Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by lung airflow limitation and can be from exposure to harmful substances. It is a common cause of death worldwide. To avoid the high morbidity and mortality associated with COPD, it must be diagnosed and treated appropriately and promptly.

COPD is a preventable and treatable slowly progressive respiratory disease of airflow obstruction involving the airways, pulmonary parenchyma, or both. The parenchyma includes any form of lung tissue, including bronchioles, bronchi, blood vessels, interstitium, and alveoli. The airflow limitation or obstruction in COPD is not fully reversible. Clients typically have symptoms of chronic bronchitis and emphysema, but the classic triad also includes asthma or a combination of the above.


COPD is caused by prolonged exposure to harmful particles or gases. Cigarette smoking is the most common cause of COPD worldwide. Other causes may include second-hand smoke, environmental and occupational exposures, and alpha-1 antitrypsin deficiency.

  • Cigarette smoking. Cigarette smoking induces macrophages to release neutrophil chemotactic factors and elastases, which lead to tissue destruction. Overall, tobacco smoking accounts for as much as 90% of COPD risk.
  • Second-hand smoke. Second-hand smoke, or environmental tobacco smoke, increases the risk of respiratory infections, augments asthma symptoms, and causes a measurable reduction in pulmonary function.
  • Environmental and occupational factors. COPD does occur in individuals who have never smoked. Although the role of air pollution in the etiology of COPD is unclear, the effect is small when compared with that of cigarette smoking. In developing countries, the use of biomass fuels for indoor cooking and heating is likely to be a major contributor to the worldwide prevalence of COPD.
  • Alpha-1 antitrypsin deficiency. Alpha-1 antitrypsin (AAT) is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and secreted into the bloodstream. One of its main purposes is to protect the lung parenchyma. AATD is the only known genetic risk factor for developing COPD and accounts for less than 1% of all cases in the United States.


COPD is estimated to affect 32 million people in the United States and is the third leading cause of death in the United States. People with COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age.

Chronic bronchitis is defined clinically as the presence of a chronic productive cough for three months during each of two consecutive years, with other causes of cough already excluded.

Emphysema is defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

Asthma is considered a distinct, separate disorder and is classified as an abnormal airway condition characterized primarily by reversible inflammation. COPD can coexist with asthma. Both of these diseases have the same major symptoms; however, symptoms are generally more variable in asthma than in COPD.


The goal of COPD management is to improve a client’s functional status and quality of life by preserving optimal lung function, improving symptoms, and preventing the recurrence of exacerbations.

  • Promote smoking cessation
  • Decrease inflammation through systemic and inhaled steroids
  • Prevent infection and COPD exacerbation
  • Improve airway clearance by reducing sputum viscosity
  • Prevent hypoxemia with oxygen therapy


In COPD, the airflow limitation is both progressive and associated with the lungs’ abnormal inflammatory response to noxious particles or gases. The inflammatory response occurs throughout the proximal and peripheral airways, lung parenchyma, and pulmonary vasculature. Because of the chronic inflammation and the body’s attempts to repair it, changes and narrowing occurs in the airways. Changes in the proximal and peripheral airways include increased numbers of goblet cells and enlarged submucosal glands, leading to hypersecretion of mucus; and thickening of the airway wall, peribronchial fibrosis, exudate in the airway, and overall airway narrowing.

In chronic bronchitis, smoke or other environmental pollutants irritate the airways, resulting in inflammation and hypersecretion of mucus. Constant irritation causes the mucus-secreting glands and goblet cells to increase in number, leading to increased mucus production. Mucus plugging of the airway reduces ciliary function, bronchial walls become thickened, and further narrowing of the lumen occurs.

In emphysema, impaired oxygen and carbon dioxide exchange results from the destruction of the walls of overdistended alveoli. The chronic inflammatory response may induce disruption of the parenchymal tissues. This end-stage process progresses slowly for many years. As the walls of the alveoli are destroyed, the alveolar surface area in direct contact with the pulmonary capillaries continually decreases, causing an increase in dead space and impaired oxygen diffusion, leading to hypoxemia.

There are two main types of emphysema, based on the changes taking place in the lung.

  • Panlobular (panacinar). There is the destruction of the respiratory bronchiole, alveolar duct, and alveolus. All airspaces within the lobule are essentially enlarged, but there is little inflammatory disease.
  • Centrilobular (centroacinar). Pathological changes take place mainly in the center of the secondary lobule, preserving the peripheral portions of the acinus. Frequently, there is a derangement of ventilation-perfusion ratios, producing chronic hypoxemia, hypercapnia, polycythemia, and episodes of right-sided heart failure.

