory muscles while breathing
• Digital clubbing
• Pursed lip breathing
• History of smoking
• Exposure to dust from work

What Findings are Relevant to the Patient’s COPD Diagnosis?

The patient’s chest x-ray showed classic signs of chronic COPD, which include hyperexpansion, dark lung fields, and a narrow heart.

This patient does not have a history of cor pulmonale ; however, the findings revealed hypertrophy of the right ventricle. This is something that should be further investigated as right-sided heart failure is common in patients with COPD.

The lab values that suggest the patient has COPD include increased RBC, Hct, and Hb levels, which are signs of chronic hypoxemia.

Furthermore, the patient’s ABG results indicate COPD is present because the interpretation reveals compensated respiratory acidosis with mild hypoxemia. Compensated blood gases indicate an issue that has been present for an extended period of time.

What Tests Could Further Support This Diagnosis?

A series of pulmonary function tests (PFT) would be useful for assessing the patient’s lung volumes and capacities. This would help confirm the diagnosis of COPD and inform you of the severity.

Note: COPD patients typically have an FEV1/FVC ratio of < 70%, with an FEV1 that is < 80%.

The initial treatment for this patient should involve the administration of low-flow oxygen to treat or prevent hypoxemia .

It’s acceptable to start with a nasal cannula at 1-2 L/min. However, it’s often recommended to use an air-entrainment mask on COPD patients in order to provide an exact FiO2.

Either way, you should start with the lowest possible FiO2 that can maintain adequate oxygenation and titrate based on the patient’s response.

Example: Let’s say you start the patient with an FiO2 of 28% via air-entrainment mask but increase it to 32% due to no improvement. The SpO2 originally was 84% but now has decreased to 80%, and his retractions are worsening. This patient is sitting in the tripod position and continues to demonstrate pursed-lip breathing. Another blood gas was collected, and the results show a PaCO2 of 65 mmHg and a PaO2 of 59 mmHg.

What Do You Recommend?

The patient has an increased work of breathing, and their condition is clearly getting worse. The latest ABG results confirmed this with an increased PaCO2 and a PaO2 that is decreasing.

This indicates that the patient needs further assistance with both ventilation and oxygenation .

Note: In general, mechanical ventilation should be avoided in patients with COPD (if possible) because they are often difficult to wean from the machine.

Therefore, at this time, the most appropriate treatment method is noninvasive ventilation (e.g., BiPAP).

Initial BiPAP Settings

In general, the most commonly recommended initial BiPAP settings for an adult patient include this following:

• IPAP: 8–12 cmH2O
• EPAP: 5–8 cmH2O
• Rate: 10–12 breaths/min
• FiO2: Whatever they were previously on

For example, let’s say you initiate BiPAP with an IPAP of 10 cmH20, an EPAP of 5 cmH2O, a rate of 12, and an FiO2 of 32% (since that is what he was previously getting).

After 30 minutes on the machine, the physician requested another ABG to be drawn, which revealed acute respiratory acidosis with mild hypoxemia.

What Adjustments to BiPAP Settings Would You Recommend?

The latest ABG results indicate that two parameters must be corrected:

• Increased PaCO2
• Decreased PaO2

You can address the PaO2 by increasing either the FiO2 or EPAP setting. EPAP functions as PEEP, which is effective in increasing oxygenation.

The PaCO2 can be lowered by increasing the IPAP setting. By doing so, it helps to increase the patient’s tidal volume, which increased their expired CO2.

Note: In general, when making adjustments to a patient’s BiPAP settings, it’s acceptable to increase the pressure in increments of 2 cmH2O and the FiO2 setting in 5% increments.

Oxygenation

To improve the patient’s oxygenation , you can increase the EPAP setting to 7 cmH2O. This would decrease the pressure support by 2 cmH2O because it’s essentially the difference between the IPAP and EPAP.

Therefore, if you increase the EPAP, you must also increase the IPAP by the same amount to maintain the same pressure support level.

Ventilation

However, this patient also has an increased PaCO2 , which means that you must increase the IPAP setting to blow off more CO2. Therefore, you can adjust the pressure settings on the machine as follows:

• IPAP: 14 cmH2O
• EPAP: 7 cmH2O

After making these changes and performing an assessment , you can see that the patient’s condition is improving.

Two days later, the patient has been successfully weaned off the BiPAP machine and no longer needs oxygen support. He is now ready to be discharged.

The doctor wants you to recommend home therapy and treatment modalities that could benefit this patient.

What Home Therapy Would You Recommend?

You can recommend home oxygen therapy if the patient’s PaO2 drops below 55 mmHg or their SpO2 drops below 88% more than twice in a three-week period.

Remember: You must use a conservative approach when administering oxygen to a patient with COPD.

Pharmacology

You may also consider the following pharmacological agents:

• Short-acting bronchodilators (e.g., Albuterol)
• Long-acting bronchodilators (e.g., Formoterol)
• Anticholinergic agents (e.g., Ipratropium bromide)
• Inhaled corticosteroids (e.g., Budesonide)
• Methylxanthine agents (e.g., Theophylline)

In addition, education on smoking cessation is also important for patients who smoke. Nicotine replacement therapy may also be indicated.

In some cases, bronchial hygiene therapy should be recommended to help with secretion clearance (e.g., positive expiratory pressure (PEP) therapy).

It’s also important to instruct the patient to stay active, maintain a healthy diet, avoid infections, and get an annual flu vaccine. Lastly, some COPD patients may benefit from cardiopulmonary rehabilitation .

By taking all of these factors into consideration, you can better manage this patient’s COPD and improve their quality of life.

Final Thoughts

There are two key points to remember when treating a patient with COPD. First, you must always be mindful of the amount of oxygen being delivered to keep the FiO2 as low as possible.

Second, you should use noninvasive ventilation, if possible, before performing intubation and conventional mechanical ventilation . Too much oxygen can knock out the patient’s drive to breathe, and once intubated, these patients can be difficult to wean from the ventilator .

Furthermore, once the patient is ready to be discharged, you must ensure that you are sending them home with the proper medications and home treatments to avoid readmission.

Written by:

John Landry is a registered respiratory therapist from Memphis, TN, and has a bachelor's degree in kinesiology. He enjoys using evidence-based research to help others breathe easier and live a healthier life.

• Faarc, Kacmarek Robert PhD Rrt, et al. Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020.
• Chang, David. Clinical Application of Mechanical Ventilation . 4th ed., Cengage Learning, 2013.
• Rrt, Cairo J. PhD. Pilbeam’s Mechanical Ventilation: Physiological and Clinical Applications. 7th ed., Mosby, 2019.
• Faarc, Gardenhire Douglas EdD Rrt-Nps. Rau’s Respiratory Care Pharmacology. 10th ed., Mosby, 2019.
• Faarc, Heuer Al PhD Mba Rrt Rpft. Wilkins’ Clinical Assessment in Respiratory Care. 8th ed., Mosby, 2017.
• Rrt, Des Terry Jardins MEd, and Burton George Md Facp Fccp Faarc. Clinical Manifestations and Assessment of Respiratory Disease. 8th ed., Mosby, 2019.

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STEVE FORD, EDITOR

• You are here: COPD

Diagnosis and management of COPD: a case study

04 May, 2020

This case study explains the symptoms, causes, pathophysiology, diagnosis and management of chronic obstructive pulmonary disease

This article uses a case study to discuss the symptoms, causes and management of chronic obstructive pulmonary disease, describing the patient’s associated pathophysiology. Diagnosis involves spirometry testing to measure the volume of air that can be exhaled; it is often performed after administering a short-acting beta-agonist. Management of chronic obstructive pulmonary disease involves lifestyle interventions – vaccinations, smoking cessation and pulmonary rehabilitation – pharmacological interventions and self-management.

