COPD is a disease of increasing public health importance around the world. COPD has emerged as the third leading cause of chronic morbidity and mortality worldwide. The disease is expected to worsen as the population ages and the worldwide use of tobacco products increases.

This article discusses the causes, clinical features, current approach to diagnosis and management, and nursing management.


COPD is the third leading cause of death and affects more than 10 million persons in the United States. It is a common, preventable, and treatable disease characterized by persistent respiratory symptoms and airflow limitation due to airway and alveolar abnormalities, usually caused by significant exposure to noxious particles or gases.


Chronic obstructive pulmonary disease is defined as a disease state characterized by airflow limitation that is not fully reversible. (GOLD – Global Initiative for Chronic Obstructive Lung Disease)

COPD includes:

  • Chronic bronchitis: Presence of chronic productive cough for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic cough have been excluded.
  • Emphysema: Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Classified into two pathologic types,
    • Centriacinar emphysema: characterized by pathological changes (enlarged air spaces) in respiratory bronchioles. Most frequently associated with cigarette smoking.
    • Panacinar emphysema characterized by the destruction of all acinar units (respiratory bronchiole, alveolar duct, and alveolus). Usually observed in patients with α1AT deficiency.
  • Small airways disease: A condition in which small bronchioles are narrowed.
Patients may have a predominance of chronic bronchitis or emphysema, and it is often difficult to determine because the conditions usually coexist.

Chronic airflow obstruction is the defining feature of COPD; chronic bronchitis without chronic airflow obstruction is not included within COPD.

Etiology and Risk Factor

  • Smoking is the #1 risk factor.
  • Environmental: air pollution, occupational exposure to noxious gases, exposure to wood smoke or other biomass fuel for cooking.
  • Host factors:
    • Genetic factors: α1-antiproteinase deficiency
    • Bronchial hyperactivity: asthma, chronic bronchitis
α1-Antitrypsin (AAT) Deficiency: α1-Antitrypsin (AAT) deficiency is an autosomal recessive disorder that may affect the lungs or liver. AAT deficiency is a genetic risk factor for COPD.

AAT is a serum protein (an α1-protease inhibitor) produced by the liver and normally found in the lungs. Its main function is to protect normal lung tissue from attack by proteases during inflammation related to cigarette smoking and infections. Severe AAT deficiency leads to destruction of lung tissues by proteases and can cause premature bullous emphysema.

Demographic factors: age, low socioeconomic status, history of childhood respiratory infections


COPD is characterized by chronic inflammation of the airways, lung parenchyma (respiratory bronchioles and alveoli), and pulmonary blood vessels.The pathogenesis of this chronic, irreversible disease is complex and involves many mechanisms.

copd pathophysiology
Source: Lewis S. M., Dirksen S. R, & Heitkemper M. M, (2014). Medical-surgical nursing: Assessment and management of clinical problems. Mosby.

Inflammation of central airways: Chronic exposure to cigarette smoke, noxious particles and gases causes abnormal inflammatory response throughout the proximal and peripheral airways, lung parenchyma, and pulmonary vasculature. The predominant inflammatory cells are neutrophils, macrophages, and lymphocytes. These inflammatory cells also attract other inflammatory mediators (e.g., leukotrienes) and proinflammatory cytokines (e.g., tumor necrosis factor). This chronic, abnormal inflammatory process causes tissue destruction and disrupts the normal defense mechanisms and repair process of the lung and finally results in structural changes in the lungs.

Excess mucus production:  Chronic productive cough is a feature of COPD with predominant chronic bronchitis. Excess mucus production is the result of the increased number of mucus-secreting goblet cells and enlarged submucosal glands. Some of the inflammatory mediators also stimulate mucus production. In addition to this, cigarette smoke-induced loss of cilia also causes decreased mucous clearance and chronic cough. chronic bronchitis

Parenchymal destruction: Inhalation of oxidants present in tobacco or air pollution causes increased activity of proteases (which break down the connective tissue of the lungs) and inhibits the antiproteases (which protect against the breakdown). The natural balance of protease/antiprotease is thus altered and results in the destruction of the alveoli and loss of the lungs’ elastic recoil.

copd diagram
Source: Lewis S. M, Dirksen S. R, & Heitkemper M. M.(2014). Medical-surgical nursing: Assessment and management of clinical problems. Mosby

Peripheral airway remodeling: The hallmark feature of COPD is airflow limitation during forced exhalation. The primary site of airflow limitation is in the smaller airways. As the peripheral airways become obstructed, the air is progressively trapped during expiration. Because of air trapping, the chest hyper expands and becomes barrel-shaped. The functional residual capacity is increased.