Epidemiology of COPD

COPD is primarily present in smokers and those greater than age 40. Prevalence increases with age and it is currently the third most common cause of morbidity and mortality worldwide. In 2015, the prevalence of COPD was 174 million and there were approximately 3.2 million deaths due to COPD worldwide. Men were found to have a pooled prevalence of 11.8% and women 8.5%.  Although current rates of COPD in men are higher than the rates in women, the rates in women have been increasing.

Signs and Symptoms

Clients diagnosed with COPD typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease. The three primary symptoms (chronic cough, sputum production, and dyspnea) often worsen over time.

Common signs and symptoms

  • Coughing usually worsens in the mornings and is productive with a small amount of colorless sputum. The cough may be intermittent and may be unproductive in some clients.
  • Breathlessness or dyspnea. Breathlessness is the most significant symptom, but it usually does not occur until the sixth decade of life. By the time FEV1 has fallen to 50% of predicted, the client is usually breathless upon minimal exertion. FEV1 is the most common variable used to grade the severity of COPD.
  • Wheezing is frequently heard on forced and unforced expiration. In addition, coarse crackles beginning with inspiration may be heard.
  • Hyperinflation or barrel-chest. In clients with COPD who have a primary emphysematous component, chronic hyperinflation leads to the “barrel chest” thorax configuration. This configuration results from a more fixed position of the ribs in the inspiratory position and from loss of lung elasticity.
  • Use of accessory muscles. As the work of breathing increases over time, the accessory muscles are recruited in an effort to breathe. Paradoxical indrawing of lower intercostal spaces is also evident, known as the Hoover sign.
  • Weight loss. Weight loss is common because dyspnea interferes with eating and the work of breathing is energy-depleting.

Chronic bronchitis characteristics include:

  • Obesity
  • Frequent cough and expectoration of sputum
  • Use of accessory muscles of respiration
  • Coarse rhonchi and wheezing
  • Edema or cyanosis, which are signs of right heart failure

Emphysema characteristics include the following:

  • Very thin clients with a barrel chest
  • Little to no cough or expectoration
  • Breathing may be assisted by pursed lips and the use of accessory muscles
  • Tripod sitting position
  • Hyperresonant chest and wheezing
  • Very distant heart sounds


The American Thoracic Society (ATS) and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria for assessing the severity of airflow obstruction are as follows:

  • Stage 1 (mild): FEV1 80% or greater of predicted
  • Stage 2 (moderate): FEV1 50 to 79% of predicted
  • Stage 3 (severe): FEV1 30 to 49% of predicted
  • Stage IV (very severe): FEV1 less than 30% of predicted


The major risk factor associated with COPD is environmental exposure and it is modifiable. Smoking cessation is the single most cost-effective intervention to reduce the risk of developing COPD and to stop its progression.

  • Smoking cessation. Healthcare providers should promote smoking cessation by explaining the risks of smoking and personalizing the “at-risk” message to the client. After giving a strong warning about smoking, healthcare providers should work with the client to set a definite “quit date”. Referral to a smoking cessation program may be helpful, with a follow-up within three to five days after the quit date.
  • Nicotine replacement. This is a first-line pharmacotherapy that reliably increases long-term smoking abstinence rates. It comes in a variety of forms, such as gums, inhalers, nasal sprays, transdermal patches, sublingual tablets, or lozenges.
  • Administration of antidepressants. Bupropion SR and nortriptyline, both antidepressants, may also increase long-term quit rates.
  • Smoking cessation resources. Various materials, resources, and programs developed by several organizations, such as the Agency for Healthcare Research and Quality, Centers for Disease Control and Prevention, and the American Lung Association can be provided by nurses to assist with this effort.

Medical Management

Once the diagnosis of COPD is established, it is important to educate the client about the disease and encourage their active participation in therapy. A comprehensive disease management strategy is associated with a lower hospitalization rate and fewer emergency department visits.