Citation: Price D, Williams N (2020) Diagnosis and management of COPD: a case study. Nursing Times [online]; 116: 6, 36-38.

Authors: Debbie Price is lead practice nurse, Llandrindod Wells Medical Practice; Nikki Williams is associate professor of respiratory and sleep physiology, Swansea University.

• This article has been double-blind peer reviewed
• Scroll down to read the article or download a print-friendly PDF here (if the PDF fails to fully download please try again using a different browser)

Introduction

The term chronic obstructive pulmonary disease (COPD) is used to describe a number of conditions, including chronic bronchitis and emphysema. Although common, preventable and treatable, COPD was projected to become the third leading cause of death globally by 2020 (Lozano et al, 2012). In the UK in 2012, approximately 30,000 people died of COPD – 5.3% of the total number of deaths. By 2016, information published by the World Health Organization indicated that Lozano et al (2012)’s projection had already come true.

People with COPD experience persistent respiratory symptoms and airflow limitation that can be due to airway or alveolar abnormalities, caused by significant exposure to noxious particles or gases, commonly from tobacco smoking. The projected level of disease burden poses a major public-health challenge and primary care nurses can be pivotal in the early identification, assessment and management of COPD (Hooper et al, 2012).

Grace Parker (the patient’s name has been changed) attends a nurse-led COPD clinic for routine reviews. A widowed, 60-year-old, retired post office clerk, her main complaint is breathlessness after moderate exertion. She scored 3 on the modified Medical Research Council (mMRC) scale (Fletcher et al, 1959), indicating she is unable to walk more than 100 yards without stopping due to breathlessness. Ms Parker also has a cough that produces yellow sputum (particularly in the mornings) and an intermittent wheeze. Her symptoms have worsened over the last six months. She feels anxious leaving the house alone because of her breathlessness and reduced exercise tolerance, and scored 26 on the COPD Assessment Test (CAT, catestonline.org), indicating a high level of impact.

Ms Parker smokes 10 cigarettes a day and has a pack-year score of 29. She has not experienced any haemoptysis (coughing up blood) or chest pain, and her weight is stable; a body mass index of 40kg/m 2 means she is classified as obese. She has had three exacerbations of COPD in the previous 12 months, each managed in the community with antibiotics, steroids and salbutamol.

Ms Parker was diagnosed with COPD five years ago. Using Epstein et al’s (2008) guidelines, a nurse took a history from her, which provided 80% of the information needed for a COPD diagnosis; it was then confirmed following spirometry testing as per National Institute for Health and Care Excellence (2018) guidance.

The nurse used the Calgary-Cambridge consultation model, as it combines the pathological description of COPD with the patient’s subjective experience of the illness (Silverman et al, 2013). Effective communication skills are essential in building a trusting therapeutic relationship, as the quality of the relationship between Ms Parker and the nurse will have a direct impact on the effectiveness of clinical outcomes (Fawcett and Rhynas, 2012).

In a national clinical audit report, Baxter et al (2016) identified inaccurate history taking and inadequately performed spirometry as important factors in the inaccurate diagnosis of COPD on general practice COPD registers; only 52.1% of patients included in the report had received quality-assured spirometry.

Pathophysiology of COPD

Knowing the pathophysiology of COPD allowed the nurse to recognise and understand the physical symptoms and provide effective care (Mitchell, 2015). Continued exposure to tobacco smoke is the likely cause of the damage to Ms Parker’s small airways, causing her cough and increased sputum production. She could also have chronic inflammation, resulting in airway smooth-muscle contraction, sluggish ciliary movement, hypertrophy and hyperplasia of mucus-secreting goblet cells, as well as release of inflammatory mediators (Mitchell, 2015).

Ms Parker may also have emphysema, which leads to damaged parenchyma (alveoli and structures involved in gas exchange) and loss of alveolar attachments (elastic connective fibres). This causes gas trapping, dynamic hyperinflation, decreased expiratory flow rates and airway collapse, particularly during expiration (Kaufman, 2013). Ms Parker also displayed pursed-lip breathing; this is a technique used to lengthen the expiratory time and improve gaseous exchange, and is a sign of dynamic hyperinflation (Douglas et al, 2013).

In a healthy lung, the destruction and repair of alveolar tissue depends on proteases and antiproteases, mainly released by neutrophils and macrophages. Inhaling cigarette smoke disrupts the usually delicately balanced activity of these enzymes, resulting in the parenchymal damage and small airways (with a lumen of <2mm in diameter) airways disease that is characteristic of emphysema. The severity of parenchymal damage or small airways disease varies, with no pattern related to disease progression (Global Initiative for Chronic Obstructive Lung Disease, 2018).

Ms Parker also had a wheeze, heard through a stethoscope as a continuous whistling sound, which arises from turbulent airflow through constricted airway smooth muscle, a process noted by Mitchell (2015). The wheeze, her 29 pack-year score, exertional breathlessness, cough, sputum production and tiredness, and the findings from her physical examination, were consistent with a diagnosis of COPD (GOLD, 2018; NICE, 2018).

Spirometry is a tool used to identify airflow obstruction but does not identify the cause. Commonly measured parameters are:

• Forced expiratory volume – the volume of air that can be exhaled – in one second (FEV1), starting from a maximal inspiration (in litres);
• Forced vital capacity (FVC) – the total volume of air that can be forcibly exhaled – at timed intervals, starting from a maximal inspiration (in litres).

Calculating the FEV1 as a percentage of the FVC gives the forced expiratory ratio (FEV1/FVC). This provides an index of airflow obstruction; the lower the ratio, the greater the degree of obstruction. In the absence of respiratory disease, FEV1 should be ≥70% of FVC. An FEV1/FVC of <70% is commonly used to denote airflow obstruction (Moore, 2012).

As they are time dependent, FEV1 and FEV1/FVC are reduced in diseases that cause airways to narrow and expiration to slow. FVC, however, is not time dependent: with enough expiratory time, a person can usually exhale to their full FVC. Lung function parameters vary depending on age, height, gender and ethnicity, so the degree of FEV1 and FVC impairment is calculated by comparing a person’s recorded values with predicted values. A recorded value of >80% of the predicted value has been considered ‘normal’ for spirometry parameters but the lower limit of normal – equal to the fifth percentile of a healthy, non-smoking population – based on more robust statistical models is increasingly being used (Cooper et al, 2017).

A reversibility test involves performing spirometry before and after administering a short-acting beta-agonist (SABA) such as salbutamol; the test is used to distinguish between reversible and fixed airflow obstruction. For symptomatic asthma, airflow obstruction due to airway smooth-muscle contraction is reversible: administering a SABA results in smooth-muscle relaxation and improved airflow (Lumb, 2016). However, COPD is associated with fixed airflow obstruction, resulting from neutrophil-driven inflammatory changes, excess mucus secretion and disrupted alveolar attachments, as opposed to airway smooth-muscle contraction.

Administering a SABA for COPD does not usually produce bronchodilation to the extent seen in someone with asthma: a person with asthma may demonstrate significant improvement in FEV1 (of >400ml) after having a SABA, but this may not change in someone with COPD (NICE, 2018). However, a negative response does not rule out therapeutic benefit from long-term SABA use (Marín et al, 2014).

NICE (2018) and GOLD (2018) guidelines advocate performing spirometry after administering a bronchodilator to diagnose COPD. Both suggest a FEV1/FVC of <70% in a person with respiratory symptoms supports a diagnosis of COPD, and both grade the severity of the condition using the predicted FEV1. Ms Parker’s spirometry results showed an FEV1/FVC of 56% and a predicted FEV1 of 57%, with no significant improvement in these values with a reversibility test.