The residual air, combined with the loss of elastic recoil, makes passive expiration difficult. This “overinflated” state causes dyspnea and limited exercise capacity.

Ventilation-perfusion (V/Q) mismatch: Continued air trapping causes destruction of alveolar walls, and bullae (large air spaces in the parenchyma) and blebs (air spaces adjacent to pleurae) can form. Bullae and blebs are not effective in gas exchange, as they do not contain the capillary bed that normally surrounds each alveolus. This results in a significant ventilation-perfusion (V/Q) mismatch and hypoxemia. Peripheral airway obstruction also results in V/Q imbalance and, combined with respiratory muscle impairment, can lead to CO2 retention, particularly in severe disease.

Pulmonary vascular changes and impaired cardiac performance: Pulmonary vascular changes may occur late in the course of COPD. The small pulmonary arteries vasoconstriction due to hypoxia. As the disease advances, the structure of the pulmonary arteries changes, resulting in the thickening of the vascular smooth muscle. Because of the loss of alveolar walls and the capillaries surrounding them, pressure in the pulmonary circulation increases resulting in mild to moderate pulmonary hypertension. Pulmonary hypertension may progress and lead to hypertrophy of the right ventricle of the heart (cor pulmonale) and may eventually lead to right-sided heart failure.

Systemic effects: Chronic abnormal inflammatory process is an underlying etiology for these systemic effects. Cardiovascular diseases commonly exist in COPD (smoking is a primary risk factor for both of them). Other common systemic diseases include cachexia (skeletal muscle wasting), osteoporosis, diabetes, and metabolic syndrome.

copd systemic effects

Clinical Manifestations

Symptoms include the following:

  • Productive cough or acute chest illness
  • Breathlessness
  • Wheezing

Cough: Productive cough is a common symptom (usually worse in the mornings and produces a small amount of colorless sputum).

Breathlessness: is the most significant symptom. When FEV1 falls to 50% of predicted, the patient becomes breathless upon minimal exertion.

Wheezing: may occur in some patients, particularly during exertion and exacerbations.

  • COPD should be considered in:
      • All patients over age 40 with 10 or more pack-years of cigarette smoking.
      • Patient who has symptoms of cough, sputum production, or dyspnea and/or a history of exposure to risk factors for the disease.
  • Patients typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease.

These include cough, worsening dyspnea, progressive exercise intolerance, sputum production, and alteration in mental status.

Systemic manifestations

  • Decreased fat-free Mass
  • Impaired systemic muscle function
  • Osteoporosis
  • Anemia
  • Depression
  • Pulmonary Hypertension
  • Corpulmonale
  • Left-sided heart failure

Physical Examination

Patients with advanced disease may experience tachypnea and respiratory distress with simple activities.

  • The respiratory rate increases in proportion to disease severity.
  • Use of accessory muscles of respiration and paradoxical indrawing of lower intercostal spaces (known as the Hoover sign) is evident.
  • In advanced cases, cyanosis, elevated jugular venous pulse (JVP), and peripheral edema can be observed.

Thoracic examination reveals the following:

  • Hyperinflation (barrel chest)
  • Wheezing (frequently heard on forced and unforced expiration)
  • Diffusely decreased breath sounds
  • Hyper resonance on percussion
  • Prolonged expiration
  • Coarse crackles beginning with inspiration may be heard.

Certain characteristics allow differentiation between a disease that is predominantly chronic bronchitis and that which is predominantly emphysema.