  • Diet. Nutritional support is an important part of comprehensive care in clients diagnosed with COPD.
  • Bronchodilators. These agents are the backbone of any COPD treatment regimen. They work by dilating airways, thereby decreasing airflow resistance. This increases airflow and decreases dynamic hyperinflation. These drugs provide symptomatic relief but do not alter disease progression or decrease mortality.
  • Beta2-agonists and cholinergic antagonists. Studies have shown that combined therapy results in greater bronchodilator response and provides greater relief. Beta2-agonists increase smooth muscle relaxation, while anticholinergic drugs provide bronchodilation with a benefit of a decrease in exercise-induced dynamic hyperinflation.
  • Smoking cessation. A smoking cessation plan is an essential part of a comprehensive management plan. Supervised use of pharmacologic agents is an important adjunct to self-help and group smoking cessation programs. Nicotine replacement therapies after smoking cessation reduce withdrawal symptoms.
  • Corticosteroids. Oral and parenteral corticosteroids significantly reduced treatment failure and the need for additional medical treatment. They increase the rate of improvement in lung function and dyspnea over the first 72 hours. Inhaled corticosteroids provide a more direct route of administration to the airways and are minimally absorbed.
  • Antibiotics. Empiric antimicrobial therapy is recommended in clients with acute exacerbation and evidence of an infectious process. The antibiotic of choice must be comprehensive and should cover all likely pathogens.
  • Mucolytics. These agents reduce sputum viscosity and improve secretion clearance. The oral agent N-acetylcysteine has antioxidant and mucokinetic properties and is sued to treat clients with COPD. they can decrease cough and chest discomfort.
  • Oxygen therapy. Oxygen administration reduces mortality rates in clients with advanced COPD because of the favorable effects on pulmonary hemodynamics. Long-term oxygen therapy improves survival 2-fold or more in hypoxemic clients with COPD.
  • AAT deficiency treatment. Available augmentation strategies for AAT levels include pharmacologic attempts to increase the endogenous production of AAT by the liver through danazol or tamoxifen and administration of purified AAT by periodic intravenous infusion or by inhalation.
  • Assisted ventilation. Progressive airflow obstruction may impair oxygenation and/or ventilation to the degree that the client requires assisted ventilation. The client may be treated with noninvasive mask ventilation or with trans laryngeal intubation and mechanical ventilation.
  • Bullectomy. Bullectomy, or removal of bullae, is a standard treatment in selected clients and may result in the expansion of compressed lung tissue and improved function. It is performed through a midline sternotomy or a lateral incision, or by video-assisted thoracoscopy.
  • Lung transplantation. Lung transplantation can be done for clients with COPD who is deemed potential candidate. The main purpose of this is to improve symptomatology and quality of life.

Assessment and Diagnosis

COPD is often evaluated in clients with relevant symptoms and risk factors. The diagnosis is confirmed by spirometry. Other tests may include a six-minute walk test, laboratory testing, and radiographic imaging.

Physical Assessment

The sensitivity of a physical examination in detecting mild to moderate COPD is relatively poor; however, physical signs are quite specific and sensitive for this disease.

  • Inspection. The client may present with retraction of the supraclavicular fossae upon inspiration, causing the shoulders to heave upward. The abdominal muscles may also contract on inspiration. In addition to breathing patterns and respiratory rates, the nurse should also observe the use of accessory muscles, such as sternocleidomastoid, scalene, and trapezius muscles, and the abdominal and internal intercostal muscles.
  • Palpation. The nurse also palpates the thorax for tenderness, masses, lesions, respiratory excursion, and vocal fremitus. Clients with emphysema exhibit almost no tactile fremitus.
  • Percussion. Percussion produces audible and tactile vibrations and allows the nurse to determine whether underlying tissues are filled with air, fluid, or solid material. Resonance with a loud intensity and low pitch signifies chronic bronchitis, while hyper resonance with a very loud intensity and lower pitch indicates emphysema.
  • Auscultation. Auscultation in COPD clients reveals wheezing upon forced and unforced expiration, diffusely decreased breath sounds, and coarse crackles beginning with inspiration.


Clients with COPD may have multiple findings as follows:


  • Significant respiratory distress in acute exacerbations
  • Muscle wasting


  • Accessory respiratory muscle use
  • Prolonged expiration
  • Wheezing
  • Pursed-lip breathing


  • Increased anterior-posterior chest wall diameter or barrel chest


  • Central cyanosis


  • Digital clubbing
  • Lower extremity edema in right heart failure

Diagnostic Testing

The formal diagnosis of COPD is made with spirometry; when the ratio of forced expiratory volume in one second over forced vital capacity is less than 70% of that predicted for a matched control, it is diagnostic for a significant obstructive defect .