GOLD (2018) guidance is widely accepted and used internationally. However, it was developed by medical practitioners with a medicalised approach, so there is potential for a bias towards pharmacological management of COPD. NICE (2018) guidance may be more useful for practice nurses, as it was developed by a multidisciplinary team using evidence from systematic reviews or meta-analyses of randomised controlled trials, providing a holistic approach. NICE guidance may be outdated on publication, but regular reviews are performed and published online.

NHS England (2016) holds a national register of all health professionals certified in spirometry. It was set up to raise spirometry standards across the country.

Assessment and management

The goals of assessing and managing Ms Parker’s COPD are to:

• Review and determine the level of airflow obstruction;
• Assess the disease’s impact on her life;
• Risk assess future disease progression and exacerbations;
• Recommend pharmacological and therapeutic management.

GOLD’s (2018) ABCD assessment tool (Fig 1) grades COPD severity using spirometry results, number of exacerbations, CAT score and mMRC score, and can be used to support evidence-based pharmacological management of COPD.

When Ms Parker was diagnosed, her predicted FEV1 of 57% categorised her as GOLD grade 2, and her mMRC score, CAT score and exacerbation history placed her in group D. The mMRC scale only measures breathlessness, but the CAT also assesses the impact COPD has on her life, meaning consecutive CAT scores can be compared, providing valuable information for follow-up and management (Zhao, et al, 2014).

After assessing the level of disease burden,  Ms Parker was then provided with education for self-management and lifestyle interventions.

Lifestyle interventions

Smoking cessation.

Cessation of smoking alongside support and pharmacotherapy is the second-most cost-effective intervention for COPD, when compared with most other pharmacological interventions (BTS and PCRS UK, 2012). Smoking cessation:

• Slows the progression of COPD;
• Improves lung function;
• Improves survival rates;
• Reduces the risk of lung cancer;
• Reduces the risk of coronary heart disease risk (Qureshi et al, 2014).

Ms Parker accepted a referral to an All Wales Smoking Cessation Service adviser based at her GP surgery. The adviser used the internationally accepted ‘five As’ approach:

• Ask – record the number of cigarettes the individual smokes per day or week, and the year they started smoking;
• Advise – urge them to quit. Advice should be clear and personalised;
• Assess – determine their willingness and confidence to attempt to quit. Note the state of change;
• Assist – help them to quit. Provide behavioural support and recommend or prescribe pharmacological aids. If they are not ready to quit, promote motivation for a future attempt;
• Arrange – book a follow-up appointment within one week or, if appropriate, refer them to a specialist cessation service for intensive support. Document the intervention.

NICE (2013) guidance recommends that this be used at every opportunity. Stead et al (2016) suggested that a combination of counselling and pharmacotherapy have proven to be the most effective strategy.

Pulmonary rehabilitation

Ms Parker’s positive response to smoking cessation provided an ideal opportunity to offer her pulmonary rehabilitation (PR)  – as indicated by Johnson et al (2014), changing one behaviour significantly increases a person’s chance of changing another.

PR – a supervised programme including exercise training, health education and breathing techniques – is an evidence-based, comprehensive, multidisciplinary intervention that:

• Improves exercise tolerance;
• Reduces dyspnoea;
• Promotes weight loss (Bolton et al, 2013).

These improvements often lead to an improved quality of life (Sciriha et al, 2015).

Most relevant for Ms Parker, PR has been shown to reduce anxiety and depression, which are linked to an increased risk of exacerbations and poorer health status (Miller and Davenport, 2015). People most at risk of future exacerbations are those who already experience them (Agusti et al, 2010), as in Ms Parker’s case. Patients who have frequent exacerbations have a lower quality of life, quicker progression of disease, reduced mobility and more-rapid decline in lung function than those who do not (Donaldson et al, 2002).

“COPD is a major public-health challenge; nurses can be pivotal in early identification, assessment and management”

Pharmacological interventions

Ms Parker has been prescribed inhaled salbutamol as required; this is a SABA that mediates the increase of cyclic adenosine monophosphate in airway smooth-muscle cells, leading to muscle relaxation and bronchodilation. SABAs facilitate lung emptying by dilatating the small airways, reversing dynamic hyperinflation of the lungs (Thomas et al, 2013). Ms Parker also uses a long-acting muscarinic antagonist (LAMA) inhaler, which works by blocking the bronchoconstrictor effects of acetylcholine on M3 muscarinic receptors in airway smooth muscle; release of acetylcholine by the parasympathetic nerves in the airways results in increased airway tone with reduced diameter.

At a routine review, Ms Parker admitted to only using the SABA and LAMA inhalers, despite also being prescribed a combined inhaled corticosteroid and long-acting beta 2 -agonist (ICS/LABA) inhaler. She was unaware that ICS/LABA inhalers are preferred over SABA inhalers, as they:

• Last for 12 hours;
• Improve the symptoms of breathlessness;
• Increase exercise tolerance;
• Can reduce the frequency of exacerbations (Agusti et al, 2010).

However, moderate-quality evidence shows that ICS/LABA combinations, particularly fluticasone, cause an increased risk of pneumonia (Suissa et al, 2013; Nannini et al, 2007). Inhaler choice should, therefore, be individualised, based on symptoms, delivery technique, patient education and compliance.

It is essential to teach and assess inhaler technique at every review (NICE, 2011). Ms Parker uses both a metered-dose inhaler and a dry-powder inhaler; an in-check device is used to assess her inspiratory effort, as different inhaler types require different inhalation speeds. Braido et al (2016) estimated that 50% of patients have poor inhaler technique, which may be due to health professionals lacking the confidence and capability to teach and assess their use.

Patients may also not have the dexterity, capacity to learn or vision required to use the inhaler. Online resources are available from, for example, RightBreathe (rightbreathe.com), British Lung Foundation (blf.org.uk). Ms Parker’s adherence could be improved through once-daily inhalers, as indicated by results from a study by Lipson et al (2017). Any change in her inhaler would be monitored as per local policy.

Vaccinations

Ms Parker keeps up to date with her seasonal influenza and pneumococcus vaccinations. This is in line with the low-cost, highest-benefit strategy identified by the British Thoracic Society and Primary Care Respiratory Society UK’s (2012) study, which was conducted to inform interventions for patients with COPD and their relative quality-adjusted life years. Influenza vaccinations have been shown to decrease the risk of lower respiratory tract infections and concurrent COPD exacerbations (Walters et al, 2017; Department of Health, 2011; Poole et al, 2006).

Self-management

Ms Parker was given a self-management plan that included:

• Information on how to monitor her symptoms;
• A rescue pack of antibiotics, steroids and salbutamol;
• A traffic-light system demonstrating when, and how, to commence treatment or seek medical help.

Self-management plans and rescue packs have been shown to reduce symptoms of an exacerbation (Baxter et al, 2016), allowing patients to be cared for in the community rather than in a hospital setting and increasing patient satisfaction (Fletcher and Dahl, 2013).

Improving Ms Parker’s adherence to once-daily inhalers and supporting her to self-manage and make the necessary lifestyle changes, should improve her symptoms and result in fewer exacerbations.

The earlier a diagnosis of COPD is made, the greater the chances of reducing lung damage through interventions such as smoking cessation, lifestyle modifications and treatment, if required (Price et al, 2011).

• Chronic obstructive pulmonary disease is a progressive respiratory condition, projected to become the third leading cause of death globally
• Diagnosis involves taking a patient history and performing spirometry testing
• Spirometry identifies airflow obstruction by measuring the volume of air that can be exhaled
• Chronic obstructive pulmonary disease is managed with lifestyle and pharmacological interventions, as well as self-management

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GOLD in Practice: Chronic Obstructive Pulmonary Disease Treatment and Management in the Primary Care Setting

Barbara p yawn.