Symptoms SignsInvestigations
Bronchitis (Blue Bloater)Chronic productive cough
Purulent sputum

Cyanosis (2º to hypoxemia and hypercapnia)
Peripheral edema from RVF
(cor pulmonale)
Crackles, wheezes
Prolonged expiration if obstructive
Frequently obese
↓ FEV1, ↓ FEV1/FVC
Normal TLC, ↓ or normal DLCO
AP diameter normal
↓ bronchovascular markings
Enlarged heart with cor pulmonale
Emphysema (Pink Puffer)Dyspnea
Minimal cough
Decreased exercise tolerance
Pink skin
Pursed-lip breathing
Accessory muscle use
Cachectic appearance Hyperinflation/barrel chest
Hyperresonant percussion
Decreased breath sounds
Decreased diaphragmatic excursion
↓ FEV1, ↓ FEV1/FVC
↑ TLC (hyperinflation)
↑ RV (gas trapping)
↑ AP diameter
Flat hemidiaphragm (on lateral
↓ cardiac silhouette
↑ retrosternal space
↓ peripheral vascular


An FEV1/FVC ratio of less than 70% establishes the diagnosis of COPD, and the severity of obstruction (as indicated by FEV1) determines the stage of COPD. COPD can be classified as mild, moderate, severe, and very severe.

ClassificationLevel of SeverityFEV1 Results
Stage IMildFEV1 80% or greater of predicted
Stage IIModerateFEV1 50-79% of predicted
Stage IIISevereFEV1 30-49% of predicted
Stage IVVery severeFEV1 less than 30% of predicted

Adapted from Global Initiative for Chronic Obstructive Lung Disease: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (updated 2013). Retrieved from

FEV1 Forced expiratory volume in the first 1 second of expirationVolume of air that can forcibly be expired in first 1 second, after full inspiration.
FVC Forced vital capacityVolume of air that can forcibly be blown out after full inspiration.
TLC Total lung capacityThe maximum volume of air present in the lungs.
FRCFunctional residual capacityVolume of air present in the lungs at the end of passive expiration.
RV RV Residual volumeThe amount of air remaining in the lungs after a maximal expiration
DLCODiffusing capacity for carbon monoxideDLCO is the carbon monoxide uptake from a single inspiration in a standard time (usually 10 seconds). It measures the diffusion of gas across the alveolar membrane which is determined by the surface area and integrity of the alveolar membrane and the pulmonary vascular bed.


  • Cor pulmonale: In COPD, chronic alveolar hypoxia causes pulmonary vasoconstriction and vascular remodeling. Chronic hypoxia also stimulates erythropoiesis, which causes polycythemia (results in increased viscosity of the blood). An anatomic reduction of the pulmonary vascular bed, as seen in emphysema with bullae, may occur. These patients thus develop increased pulmonary vascular resistance and pulmonary hypertension. Pulmonary hypertension causes increased pressures on the right side of the heart (normally the right ventricle and pulmonary circulatory system are low-pressure systems compared with the left ventricle and systemic circulation) and eventually, right-sided heart failure develops.
copd complication
Source: Lewis S. M., Dirksen S. R, & Heitkemper M. M, (2014). Medical-surgical nursing: Assessment and management of clinical problems.Mosby
  • COPD Exacerbations: According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, a COPD exacerbation is an acute event in the natural course of the disease. The primary causes of exacerbations are bacterial or viral infections. Exacerbations are signaled by an acute change in the patient’s usual dyspnea, cough, and/or sputum.
  • Acute Respiratory Failure: Patients with severe COPD who have exacerbations are at risk for respiratory failure.
  • Spontaneous Pneumothorax: Spontaneous pneumothorax occurs in a small fraction of patients with emphysema.
  • Depression and Anxiety: Patients with COPD experience may experience depression and anxiety as the disease progresses.


Pulmonary Function Tests:

  • Spirometry: The formal diagnosis of COPD is made with spirometry. When the ratio of forced expiratory volume in 1 second over forced vital capacity (FEV1/FVC) is less than 70% of that predicted for a matched control, it is diagnostic for a significant obstructive defect.
  • Lung volume measurements: may show an increase in total lung capacity, functional residual capacity, and residual volume. The vital capacity often decreases.
Diagnostic Considerations
  • History and physical examination
  • Pulmonary function tests
  • ABG
  • Serum electrolytes, BNP
  • Sputum analysis/culture
  • Chest x-ray/CT
  • Serum α1-antitrypsin level
  • Six-minute walk test
  • BODE Index

Arterial blood gas (ABG) analysis: helps to assess the acuteness and severity of disease exacerbation. Mild COPD patients may have mild to moderate hypoxemia without hypercapnia. As the disease condition progresses, hypoxemia worsens and hypercapnia may develop. In chronic CO2 retainers, renal compensation occurs and thus, pH usually is near normal. Any pH below 7.3 may be a sign of acute respiratory compromise.