  • Spirometry. This is used to evaluate airflow obstruction, which is determined by the ratio of FEV1 to FVC. With obstruction, the client either has difficulty exhaling or cannot forcibly exhale air from the lungs, reducing FEV1. Spirometry is also used to determine the reversibility of obstruction after the use of bronchodilators.
  • Arterial blood gas analysis. ABG analysis provides the best clues as to the acuteness and severity of disease exacerbation. Clients with mild COPD have mild to moderate hypoxemia without hypercapnia. pH usually is near normal. Lung mechanics and gas exchange worsen during acute exacerbations.
  • Serum chemistries. Clients with COPD tend to retain sodium. Additionally, serum potassium should be monitored carefully, because diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels.
  • Alpha1-antitrypsin. Measure alpha1-antitrypsin (AAT) in all clients younger than 40 years, in those with a family history of emphysema at an early age, or in clients with emphysematous changes with no smoking history. The diagnosis of severe AAT deficiency is confirmed when the serum level falls below the protective threshold value of 11 mmol/L.
  • Sputum evaluation. In clients with stable chronic bronchitis, the sputum is mucoid and macrophages are the predominant cells. With an exacerbation, sputum becomes purulent because of the presence of neutrophils.
  • Chest radiography. Frontal and lateral chest radiographs of clients with emphysema reveal signs of hyperinflation. Chronic bronchitis is associated with increased broncho vascular markings and cardiomegaly.
  • Computed tomography. High-resolution CT scanning is more sensitive than standard chest radiography and is highly specific for diagnosing emphysema.
  • Pulmonary function tests. PFTs are essential for the diagnosis and assessment of the severity of the disease, and they are helpful in following its progress. Lung volume measurements often show an increase in total lung capacity, functional residual capacity, and residual volume. FEV1 is the most commonly used index of airflow obstruction.
  • Six-minute walking distance. The distance walked in six minutes (6MWD) is a good predictor of all-cause and respiratory mortality in clients with moderate COPD.


In diagnosing COPD, several differential diagnoses must be ruled out. The primary differential diagnosis is asthma. It may be difficult to differentiate between a client with COPD and one with chronic asthma. Other diseases that must be considered in the differential diagnosis include heart failure, bronchiectasis, tuberculosis, obliterative bronchiolitis, and diffuse panbronchiolitis.


Respiratory insufficiency and failure are major life-threatening complications of COPD. The acuity of the onset and the severity of respiratory failure depend on baseline pulmonary function, pulse oximetry, or ABG values, comorbid conditions, and the severity of other complications of COPD. this may necessitate ventilatory support until other acute complications can be treated. Other complications of COPD include pneumonia, chronic atelectasis, pneumothorax, and pulmonary arterial hypertension or cor pulmonale.

Nursing Management

Nursing management is vital in the care of clients diagnosed with COPD because of its focus on education, self-management, medication management, symptom control, oxygen therapy, rehabilitation, collaboration, and preventive care. By providing comprehensive and client-centered care, nurses contribute significantly to enhancing client outcomes for COPD.

Nursing Assessment

Assessment involves obtaining information about current symptoms as well as previous disease manifestations. Most clients with COPD seek medical attention late in the course of their disease. With retroactive questioning, a multi-year history can be elicited.

Subjective Cues

  • Dyspnea
  • Tachypnea
  • Respiratory distress
  • Progressive exercise intolerance
  • Acute chest illness
  • Fatigue

Objective Cues

  • Productive cough
  • Increased respiratory rate
  • Use of accessory muscles when breathing
  • Paradoxical indrawing of lower intercostal spaces
  • Barrel chest
  • Excessive sputum production
  • Wheezing
  • Coarse crackles
  • Diffusely decreased breath sounds
  • Cyanosis
  • Decreased fat-free mass
  • Edema
  • Weight gain
  • Cachexia
  • Tripod sitting position

Nursing Diagnosis

Nursing diagnoses applicable for a client diagnosed with COPD include:

  • Ineffective airway clearance related to bronchospasm and increased production of sputum
  • Impaired gas exchange related to altered oxygen supply or alveoli destruction
  • Imbalance nutrition: less than body requirements related to fatigue, sputum production, or dyspnea
  • Deficient knowledge related to lack of information or misinterpretation of information, cognitive limitation
  • Self-care deficit related to intolerance to activity and decreased strength and endurance
  • Risk for infection related to decreased ciliary action or stasis of secretions

See also 

Nursing Care Planning and Goals

The goals appropriate for the care of a client diagnosed with COPD are:

  •  The client will maintain airway patency.
  • The client will participate in measures to facilitate gas exchange.
  • The client will improve their nutritional intake.
  • The client will engage in behaviors to prevent complications and slow the progression of their condition.
  • The client will understand information about their disease process and prognosis, and adhere to the treatment regimen.