1 Department of Family and Community Health, University of Minnesota, Minneapolis, MN, USA

2 COPD Foundation, Miami, FL, USA

Matthew L Mintz

3 Department of Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC, USA

Dennis E Doherty

4 Division of Pulmonary, Critical Care and Sleep Medicine, University of Kentucky, Lexington, KY, USA

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality. Early detection and appropriate treatment and management of COPD can lower morbidity and perhaps mortality. Clinicians in the primary care setting provide the majority of COPD care and are pivotal in the diagnosis and management of COPD. In this review, we provide an overview of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020 report, with a focus on the management of COPD in the primary care setting. We discuss the pathophysiology of COPD; describe COPD risk factors, signs, and symptoms that may facilitate earlier diagnosis of COPD; and reinforce the importance of spirometry use in establishing the diagnosis of COPD. Disease monitoring, as well as a review of the 2020 GOLD treatment recommendations, is also discussed. Patients and families are important partners in COPD management; therefore, we outline simple steps that may assist them in caring for those affected by COPD. Finally, we discuss nonpharmacological treatment options for COPD, COPD monitoring tools that may aid in the evaluation of disease progression and response to therapy, and the importance of developing a COPD action plan on an individualized basis.

Introduction

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality. COPD is the seventh leading cause of years of life lost globally, and lower respiratory disease is the fourth leading cause of death in the United States. 1 , 2 In the United States, the age-standardized COPD-related death rate was 39.1 deaths per 100,000 in 2014 (44.3 in men and 35.6 in women per 100,000). 3 COPD symptoms can be debilitating and prevent patients and their families from leading normal lives. Because of breathlessness, the level of daily physical activity is typically lower in patients with COPD than in healthy controls. 4 Additionally, patients with COPD often have comorbidities such as anxiety, depression, osteoporosis, and cardiovascular disease, 5 which further impact their overall health, quality of life (QoL), functional status, and clinical outcomes. COPD is also associated with substantial socioeconomic impact, with high direct and indirect costs—estimated at $36 billion annually—burdening the health care system. 6 Direct costs predominantly result from exacerbations leading to emergency department (ED) visits, hospital admissions and readmissions, and unscheduled office visits. 6 , 7 Clearly, COPD impacts not only patients but also the society as a whole and this impact can be reduced with early identification and appropriate treatment and management. 8 , 9

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) report includes recommended strategies for the diagnosis, treatment, and management of COPD. 5 The COPD Foundation (COPDF) also provides a brief, point-of-care pocket consultant guide that serves as a short summary to aid clinical decision-making during office, ED, or hospital visits. 10 In this review, we provide an overview of the GOLD 2020 report, with a focus on recommendations for the treatment and management of COPD in the primary care setting.

Pathophysiology of COPD

COPD results from chronic inflammation of the airways, which leads to thickening of airway walls, increased mucus production, and eventually permanent changes in lung structure 11 ( Figure 1 ). Lung changes may include the destruction of lung parenchyma including air sac (alveolar) walls, resulting in fibrosis of the small airways (emphysema) and loss of elasticity. 12 These structural changes may cause increased resistance to airflow, significant air trapping, and ultimately hyperinflation, all of which may manifest as breathlessness, cough, and increased phlegm production. 11

Pathophysiology of chronic obstructive pulmonary disease. During the time course of COPD, inflammation of the airways can lead to thickening of the airway walls, increased mucus production, and damage to alveoli and alveolar ducts that leads to enlargement of the air spaces/emphysema, and potentially to air-trapping. 11

Chronic lung inflammation in COPD is generally characterized by increased neutrophils, activated macrophages, and activated CD8 + T lymphocytes. 12 The predominant increase in types of inflammatory cells differs between COPD and asthma ( Table 1 ). 12 Macrophages facilitate the recruitment of other inflammatory cells (such as neutrophils) and the release of mediators and proteases, which may lead to emphysema. 13 A subset of COPD patients have predominant eosinophilic inflammation even in the absence of exacerbations. 14

Differences Between COPD and Asthma Pathophysiology and Symptoms

Notes: Adapted from Am J Med, 117(Suppl12A). Doherty DE. The pathophysiology of airway dysfunction, 11–23, Copyright (2004), with permission from Elsevier. 12

Abbreviations: COPD, chronic obstructive pulmonary disease; FEV 1 , forced expiratory volume in 1 second; HLA-DR + , human leukocyte antigen-DR; VLA-1 + , very late activation antigen-1.

Patients and families require accurate but simple explanations of COPD pathophysiology that can help them understand this chronic condition, its symptoms, and recommended pharmacological and nonpharmacological therapies. For example, when discussing dyspnea or shortness of breath, clinicians can explain that patients with even mild-to-moderate COPD can inhale a high volume of air (approaching total lung capacity). However, they may be able to exhale only a portion of the inhaled volume, resulting in air trapping and hyperinflation. 15 As patients breathe more rapidly (eg, during exercise), they have even shorter time for exhalation and, less and less “room” to breathe in (ie progressively increased end-expiratory lung volume and decreased inspiratory capacity), both of which enhance dyspnea or shortness of breath because of inability to “get air in.” This phenomenon can be illustrated by asking the patient to take a deep breath in, exhale only a small amount of the breath (air trapping), and then attempt to take in three quick breaths. The patient will experience acute dyspnea and discomfort, as they will have more difficulty with inhalation because of residual air in the lungs (ie hyperinflation). This maneuver mimics what happens with hyperinflation during rest (static hyperinflation) and also during increased activity (dynamic hyperinflation) when the respiratory rate is faster. 15 Exertion leaves less time to exhale and, consequently no room to let new air in. Common descriptors of air trapping, which are important to know to understand patients’ experiences and estimating disease severity, include “air hunger,” “unsatisfied” or “unrewarded” inhalation, “shallow breathing,” “suffocating,” and “cannot get a deep breath.” 15 , 16

Patient Presentation

Patients with COPD commonly present with dyspnea, chronic cough, and/or sputum production, and occasionally wheezing ( Table 1 ). 5 Unfortunately, delayed diagnosis is common and many patients present only after they have experienced ≥1 exacerbation, often mistakenly labeled as recurrent bronchitis. 17 Early diagnosis and treatment are essential to improve patients’ lung function, functional status, and QoL, and to reduce exacerbations. 18 COPD can be detected early on if the clinicians consider COPD as part of their differential diagnosis. For example, when a patient is >40 years old and has recurrent acute bronchitis or bad colds that last for weeks, COPD should be suspected even if the patient is a nonsmoker. Of note, women are less likely to be suspected of having or diagnosed with COPD than men with similar symptoms, 19 possibly because, COPD traditionally was considered a “male” disease. However, various factors, including smoking, have contributed to the rising prevalence of COPD in women. 20 Clinicians can also increase the likelihood of detecting COPD by asking targeted questions focused on respiratory symptoms (eg, changes in the ability to do activities or changes in lifestyle because of shortness of breath). Patients often attribute these symptoms to being “old, overweight, or out of shape”. Questions such as “Do you get or have you ever gotten short of breath when you climb a flight of stairs or walk up a hill?” are more specific and easier for patients to answer than a vague question such as “Do you get short of breath?” Useful tools that are available to identify and assess baseline symptomatology can be used to monitor changes in severity over time. The modified Medical Research Council (mMRC) dyspnea scale comprises five statements that describe a range of dyspnea effects in increasing order of severity. Use of this questionnaire is recommended in the GOLD 2020 report 5 ( Supplementary Table 1 ). Although this questionnaire may be helpful for the initial identification of breathlessness and support evaluation for COPD, 21 it is less useful for monitoring over time because moving from one grade to the next requires a very large change in functional abilities. Alternatively, the COPD Assessment Test (CAT), comprising eight items that are each scored using a 6-point scale (0–5), is useful in assessing the symptomatic impact of COPD. A higher CAT score indicates poorer health. CAT is more sensitive in detecting improvements with treatment or a decline of disease progression or exacerbations ( Supplementary Figure 1 ). 5 , 22 Supplementary Videos 1 and 2 .