Serum Chemistries: Monitor serum sodium and potassium levels. Patients with COPD tend to retain sodium. Beta-adrenergic agonists, theophylline and diuretics, act to lower potassium levels. Beta-adrenergic agonists also causes increased renal excretion of serum calcium and magnesium.

Alpha1-Antitrypsin: AAT should be measured in all patients younger than 40 years, in those with a family history of emphysema at an early age, or patients with emphysematous changes with no smoking history.

Sputum evaluation and sputum culture: An increase in the quantity of sputum production and the presence of neutrophils is often a sign of an acute exacerbation. The pathogens cultured most frequently during exacerbations are Streptococcus pneumonia, Haemophilus influenzae and Pseudomonas aeruginosa.

B-Type Natriuretic Peptide: By measuring BNP, CHF and COPD exacerbations can be differentiated.

Chest Radiography: Chest radiographs of emphysematous patients reveal signs of hyperinflation, including flattening of the diaphragm, increased retrosternal air space, and a long, narrow heart shadow. In chronic bronchitis increased bronchovascular markings and cardiomegaly can be seen. In pulmonary hypertension, the hilar vascular shadows are prominent, with possible right ventricular enlargement.

Computed Tomography: High-resolution CT is more sensitive than standard chest radiography and is highly specific for diagnosing emphysema (outlined bullae are not always visible on a chest radiograph).

Two-Dimensional Echocardiography: Even with severe COPD, the degree of pulmonary hypertension is usually only mild to moderate and hence, findings of severe pulmonary hypertension on echocardiogram or cardiac catheterization warrant further workup.

Six-Minute Walking Distance: The distance walked in 6 minutes (6MWD) is a good predictor of mortality in patients with moderate COPD. Patients who desaturate during the 6MWD have a higher mortality rate than do those who do not desaturate.

BODE index: The BODE index is a multidimensional scoring system used to test patients who have been diagnosed with COPD and to predict mortality. The index uses the four factors to predict risk of death from the disease – Body-mass index, airflow Obstruction, Dyspnea, and Exercise capacity.

The BODE index will result in a score of zero to ten dependent upon FEV1, body-mass index, the distance walked in six minutes, and the modified MRC dyspnea scale. Greater score means higher probability the patient will die from COPD.

bode index

Other Studies

  • Pulse oximetry: when combined with clinical observation, provides instant feedback on a patient’s status.
  • Electrocardiography: Electrocardiography can be used in establishing that hypoxia is not resulting in cardiac ischemia and that the underlying cause of respiratory difficulty is not cardiac in nature.
  • Right-Sided Heart catheterization: to measure pulmonary artery pressures directly and to gauge the response to vasodilators.
  • Hematocrit: Chronic hypoxemia may lead polycythemia (hematocrit greater than 52% in men or 47% in women is indicative of polycythemia).


  • Alpha1-Antitrypsin (AAT) Deficiency
  • Asthma COPD overlap syndrome
  • Bronchitis
  • Chronic Cough
  • Congestive heart failure
  • Emphysema
  • Nicotine Addiction
  • Pulmonary Embolism (PE)


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

Smoking Cessation: Cessation of cigarette smoking is the most important intervention that can impact the natural history of COPD.

Prevention of infections: COPD patients are extremely susceptible to pulmonary infections.

Recommended for all patients with COPD
  • Annual influenza virus vaccination
  • Pneumococcal vaccination


Drug Therapy: Drugs are given in a stepwise fashion according to the severity of airflow obstruction.