Nursing Interventions for COPD

  • Auscultate breath sounds and note adventitious sounds.
  • Assess and monitor the respiratory rate.
  • Note the presence and degree of dyspnea. Use a 0 to 10 scale or the American Thoracic Society’s Grade of Breathlessness Scale to rate breathing difficulty.
  • Assess and monitor skin and mucous membranes for cyanosis.
  • Monitor the level of consciousness and mental status.
  • Evaluate the level of activity intolerance.
  • Monitor vital signs and cardiac rhythm.
  • Assess dietary habits and recent food intake.
  • Assist the client to maintain a comfortable position or elevate the head of the bed.
  • Allow the client to lean on or over a bed table or sit on the edge of the bed to facilitate breathing.
  • Encourage and assist with diaphragmatic or pursed-lip breathing exercises.
  • Explain and reinforce explanations of the disease process and encourage the client and caregivers to ask questions.
  • Promote an increase in fluid intake to 3,000 mL per day as tolerated or as recommended by the healthcare provider.
  • Encourage expectoration of sputum; suction as necessary.
  • Encourage a rest period of one hour before and after meals.
  • Administer medications such as bronchodilators, corticosteroids, beta-agonists, leukotriene agonists, antibiotics, analgesics, or anti-inflammatory drugs.
  • Assist with respiratory modalities, such as spirometry and chest physiotherapy.
  • Provide supplemental oxygen therapy with humidification.
  • Assist with noninvasive positive-pressure ventilation or intubation and mechanical ventilation.
  • Consult with a dietitian or nutritionist to provide easily digested, nutritionally balanced meals.

Emergency Interventions

  • Provide supplemental oxygen as indicated.
  • Administer a short-acting inhaled bronchodilator as first-line therapy.
  • Administer corticosteroids and antibiotics.
  • Prepare the client for admission or transfer to the intensive care unit.
  • Assist with endotracheal ventilation and mechanical ventilation preparation.

Nursing Evaluation

After the implementation of nursing interventions, the nurse evaluates if the desired goals and outcomes were achieved. The nurse needs to ensure that:

  • Ventilation/oxygenation is adequate to meet self-care needs.
  • The nutritional intake meets caloric needs.
  • The infection is treated or prevented.
  • The disease process, prognosis, and therapeutic regimen are understood.
  • The plan is in place to meet the needs of the client after discharge.

Discharge and Home Care Guidelines

For clients discharged to their homes, monitoring should be performed on a continual basis based on the following parameters, which help in the overall management of the disease.

  • The nurse should educate the client and family members about self-management.
  • Nurses are key in promoting smoking cessation and educating clients about its importance.
  • Set and accept realistic short-term and long-range goals with the client.
  • Instruct the client to avoid extremes of hot and cold, air pollutants, and high altitudes.
  • Promote sufficient rest and sleep.
  • The nurse must review educational information and have the client demonstrate correct pMDI use before discharge, during follow-up visits, and during home visits.
  • Refer the client for home, community-based, or transitional care.
  • The nurse provides education and breathing retraining necessary to optimize the client’s functional status.
  • The nurse also directs the client to community resources, such as pulmonary rehabilitation programs and smoking cessation programs.
  • Provide information about decision-making in end-of-life scenarios and the aggressiveness of care near the end of life.

Nursing Documentation

The focus of documentation on a client diagnosed with COPD should include the following:

  • Assessment findings, including respiratory rate, the character of breath sounds; frequency, amount, and appearance of secretions; the presence of cyanosis; laboratory findings, and mentation levels
  • Conditions that may interfere with the oxygen supply
  • Plan of care or interventions and who is involved in the planning
  • Ventilator settings, liters of supplemental oxygen
  • Teaching plan
  • Client’s responses to treatment/teaching and actions performed
  • Attainment/progress toward desired outcomes
  • Modifications to plan of care
  • Long-range needs and identifying who is responsible for actions to be taken
  • Community resources for equipment or supplies postdischarge
  • Specific referrals made


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  2. Cheever, K. H., & Hinkle, J. L. (2018). Brunner & Suddarth’s Textbook of Medical-surgical Nursing. Wolters Kluwer.
  3. Doenges, M. E., Moorhouse, M. F., & Murr, A. C. (2006). Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales. F.A. Davis.
  4. Moorhouse, M. F., Doenges, M. E., & Murr, A. C. (2010). Nursing Care Plans: Guidelines for Individualizing Client Care Across the Life Span. F.A. Davis Company.
  5. Mosenifar, Z., & Oppenheimer, J. J. (2022, June 3). Chronic Obstructive Pulmonary Disease (COPD): Practice Essentials, Background, Pathophysiology. Medscape Reference. Retrieved June 18, 2023, from


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