COPD Risk Factors

In addition to understanding patients’ symptoms, knowledge of COPD risk factors is important. As major risk factors for COPD, current and past smoking history must be assessed. 5 Nonsmokers exposed to second-hand smoke in childhood and adult years are also at an increased risk of developing COPD. 23 Cigarette smoking was rated as the cause of COPD in 50%–70% of patients in developed countries. 24 Genetics also contributes to the risk of developing COPD. In a meta-analysis of genome-wide association studies, several genetic loci were associated with COPD pathophysiology. 25 Serine protease α1-antitrypsin deficiency, found in 1%–3% of patients with COPD, is the most widely reported genetic factor that increases COPD risk. 26 Other COPD risk factors include occupational exposure (eg, to dust, vapors, organic materials, fumes, and chemicals), indoor and outdoor air pollutants (including biomass fuels), and aging. 5

Diagnosis begins with clinical suspicion, usually in patients who report shortness of breath with activity. Overall, symptomatic, at-risk individuals who require spirometry and evaluation for COPD include those with recurring respiratory events (eg, acute bronchitis, bad colds, chronic cough, and excess sputum production), history of risk factors, decrease in activities because of dyspnea, and/or a family history of COPD. 5

Spirometry is essential and required to confirm a COPD diagnosis. 5 It also is useful for tracking treatment response, potentially adjusting medications, and monitoring disease progression. When rapid disease progression is identified, further evaluation and referral to a lung specialist are indicated. 5 A postbronchodilator (10–15 minutes after 2–4 puffs of a short-acting bronchodilator) forced expiratory volume in 1 second (FEV 1 ) to forced vital capacity (FVC) ratio of <0.70 confirms the presence of persistent or fixed airflow limitation. FVC is the maximal volume of air that can be forcibly exhaled after taking in the deepest breath possible, and FEV 1 is the maximal volume of air exhaled in the first second during an FVC maneuver ( Figure 2 ). 5

Diagnosis, assessment, initial, and follow-up treatment of COPD.

Despite recommendations, spirometry is not regularly used in clinical practice. 27 Underuse of spirometry in primary care settings is attributed to uncertainty about the benefit of COPD diagnosis, lack of time and resources, unfamiliarity with the technique, and/or difficulty in interpreting results. 28 , 29 However, spirometry is required to confirm a COPD diagnosis, can be performed in primary care practice using an office-based system, 30 and is a billable procedure reimbursed by payors. Although patients can be referred to specialists and hospitals for spirometry, follow-through may be limited; therefore, spirometry can and should be done in primary care offices. 31

Assessment of Airflow Limitation Severity, Symptoms, and Exacerbation Frequency

Once a COPD diagnosis is confirmed, spirometry findings can also be used to determine the severity of airflow limitations ( Figure 2 ), which is based on the patient’s FEV 1 relative to normal values. 5 However, treatment decisions are based on symptoms and history of exacerbations treated at home and in the hospital. Per the GOLD 2019 report, symptom burden and exacerbation frequency in the prior year are used to categorize patients into GOLD group A (few symptoms and 0–1 exacerbations not leading to hospitalization), group B (more symptoms and 0–1 exacerbations not leading to hospitalization), group C (few symptoms but ≥2 exacerbations or ≥1 exacerbation leading to hospitalization), or group D (more symptoms and ≥2 exacerbations or ≥1 exacerbation leading to hospitalization) to guide initial pharmacological therapy ( Figure 2 ). 5

Treatment of COPD

After categorizing a patient as belonging to GOLD group A, B, C, or D, the GOLD treatment algorithm ( Figure 2 ) can be used to determine appropriate initial pharmacological treatment, which should be complemented with nonpharmacological approaches as appropriate.

Pharmacological Interventions

Bronchodilators—the first-choice pharmacotherapy for COPD across all patient groups—increase airway diameter and decrease air trapping, thereby improving airflow and reducing dyspnea. 5 GOLD group A patients should be offered a bronchodilator (short- or long-acting), if symptoms are present. A long-acting muscarinic antagonist (LAMA) or a long-acting β 2 -agonist (LABA) is suggested as initial treatment for GOLD group B patients, and—because of their complementary mechanisms of action—dual bronchodilator therapy with a LAMA and a LABA can be considered for highly symptomatic (CAT score ≥20) patients. LAMA monotherapy improves lung function and reduces exacerbations and is suggested for initial pharmacological treatment in GOLD group C ( Figure 2 ). While initial therapy with LAMA is recommended for group GOLD group D patients, starting with a LAMA+LABA combination may be more appropriate because many of these patients are highly symptomatic (eg, CAT >20). Although commonly used as monotherapy for asthma control, inhaled corticosteroids (ICS) are not approved worldwide for use as monotherapy in COPD patients of any severity. Long-term ICS use is associated with safety concerns such as an increased risk of pneumonia, active tuberculosis, and osteoporosis. 32 However, LABA+ICS may be the first-choice treatment in COPD GOLD group D patients with a history of asthma or blood eosinophil counts ≥300 cells/μL. 5 Once recommended initial therapy is implemented, patients should be reassessed for treatment response. According to recommendations in the GOLD 2020 report, if response to initial therapy is not appropriate, follow-up treatment based on the patients’ symptoms and exacerbations—and not on their initial GOLD group classification—should be provided ( Figure 2 ). Separate treatment algorithms are provided based on the need to treat dyspnea or prevent exacerbations.

For patients with persistent breathlessness or exercise limitation despite long-acting bronchodilator monotherapy, 5 step-up to a LAMA+LABA is recommended. If dual bronchodilator therapy does not improve symptoms, step down to monotherapy, or switching inhalers or molecules are recommended. When patients experience persistent breathlessness or exercise limitation despite LABA+ICS therapy, triple therapy with a LAMA+LABA+ICS may be considered. However, if ICS was inappropriately indicated to treat patients without a history of exacerbations, caused side effects, or did not yield any response, switching to a LAMA+LABA is recommended.

For patients who continue to experience exacerbations despite long-acting bronchodilator monotherapy, step-up to a LAMA+LABA or LABA+ICS (in patients with a history of hospitalizations for COPD exacerbations, with ≥2 moderate COPD exacerbations per year, eosinophil counts >300 cells/μL, or a history of asthma) is recommended. 5 For patients who continue to exacerbate despite maximal LAMA+LABA, triple therapy is recommended if eosinophil counts ≥100 cells/μL and roflumilast or azithromycin is recommended if eosinophil counts <100 cells/μL.

While ICS therapy has a role in COPD management, there may be a current over-use based on the GOLD 2020 treatment algorithms. 33 In 2019, some of the recommendations surrounding the use of ICS in GOLD were changed due to concerns of over-use of ICS, but these recommendations were revised in 2020 to reflect the importance of ICS in certain circumstances, such as hospitalization for exacerbation. Whether, when, and how non-recommended ICS treatment can be withdrawn safely should be considered, particularly in patients who had ICS initiated despite no or infrequent exacerbations, especially if they also have low eosinophil counts. In the INSTEAD trial, 34 non-exacerbating patients with moderate COPD were switched from salmeterol+fluticasone (a LABA+ICS) to indacaterol (a LABA) without a significant change in exacerbation rate. Patients in this trial were at low risk of exacerbations and should not have been prescribed ICS based on the GOLD 2020 treatment algorithm. Similarly, withdrawal of ICS did not increase exacerbation rates in the WISDOM 35 and SUNSET 36 trials, which included patients with severe/very severe and moderate-to-severe COPD, respectively.