copd gold drug therapy




  1. Bronchodilators and anticholinergics: Bronchodilators and/or anticholinergic drugs are used for symptomatic benefit in patients with COPD. The inhaled route is preferred.
  • Short-acting β2-agonists (such as salbutamol and terbutaline), or the anticholinergic ipratropium bromide, may be used for patients with mild disease
  • Longer acting β2-agonists (e.g., salmeterol, formoterol and indacaterol), or the anticholinergic tiotropium bromide, are more appropriate for patients with moderate to severe disease.
  • Oral bronchodilators may be used in patients who cannot use inhaled devices efficiently. Theophylline preparations improve breathlessness and quality of life, but their use is limited by side-effects and drug interactions.
  1. Corticosteroids: Inhaled corticosteroids are currently recommended in patients with severe disease (FEV1 < 50%) who report two or more exacerbations requiring antibiotics or oral steroids per year. ICS reduce the frequency and severity of exacerbations. Oral corticosteroids are useful during exacerbations but long term therapy contributes to osteoporosis and impaired skeletal muscle function and should be avoided.
  2. Antibiotics: Antibiotics are commonly prescribed to COPD patients to prevent/treat acute exacerbations.
  3. Other Agents
    • N-acetyl cysteine: has been used in patients with COPD for both its mucolytic and antioxidant properties.
    • Phosphodiesterase 4 inhibitor: Roflumilast has been shown to reduce the frequency of exacerbation in patients who have moderate or severe (FEV1 less than 50% of predicted) COPD and chronic bronchitis, with frequent exacerbations and are taking LABA/inhaled corticosteroid with or without a LAMA.

Oxygen Therapy: Long-term continuous O2 therapy-LTOT (more than 15 hr/day) increases survival and improves exercise capacity and mental status in hypoxemic patients.

Breathing Retraining: The main types of breathing retraining exercises are:

(1) pursed-lip breathing and (2) diaphragmatic breathing

  • Pursed-lip breathing (PLB) is used to prolong exhalation and thereby preventing bronchiolar collapse and air trapping.
  • Diaphragmatic (abdominal) breathing uses diaphragm instead of the accessory muscles of the chest to (1) achieve maximum inhalation and (2) to slow the respiratory rate. However, the use of diaphragmatic breathing in patients with COPD may increase the work of breathing and dyspnea. Patients with moderate to severe COPD with marked hyperinflation are poor candidates for diaphragmatic breathing.

Airway Clearance Techniques: ACTs include effective coughing, chest physiotherapy, airway clearance devices, and high frequency chest ventilation.

  • Effective Coughing. Many patients with COPD have developed ineffective coughing patterns that do not adequately clear their airways of sputum. The patient must cough effectively to bring the secretions to the central airways to expectorate them. Huff coughing is an effective method to clear the airways.

effective huff coughing





  • Chest Physiotherapy: Chest physiotherapy (CPT) is primarily used for patients with excessive bronchial secretions who have difficulty clearing them (e.g., cystic fibrosis, bronchiectasis). CPT consists of postural drainage, percussion, and vibration.

Nutritional Therapy: Many COPD patients in the advanced stages are underweight with loss of muscle mass and cachexia. Weight loss is a predictor of a poor prognosis and increased frequency of COPD exacerbations. Nutritional support is an important part of comprehensive care in patients with COPD.

  • A diet high in calories and protein, moderate in carbohydrate, and moderate to high in fat is recommended and can be divided into five or six small meals a day.
  • High-protein, high-calorie nutritional supplements can be offered between meals.
  • Fluid intake should be at least 3 L/day unless contraindicated by other medical conditions.
  • Fluids should be taken between meals (rather than with them) to prevent excess stomach distention and to decrease pressure on the diaphragm.
  • Sodium restriction may be indicated if there is accompanying heart failure.

Surgical Therapy for COPD: Three different surgical procedures have been used in severe COPD.

  • Lung volume reduction surgery (LVRS): The goal of this surgery is to reduce the lung volume by removing the most diseased lung tissue so the remaining healthy lung tissue can perform better. Reducing the size of the hyperinflated emphysematous lungs results in decreased airway obstruction and increased room for the remaining normal alveoli to expand and function.
  • Bullectomy: used for carefully selected patients with emphysematous COPD who have large bullae (larger than 1 cm). The bullae are usually resected via thoracoscope.
  • Lung transplantation: benefits carefully selected patients with advanced COPD. Although single-lung transplant is the most commonly used technique because of a shortage of donors, bilateral transplantation can be performed.

Acute Exacerbations of COPD

Acute exacerbations of COPD are characterized by an increase in symptoms and deterioration in lung function and health status.


  • Sustained (>48 h) episodes of increased dyspnea and cough and change in the amount and character of sputum.

Etiology: viral /bacterial infections, air pollution


  • Classic signs of exacerbation are an increase in dyspnea, sputum volume, or sputum purulence.
  • Patients may also have nonspecific complaints of malaise, insomnia, fatigue, depression, confusion, decreased exercise tolerance, increased wheezing, or fever without other causes.


  • O2: target 88-92% SaO2 for CO2 retainers
  • Bronchodilators by MDI with spacer or nebulizer
    • SABA + anticholinergic, e.g. salbutamol and ipratropium bromide via nebulizers × 3 back-to-back q15min
  • Systemic corticosteroids: IV solumedrol or oral prednisone
  • Antibiotics for exacerbations with sputum purulence, ICU admission, or non-invasive ventilation (NIV use)
    • 1st line: Amoxicillin-Clavulanic Acid
    • If allergic to penicillin, Fuoroquinolone or doxycycline
  • Post exacerbation: Pulmonary rehabilitation with general conditioning to improve exercise tolerance

ICU admission and mechanical ventilation for life-threatening exacerbations

  • Ventilatory support
    • Non-invasive: NIPPV, BiPAP
    • Conventional mechanical ventilation: indicated for patients with severe respiratory distress despite initial therapy, life-threatening hypoxemia, severe hypercarbia and/or acidosis, markedly impaired mental status, respiratory arrest, hemodynamic instability, or other complications.

Nursing Management

 Nursing Assessment

Nursing assessment should include the following

  • Obtain a clear history of the disease process and assess for exposure to risk factors.
  • Obtain information about current symptoms as well as previous disease manifestations.
  • Assess the patient’s vital signs, review the results of diagnostic tests performed.

Nursing Priorities

  • Maintain airway patency
  • Improve breathing pattern and reduction of symptoms
  • Assist with measures to facilitate gas exchange.
  • Improve  activity and exercise tolerance
  • Improve nutrition

Nursing Diagnosis

  • Ineffective airway clearance
  • Ineffective Breathing Pattern
  • Impaired Gas Exchange
  • Activity Intolerance
  • Imbalanced Nutrition: Less Than Body Requirements


The overall goals are that the patient with COPD will have:

  • A patent airway
  • Improved breathing pattern and relief from symptoms
  • Normal respiratory parameters and ABG values
  • Ability to perform ADLs and improved exercise tolerance
  • No complications related to COPD
Nursing Care Plan of COPD

Nursing Diagnosis: Ineffective airway clearance 

Related to

  • Expiratory airflow obstruction
  • Ineffective cough
  • Decreased airway humidity
  • Tenacious secretions as evidenced by
  • Ineffective or absent cough
  • Presence of abnormal breath sounds
  • Absence of breath sounds

As evidenced by

  • Ineffective or absent cough
  • Presence of abnormal breath sounds
  • Absence of breath sounds

Desired outcome: Patient maintains a clear airway by effectively coughing as evidenced by clear lung sounds on auscultation.

Assist the patient to sitting position with head slightly flexed, shoulders relaxed, and knees flexed. This position promotes comfort and optimal gas exchange by enabling maximal chest expansion, using activation of accessory muscles during inspiration and gravity during expiration.
Encourage slow, deep breathing; turning; and coughing. Helps to mobilize pulmonary secretions.
Regulate fluid intake to optimize fluid balance.Adequate hydration helps to liquefy secretions for easier expectoration.
Perform endotracheal or nasotracheal suctioning as appropriate. To clear the airway.
Administer bronchodilator agents and use airway clearance devicesTo facilitate clearance of retained secretions and increase ease of breathing.

Nursing Diagnosis: Ineffective Breathing Pattern

Related to alveolar

  • Hypoventilation
  • Anxiety
  • Chest wall alterations
  • Hyperventilation as evidenced by
  • Dyspnea
  • Increased anteroposterior diameter of chest
  • Nasal flaring
  • Orthopnea
  • Prolonged expiration
  • Pursed-lip breathing
  • Use of accessory muscles to breathe

As evidenced by

  • Dyspnea
  • Increased anteroposterior diameter of chest
  • Nasal flaring
  • Orthopnea
  • Prolonged expiration
  • Pursed-lip breathing
  • Use of accessory muscles to breathe

Desired Outcome: Following treatment/intervention, the patient’s breathing pattern improves as evidenced by reduction in or absence of reported dyspnea and related symptoms.