To avoid potentially difficult decisions regarding stepping down treatment, ICS should be initiated only when recommended, and not in patients with no or infrequent exacerbations or in patients whose exacerbations can be controlled with dual bronchodilator therapy.

In addition to deciding on appropriate initial and maintenance medications, COPD clinicians should also consider which inhaler is optimal for each patient. Prescribing an inhaler based on patient characteristics and preferences, and training patients on correct inhaler use, will lead to better adherence. 5 During follow-up, inhaler technique and adherence should be assessed. If not optimal, switching to a different inhaler device may be considered. 5

Nonpharmacological Interventions

Pharmacological therapy for COPD should be complemented with nonpharmacological approaches, including behavioral therapies and pulmonary rehabilitation, as appropriate. Assessment of smoking history and initiation of a cessation program, if necessary, must be a part of all COPD patients’ treatment plans. Because relapses are common, smoking status and second-hand smoke exposure should be continually monitored over time. Reinforcement to remain a sustained quitter or encouragement to stop smoking should be given at each opportunity.

Other nonpharmacological approaches at diagnosis, based on GOLD 2020, include referring GOLD group A-D patients to pulmonary rehabilitation including exercise training, promoting physical activity, encouraging adherence to the prescribed medication, and prescribing vaccinations. 5 Recommendations for nonpharmacological management of COPD at diagnosis and during follow-up are summarized in Figure 3 . Teaching COPD patients breathing techniques aimed at improving respiratory muscle strength and decreasing air trapping in the lungs, which can reduce the sense of dyspnea is also beneficial. 5 Pursed-lip breathing, which reduces heightened air trapping by a mechanical maneuver, is a practical and simple technique that can be taught quickly and can make a substantial difference to patients ( Supplementary Figure 2 ). Pulmonary rehabilitation improves symptoms, reduces hospital readmissions, increases activity levels, and decreases levels of anxiety and depression. 5 , 37 Although programs can be difficult to implement in some areas, largely because of low reimbursement rates, pulmonary rehabilitation is one of the single best treatments for patients with COPD. 37 Exercise programs, disease education, and setting activity goals for patients can be helpful when pulmonary rehabilitation is not available. 5 Finally, ensuring that patients with COPD receive all indicated immunizations (eg, influenza, pneumococcal pneumonia, 5 Tdap, and Zoster) is important to overall patient care and may help to reduce exacerbations and other poor outcomes.

Nonpharmacological management of COPD at diagnosis and follow-up.

Referral to a pulmonologist may be considered at diagnosis, at discharge after hospitalization for an exacerbation, or when symptoms progressively deteriorate. 5

Chronic Disease Management

Chronic disease management involves regular evaluation to monitor disease progression and treatment response. For COPD, important aspects include monitoring symptom burden and exacerbation frequency, reviewing and observing device/inhaler technique, reviewing medication adherence, and updating any action plans. But, patient evaluation and treatment are a continuous process and cannot be accomplished in a single visit. A COPD action plan should be developed and individualized for each patient; however, development is often not logical or feasible until the second or third visit. The COPDF action plan, 38 which was designed to improve communication between clinicians and patients with COPD, and to encourage disease self-management, should be considered ( Supplementary Figure 3 ). Further, while these regular evaluations are essential to achieve optimal treatment outcomes, evidence indicates clinicians and patients do not necessarily appreciate their importance. For example, according to results of quantitative, web-based, descriptive, cross-sectional surveys of clinicians and patients with COPD in the United States, both groups had limited concerns about proper device use. 39 Less than half of the clinicians surveyed reported assessing device technique in every newly diagnosed patient, and many reported not routinely assessing and inconsistently educating about proper device use. Not surprisingly, incorrect inhaler use led to poor clinical outcomes.

Patient education is important in ensuring successful disease management and optimal medication adherence and compliance. Regular demonstrations and direct observations of patients’ use of their medication delivery systems should be done at each visit to ensure proper use. In addition, patients should be reminded that although serious, COPD symptom burden and progression may be modifiable with treatment and behavioral changes.

As mentioned, an important aspect of patient education is smoking cessation. 40 Motivating current smokers with COPD to quit may be particularly challenging because they continue to smoke despite disease symptoms. “Lung age” may be a useful tool to demonstrate the effects of cigarette smoking and is known to increase smoking cessation rates. 40 In addition, spirometry curves ( Figure 4 ) are helpful in demonstrating that quitting smoking even at a late age can reduce morbidity and mortality. 40–42

Effects of smoking on COPD risk and lung age.

Ensuring continuity of care over time is central to chronic disease management programs, including those for COPD. During repeated visits, clinicians must confirm that patients are prescribed and are taking appropriate COPD maintenance therapy, addressing smoking cessation, offered support for an increased activity or pulmonary rehabilitation, and considered as candidates for palliative (not just end-of-life) care. All of these activities are especially important following any hospital admission for an exacerbation.

Conclusions

COPD is a leading cause of morbidity and mortality in the United States. Because most patients with COPD are managed in the primary care setting, primary care clinicians play a pivotal role in appropriately managing COPD. Following up-to-date treatment recommendations such as those provided in the GOLD 2020 strategy report, engaging in chronic disease management, and investing in patient education are important to achieve the greatest benefits of COPD treatment.

Acknowledgments

The authors meet the criteria for authorship as recommended by the International Committee of Medical Journal Editors. The authors received no direct compensation related to the development of the manuscript. Writing, editorial support, and formatting assistance were provided by Suchita Nath-Sain, PhD, Michelle Rebello, PhD, and Maribeth Bogush, PhD, of Cactus Life Sciences (part of Cactus Communications), which was contracted and compensated by Boehringer Ingelheim Pharmaceuticals, Inc. (BIPI) for these services. BIPI was given the opportunity to review the manuscript for medical and scientific accuracy, as well as intellectual property considerations.

Funding Statement

Writing, editorial support, and formatting service for this review was funded by Boehringer Ingelheim Pharmaceuticals, Inc.

Abbreviations

CAT, COPD Assessment Test; CD, Cluster differentiation; COPD, Chronic Obstructive Pulmonary Disease; COPDF, Chronic Obstructive Pulmonary Disease foundation; ED, Emergency department; FEV 1 , Forced expiratory volume in 1 second; FVC, Forced vital capacity; GOLD, Global Initiative for Chronic Obstructive Lung Disease; ICS, Inhaled corticosteroids; LABA, Long-acting β 2 -agonist; LAMA, Long-acting muscarinic antagonist; mMRC, modified Medical Research Council; QoL, Quality of life; Tdap, Tetanus, diphtheria, and pertussis combination vaccine.

Author Contributions

All authors made a significant contribution to the conception and interpretation of the article; took part in critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

BPY served on advisory boards for Boehringer Ingelheim, AstraZeneca, TEVA, and GlaxoSmithKline (GSK) and received consulting fees from GSK related to COPD; and received grants from the COPD Foundation, Boehringer Ingelheim, and National Heart, Lung, and Blood Institute (NHLBI), outside the submitted work. MLM received speaking and consulting fees from GSK, Mylan, and Boehringer Ingelheim, outside the submitted work. DED served on advisory boards and received speaker fees from AstraZeneca and Boehringer Ingelheim and received grants from Boehringer Ingelheim and NHLBI outside of the submitted work. The authors report no other conflicts of interest in this work.

Acute exacerbation of chronic obstructive pulmonary disease

• Overview  
• Theory  
• Diagnosis  
• Management  
• Follow up  
• Resources  

When viewing this topic in a different language, you may notice some differences in the way the content is structured, but it still reflects the latest evidence-based guidance.