Assess respiratory and oxygenation status as indicated by the patient’s condition. Report significant findings.Signs of respiratory distress should be reported promptly for immediate intervention.
Auscultate breath sounds noting areas of decreased or absent ventilation and presence of adventitious sounds (crackles, wheezes, rhonchi).A decrease in breath sounds or presence of adventitious breath sounds may indicate respiratory status change and necessitate prompt intervention.
Elevate head of the bed and provide an over bed table for the patient to lean on.To minimize respiratory efforts
Encourage slow, deep breathing; turning; and coughing. To promote effective breathing techniques and secretion mobilization.
Administer medications (e.g., bronchodilators and inhaled/oral corticosteroids or a combination of these).Helps to promote airway patency and gas exchange.
Corticosteroids combined with a long-acting beta-2 agonist are more effective than any one individual treatment in reducing exacerbations and overall improvement of lung function.
Monitor for tachycardia and dysrhythmias.

Advise the patient about the increased risk for pneumonia.
These are side effects of bronchodilator therapy.
Corticosteroid use also carries an increased risk for pneumonia.
Deliver humidified oxygen as prescribed and monitor the patient’s response..Delivering O2 with humidity will help minimize convective losses of moisture, decreasing dry mucous membranes and enhancing lung compliance.
Monitor pulse oximetry readings and titrate oxygen to keep SpO2 between 88%-92%.SpO2 saturation at 87% or less can indicate need for initiating or increasing O2
Monitor for respiratory muscle fatigue.To determine a need for ventilatory assistance.

Nursing Diagnosis: Impaired Gas Exchange

Related to

  • Alveolar hypoventilation

As evidenced by

  • Headache on awakening
  • PaCO2 ≥45 mm Hg, PaO2 <60 mm Hg,
  • SaO2 <90% at rest

Desired Outcomes: Optimally within 1-2 hr following treatment/intervention or by discharge, the patient has adequate gas exchange as evidenced by respiratory rate (RR) of 12-20 breaths/min and normal/improved ABG values.

Assess for signs and symptoms of hypoxia and report significant findings.Hypoxia (evidenced by agitation, anxiety, restlessness, changes in mental status or level of consciousness [LOC]) indicates oxygen deficiency and necessitates prompt treatment.
Auscultate breath sounds q2-4h and as indicated by the patient’s condition and report significant findings.A decrease in breath sounds or an increase in adventitious breath sounds (crackles, wheezes, rhonchi) may indicate respiratory status change and necessitate prompt intervention.
Deliver humidified oxygen as prescribed, and monitor the patient’s response.Long-term oxygenation for chronic hypoxemia has been shown to reduce mortality. Delivering O2 with humidity will help minimize convective losses of moisture, decreasing dry mucous membranes and enhancing lung compliance.
Monitor the effectiveness of O2 therapy (e.g., pulse oximetry, ABGs). Titrate oxygen to keep SpO2 between 88%-92%.To evaluate patient response to therapy. SpO2 at 87% or less can indicate need for O2 therapy. SpO2 at 93% or more can indicate need for decreasing O2 therapy.
Position the patient in high Fowler’s position, with the patient leaning forward and elbows propped on the over-the-bed table.This position promotes comfort and optimal gas exchange by enabling maximal chest expansion, using activation of accessory muscles during inspiration and gravity during expiration.
Administer noninvasive positive pressure ventilation (NIPPV) as prescribed.NIPPV has been shown to increase blood pH, reduce Paco2, and reduce severity of dyspnea in the first 4 hr of treatment, possibly eliminating the need for mechanical ventilation in some patients.
Explain, as indicated, that mechanical ventilation may be necessary and this would necessitate intensive care support.Exacerbations of COPD or complications may require endotracheal intubation and short-term mechanical ventilation. Goals and possible outcomes should be discussed with the patient and/or significant others BEFORE intubation and mechanical ventilation are instituted, if possible.
Monitor serial ABG values as indicated by the patient’s condition. To assess the patient’s response to the therapy. PaO2 likely will continue to decrease as the patient’s disease progresses. Patients with chronic CO2 retention may have chronically compensated respiratory acidosis with a low normal pH (7.35-7.38) and a Paco2 greater than 50 mm Hg.

Nursing Diagnosis: Activity Intolerance

Related to

  • Fatigue
  • Imbalance between oxygen supply and demand due to inefficient work of breathing

As evidenced by

  • Decreased exercise tolerance
  • Easy fatiguability
  • Dyspnea on excertion
    Verbalization of inability to perform ADLs

Desired Outcome: The patient reports decreasing dyspnea during activity or exercise and rates perceived exertion at 3 or less on a 0-10 scale.

Monitor the patient’s respiratory response to activity, including assessment of oxygen saturations.Individuals with COPD may become hypoxic during increased activity and require oxygen therapy to prevent hypoxemia, which increases the risk for exacerbations of the COPD.
Maintain prescribed activity levels, and explain rationale to the patient.Prescribed activity levels will increase the patient’s stamina while minimizing dyspnea.
Allow at least 90 min between activities for undisturbed rest.Decreases oxygen demand and enables adequate physiologic recovery.
Assist with active range-of-motion (ROM) exercises.ROM exercises help build stamina and prevent complications of decreased mobility.
Request consultation from pulmonary rehabilitation.A comprehensive program includes exercise training, nutrition counseling, and education and provides benefits to patients with all stages of COPD.
Pulmonary rehabilitation is strongly recommended for any patient with an FEV1 less than 50%. Patients who have completed a pulmonary rehabilitation program have been shown to experience improved quality of life and slowed progression of the disease.

Nursing Diagnosis: Imbalanced Nutrition: less than body requirements

 Related to
  • Decreased intake occurring with fatigue and anorexia

As evidenced by

  • Refusing meals or eating only small quantity
  • Cachectic appearance
Assess food and fluid intake. This assessment provides data that will determine need for dietary consultation.
Provide the diet in small, frequent, high caloric meals that are nutritious and easy to consume.Small meals are easier to consume in individuals who are fatigued. Patients with COPD expend an extraordinary amount of energy simply on breathing and require high caloric meals to maintain body weight and muscle mass.
Request consultation with a dietitian as indicated. Such a consultation enables a comprehensive nutritional assessment and possible additional therapies, including nutritional counseling related to the disease process.
For patients who require an oxygen mask or NIPPV and are able to eat, consult with respiratory therapy for the most appropriate device to allow the patient to eat.Attempting oral intake while using NIPPV may result in aspiration. Changing devices for short periods to enable the patient to eat may avoid the need for enteral or parental nutrition support.
When not otherwise indicated, encourage fluid intake (2.5 L/day or more).Adequate hydration helps decrease sputum viscosity for patients with chronic increased sputum production.
Discuss with the patient and significant others the importance of good nutrition in the treatment of COPD.This information optimally will promote adequate nutrition and stable body weight. A knowledgeable patient is more likely to adhere to the treatment plan.


In this phase the effectiveness of nursing care to meet the set goals are evaluated. An effective nursing care plan will help the client with COPD to achieve the goals and the patient

  • Maintains a patent airway
  • Shows normal/improved breathing pattern
  • Will have normal respiratory parameters
  • Shows improved exercise tolerance and will be able to perform ADLs
  • Maintains stable body weight and free from cachexia
  • Remains free from disease related complications
See Also


  1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2019 report.
  2. Kasper DL, Fauci AS, Hauser S, et al, editors. Harrison’s principles of internal medicine, 19th ed (2015). New York: The McGraw-Hill Companies. Page no 1700-1710
  3. Colledge, N. R., Walker, et al, editors. 22nd edition (2014). Davidson’s principles and practice of medicine. Edinburgh: Churchill Livingstone/Elsevier. Page no 673-680
  4. In Papadakis, M. A., In McPhee, S. J., & In Rabow, M. W. (2020). Current medical diagnosis & treatment 2020. McGraw-Hill Education. Page no 655-660
  5. Lewis S. M., Dirksen S. R, & Heitkemper M. M, (2014). Medical-surgical nursing: Assessment and management of clinical problems. Mosby Publications, Page no 580-590.
  6. Hinkle, J. L., & Cheever, K. H. (2014). Brunner & Suddarth’s textbook of medical-surgical nursing. Lippincott Williams & Wilkins. Page no 1334-1340
  7. De Torres, Juan & Casanova, Ciro & Garcini, Angela & Aguirre-Jaime, Armando & Celli, Bartolomé. (2007). COPD heterogeneity: Gender differences in the multidimensional BODE index. International journal of chronic obstructive pulmonary disease. 2. 151-5.
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