Acute exacerbation of chronic obstructive pulmonary disease (COPD) typically presents with an increased level of dyspnoea, worsening of chronic cough, and/or an increase in the volume and/or purulence of the sputum produced.

May represent the first presentation of COPD, usually associated with a history of tobacco exposure.

Treatment includes bronchodilators, systemic corticosteroids, and antibiotics.

Antibiotics may be reserved for exacerbations thought to be due to bacteria. An acute change in the volume and colour of sputum produced is suggestive of a bacterial trigger.

COPD is a heterogeneous lung condition. COPD is characterised by chronic respiratory symptoms (dyspnoea, cough, sputum production, and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction. [1] Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: 2023 report. 2023 [internet publication]. https://goldcopd.org/2023-gold-report-2

An exacerbation of COPD may be defined as an event characterised by increased dyspnoea and/or cough and sputum that worsens in <14 days and may be accompanied by tachypnoea and/or tachycardia. An acute exacerbation of COPD is often associated with increased local and systemic inflammation caused by infections, pollution, or other insult to the airway. [1] Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: 2023 report. 2023 [internet publication]. https://goldcopd.org/2023-gold-report-2

Typically, COPD exacerbations are characterised by a worsening of airflow obstruction over and above baseline measurements, related to increased airway wall inflammation, mucus production, and/or bronchoconstriction. Several conditions including pneumonia, pulmonary embolus, and congestive heart failure can also worsen respiratory symptoms in patients with COPD; these must be differentiated from an acute exacerbation of COPD.

History and exam

Key diagnostic factors.

• increased sputum purulence and volume
• chest tightness/chest pain
• tachycardia
• risk factors
• cor pulmonale

Other diagnostic factors

• signs of respiratory failure
• gastro-oesophageal reflux and/or swallowing dysfunction

Risk factors

• bacterial infection
• viral infection
• atypical bacterial infection
• change in weather

Diagnostic investigations

1st investigations to order.

• arterial blood gas (in hospital)
• pulse oximetry (in hospital and in the community)
• ECG (in hospital and in the community if available)
• FBC with platelets (in hospital)
• urea, electrolytes, and creatinine (in hospital)
• CRP (in hospital)
• CXR (in hospital)
• sputum microscopy, culture, and Gram stain (in hospital)
• vitamin D (in hospital or in the community)

Investigations to consider

• blood cultures
• respiratory virus diagnostics
• cardiac troponin
• serum theophylline level
• pro-brain natriuretic peptide (BNP)
• CT scan of chest

Emerging tests

• procalcitonin
• point-of-care CRP
• eosinophil count

Treatment algorithm

On presentation, after stabilisation, contributors, expert advisers, jonathan bennett, md.

Honorary Professor of Respiratory Sciences

University of Leicester

Respiratory Consultant

Glenfield Hospital

JB is Chair of the British Thoracic Society (BTS). He is also deputy medical director RCP Invited service Reviews, and speaker at National Society (eg., BTS), Primary Care respiratory Society, Society Cardiothoracic Surgeons meetings.

Disclosures

JB declares that he has no competing interests.

Richard Russell

Specialty Registrar in Respiratory Medicine

RJR received sponsorship from AstraZeneca to attend a conference, May 2018 (covering travel, accommodation, and conference fee).

Acknowledgements

BMJ Best Practice would like to gratefully acknowledge the previous team of expert contributors, whose work has been retained in parts of the content:

Carolyn L. Rochester MD

Associate Professor

Yale University School of Medicine

VA Connecticut Healthcare System

Richard A. Martinello MD

Veterans Health Administration

Office of Public Health

CLR serves on the COPD scientific advisory board for GlaxoSmithKline Pharmaceuticals but has no competing interests pertaining to this publication. RAM declares that he has no competing interests.

Peer reviewers

Carlos echevarria.

Consultant Respiratory Physician

Royal Victoria Infirmary

Newcastle upon Tyne

CE declares that he has no competing interests.

Emma Quigley

Section Editor, BMJ Best Practice

EQ declares that she has no competing interests.

Tannaz Aliabadi-Oglesby

Lead Section Editor, BMJ Best Practice

TAO declares that she has no competing interests.

Julie Costello

Comorbidities Editor, BMJ Best Practice

JC declares that she has no competing interests.

Adam Mitchell

Drug Editor, BMJ Best Practice

AM declares that he has no competing interests.

Expert advisers: comorbidities

Martyn patel, bmbch, frcp, ma.

Consultant, Older People's Medicine

Norfolk and Norwich University Hospitals

NHS Foundation Trust

MP is a contributor to the Oxford Textbook of Otolaryngology, Oxford University Press, 2021, having written a chapter about mental capacity law, for which he received no fee. MP is the NHS representative on the board for Norwich Institute for Healthy Ageing (unpaid role). MP has spoken at the International Forum on Quality and Safety in Healthcare, virtual conference in November 2020 for which he received no fee.

Paul Cockwell, PhD, FRCP

Consultant Nephrologist

Queen Elizabeth Hospital Birmingham

Professor of Nephrology (honorary)

University of Birmingham

PC is president of UK Kidney Association (UKKA), which is the professional organisation that supports healthcare professionals involved in care for, and research, innovation and education in, kidney disease. UKKA has a broad remit with relationships with multiple partners and includes responsibility for UK Kidney Week, the major educational meeting for UK kidney professionals. PC holds grant funding from Kidney Research UK in areas related to chronic kidney disease, and has recently (within the last 3 years) held grants from the EU, NIHR, and MRC in research in areas related to chronic kidney disease. PC has a non-remunerated research partnership with Boehringer Ingelheim into the epidemiology of chronic kidney disease. PC is author of the BMJ Learning module on chronic kidney disease.

Rajiv Sankaranarayanan, MBBS, FRCP (Lon), FESC, FHFA, PhD

Consultant Cardiologist and Heart Failure Lead

Liverpool University Hospitals NHS Foundation Trust

Liverpool Centre for Cardiovascular Science and NIHR Research Scholar and Honorary Senior Clinical Lecturer

University of Liverpool

RS has research grants from the British Heart Foundation, the NIHR, NHSX (Transformation Agency), AstraZeneca, Biotronik, and the University of Liverpool. RS has received speaker fees/honoraria and travel reimbursement for conferences from AstraZeneca, Novartis, Vifor, Medtronic, Biotronik, Pfizer, Daaichi Sankyo, and Boehringer. RS has been appointed to: NHS England PIFU Pathway Committee for Heart Failure (2021); British Society for Heart Failure Digital Pathway, Discharge and Virtual Ward Pathway panels; British Cardiac Society Digital and Communications Committee (2020); NIHR Research Scholar (Feb 2020); Clinical Advisory Board of UK’s patient-led charity Pumping Marvellous (2020); and NHS England HF Virtual Ward committee.

Rachael Evans, MBChB, FRCP (UK), PhD

Associate Professor (Clinical)

Honorary Consultant Respiratory Physician

RAE has given lectures for non-promotional industry-led sessions on long COVID and provided consultancy for GSK, AstraZeneca, Boehringer, and Chiesi, for individual payment and travel expenses totalling <£4000.

Gerry Rayman, MD, FRCP

Consultant Physician and Head of Service

Diabetes and Endocrine Centre and the Diabetes Research Unit

Ipswich Hospitals NHS Trust

GR received funding from Novo Nordisk in 2022 to attend the EASD conference. GR undertakes several research projects on behalf of East Suffolk and North Essex NHS Foundation Trust for pharmaceutical companies which are on the NIHR portfolio (he does not receive payment himself for these). GR has received lecture fees from Abbott Diabetes UK and Lilly UK.

Sotiris Posporelis, MD, MRCPsych

Consultant Liaison Neuropsychiatrist

King’s College Hospital

South London and Maudsley NHS Foundation Trust

Honorary Senior Clinical Lecturer

Institute of Psychiatry, Psychology & Neuroscience

King’s College London

SP declares that he has no competing interests.

Asangaedem Akpan, MPH, FRCP

Consultant Geriatrician

Bunbury Regional Hospital

Western Australia Country Health Service

Western Australia

Visiting Professor

University of Cumbria

Honorary Clinical Associate Professor

AA has a limited company that is seeking consultancy work offering reviews of healthcare services, facilitation of workshops, advice/review of publications. AA has received honorariums for giving lectures on behalf of Profile Pharma in 2021. AA was invited to be on a panel at the British Society for Heart Failure conference in 2022 with all expenses paid and has been invited to contribute to the European Union geriatric medicine conference (free conference registration) and British Society for Heart Failure conference (accommodation and travel expenses covered) in 2022. AA sat on the National Institute for Health and Care Excellence Quality Standards Committee on urinary tract infections in adults as an expert committee member in 2022 and is Deputy Chair of the British Geriatrics Society England Council and Ageing Specialty Research Lead CRN NWC. AA has received research funding from the Liverpool CCG and Applied Research Collaborative 2021-2022. AA contributed to developing a heart failure pathway tool for the British Society for Heart Failure in 2022. AA sits on advisory committees for the following research studies - VOICE2 (development and testing of communication skills training for hospital healthcare practitioners caring for people living with dementia), SWOP (social work in older people), and CFIN (cognitive frailty interdisciplinary network) 2022 -2023.

Acknowledgement: Professor Sanjay Agrawal

BMJ Best Practice would like to gratefully acknowledge Professor Sanjay Agrawal, National Speciality Advisor for tobacco dependency at NHS England and Chair of Royal College of Physicians tobacco advisory group, for his advice on the comorbidity content for 'current smoker'.

Professor Sanjay Agrawal, MBChB, FRCP

Consultant in Respiratory and Intensive Care Medicine

University Hospitals of Leicester NHS Trust

SA declares that he has no competing interests.

Acknowledgement: Dr Hamish McAuley

BMJ Best Practice would like to gratefully acknowledge Dr Hamish McAuley for his previous involvement in the creation of comorbidity content relevant to asthma and COPD.

Hamish McAuley, MBBS, BSc, MRCP

Clinical Research Fellow

Specialist Registrar (ST5)

Respiratory Biomedical Research Unit

HM declares that he has no competing interests.

Peer reviewers: comorbidities

Add your patient's comorbidities for tailored treatment recommendations

If your patient is pregnant or a child, do not select comorbidities using this tool. Use the standard algorithm and seek specialist advice on comorbidities.

• Chronic kidney disease (CKD)
• Hypertension
• Coronary artery disease
• Heart failure

If your patient has both Asthma and COPD, select the predominant condition and tailor your management to the individual.

other considerations

• Suspected frailty
• Tobacco dependence

Differentials

• Coronavirus disease 2019 (COVID-19)
• Acute exacerbation of asthma
• Congestive heart failure
• Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: 2023 report
• Chronic obstructive pulmonary disease in over 16s: diagnosis and management

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BAP-65 prediction of in-hospital mortality and need for mechanical ventilation in COPD Opens in new window

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COPD: what is it?

COPD: what treatments work?

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Pathophysiology and Clinical Presentation

The lungs are the main organ of the respiratory system. Their main function is to assist in the exchange of oxygen and carbon dioxide using the air that we inhale (McCance & Huether, 2019). The right lung has three lobes and the left lung has two lobes. The pulmonary artery brings deoxygenated blood to the capillaries that form respiratory membranes with the alveoli (McCance & Huether, 2019). The alveoli will perform gas exchange, and then the pulmonary veins will return the now oxygenated blood back to the heart so that it can be sent throughout the body (McCance & Huether, 2019). Around the lungs is the pleura which is made up of two layers, the visceral and parietal pleural layers. Between these two layers there is a small amount of pleural fluid that works as a lubricant to prevent any friction, as well as an adhesive to bring the lungs to the thoracic wall so that it can assist in the movement of lungs with every breath (McCance & Huether, 2019). With normal lung function, the alveoli in the lungs have strong elastic walls that allow air to expand and contract the little sacs. The bronchioles are nice and clear and allow air to flow in and out of them smoothly (McCance & Huether, 2019). This is normal lung function. 

COPD is Chronic Obstructive Pulmonary Disease. This is a lung disease that is obstructive in nature, irreversible, and can get worse over time (McCance & Huether, 2019). COPD is a common disease that is preventable. There are two main conditions that cause COPD. One is emphysema , and the other is chronic bronchitis . In some situations, you may find a genetic susceptibility such as in the case of alpha-1 antitrypsin deficiency (McCance & Huether, 2019).  COPD is the third leading cause of death in the United States and the sixth leading cause of death worldwide (McCance & Huether, 2019).

COPD happens when the lungs are exposed to harmful particles and gases which cause the lungs to have an abnormal inflammatory response (McCance & Huether, 2019). The most common harmful cause is cigarette smoking. COPD can also occur from exposure to occupational dusts and chemicals, indoor air pollution (such as fuels used for cooking and heating), outdoor air pollution, any factor involved in lung growth during gestation and childhood, and genetic susceptibilities such as a mutation in the alpha-1 antitrypsin gene (McCance & Huether, 2019). In both chronic bronchitis and emphysema you will see involvement of neutrophils, macrophages, and lymphocytes to the lungs, which will lead to inflammation, oxidative stress, extracellular matrix proteolysis, and apoptotic and autophagic cell death, all of which cause progressive damage (McCance & Huether, 2019). 

Chronic bronchitis is one type of COPD. In chronic bronchitis, patients exhibit a chronic productive cough and experience excess mucus build up that leads to irritation and mucus throughout the large and small airways of the lungs (McCance & Huether, 2019). The lining within the airways becomes swollen and irritated and the cilia function becomes impaired, making it harder to breathe. This happens for at least three months of the year and for at least two years in a row. These patients will end up with a ventilation-perfusion mismatch with hypoxemia (Department of Pulmonary Rehab, 2009). 

Imagine retrieved from mayoclinic.org

Emphysema is a second type of COPD. It is a disease of the alveoli. In emphysema, there is irritation to the alveoli in the lungs which eventually leads to damage and a reduction of air exchange in the lungs (McCance & Huether, 2019).  This makes it hard for the patient to be able to move oxygen into the blood or take carbon dioxide out of the blood. Patients with emphysema will have permanent enlargement of the gas-exchange airways as well as damage to the walls of the alveoli (McCance & Huether, 2019). They lose their normal elasticity that allowed them to expand and contract, letting air in and out as with normal, healthy alveoli (Department of Pulmonary Rehab, 2009). 

Clinical Presentation:

Often with COPD, patients you will see some combination of both presentations seen in chronic bronchitis and emphysema. 

In review, COPD causes the flow of air out of the lungs to be blocked. The air is therefore trapped in the lungs, making it hard for the lungs to send the right amount of oxygen to the rest of the body (McCance & Huether, 2019). Patients can breathe air in, but getting air out is a challenge. Often, these patients will present with coughing (which can be productive or nonproductive), wheezing, shortness of breath that gets worse with exertion, and feelings of tightness in the chest (Department of Pulmonary Rehab, 2009). 

The main causes of COPD are smoking, exposure to secondhand smoke, and working in environments where you are breathing in toxic dusts, fumes or gases (McCance & Huether, 2019).

Patients with COPD need to understand that this disease is chronic, obstructive in nature, and progressive over time. This means that they cannot reverse the disease, but they can stop it in its tracks and keep it from getting worse. One of the best ways to do this is to stop smoking if the patient is a smoker (Department of Pulmonary Rehab, 2009). 

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