Acute Respiratory: Chapter 20 pg. 603-630 COPD

air trapping: incomplete emptying of alveoli during expiration due to loss of lung tissue elasticity (emphysema), bronchospasm (asthma), or airway obstruction

alpha1-antitrypsin deficiency: genetic disorder resulting from deficiency of alpha1-antitrypsin, a protective agent for the lung; increases patient’s risk for developing panacinar emphysema even in the absence of smoking

asthma: a heterogeneous disease, usually characterized by chronic airway inflammation; defined by history of symptoms such as wheeze, shortness of breath, chest tightness, and cough that vary over time and in intensity

bronchiectasis: chronic, irreversible dilation of the bronchi and bronchioles that results from the destruction of muscles and elastic connective tissue; dilated airways become saccular and are a medium for chronic infection

chest percussion: manually cupping hands over the chest wall and using vibration to mobilize secretions by mechanically dislodging viscous or adherent secretions in the lungs

chest physiotherapy (CPT): therapy used to remove bronchial secretions, improve ventilation, and increase the efficiency of the respiratory muscles; types include postural drainage, chest percussion, and vibration, and breathing retraining

chronic bronchitis: a disease of the airways defined as the presence of cough and sputum production for at least a combined total of 3 months in each of 2 consecutive years

chronic obstructive pulmonary disease (COPD): disease state characterized by airflow limitation that is not fully reversible; sometimes referred to as chronic airway obstruction or chronic obstructive lung disease

desaturate: a precipitous drop in the saturation of hemoglobin with oxygen

dry-powder inhaler (DPI): a compact, portable inspiratory flow–driven inhaler that delivers dry-powder medications into the patient’s lungs

emphysema: a disease of the airways characterized by destruction of the walls of overdistended alveoli

flutter valve: portable handheld mucous clearance device; consisting of a tube with an oscillating steel ball inside; upon expiration, high-frequency oscillations facilitate mucous expectoration

fraction of inspired oxygen (FiO2): concentration of oxygen delivered (e.g., 1.0 equals to 100% oxygen)

hypoxemia: decrease in arterial oxygen tension in the blood

hypoxia: decrease in oxygen supply to the tissues and cells

polycythemia: increase in the red blood cell concentration in the blood; in COPD, the body attempts to improve oxygen-carrying capacity by producing increasing amounts of red blood cells

postural drainage: positioning the patient to allow drainage from all lobes of the lungs and airways

pressurized metered-dose inhaler (pMDI): a compact, portable patient-activated pressurized medication canister that provides aerosolized medication that the patient inhales into the lungs

small-volume nebulizer (SVN): a handheld generator-driven medication delivery system that provides aerosolized liquid medication that the patient inhales into the lungs

spirometry: pulmonary function tests that measure specific lung volumes (e.g., FEV1, FVC) and rates (e.g., FEF25%–75%); may be measured before and after bronchodilator administration

vibration: a type of massage given by quickly tapping the chest with the fingertips or alternating the fingers in a rhythmic manner, or by using a mechanical device to assist in mobilizing lung secretions

Chronic pulmonary disorders are a leading cause of morbidity and mortality in the United States. Nurses care for patients with chronic pulmonary disease across the spectrum of care, from outpatient and home care to emergency department (ED), critical care, and hospice settings. To care for these patients, nurses not only need to have astute assessment and clinical management skills, but they also need knowledge of how these disorders can affect quality of life. In addition, the nurse’s knowledge of palliative and end-of-life care is important for applicable patients. Patient and family education is an important nursing intervention to enhance self-management in patients with any chronic pulmonary disorder.Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable slowly progressive respiratory disease of airflow obstruction involving the airways, pulmonary parenchyma, or both (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2019). 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. Most patients with COPD present with overlapping signs and symptoms of emphysema and chronic bronchitis, which are two distinct disease processes.

COPD may include diseases that cause airflow obstruction (e.g., emphysema, chronic bronchitis) or any combination of these disorders. Other diseases such as cystic fibrosis (CF), bronchiectasis, and asthma are classified as chronic pulmonary disorders. 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. This chapter discusses COPD as a disease and describes chronic bronchitis and emphysema as distinct disease states, providing a foundation for understanding the pathophysiology of COPD. Bronchiectasis, asthma, and CF are discussed separately.

While COPD and lower respiratory diseases are the fourth leading cause of death for people of all ages in the United States, they are the third leading cause of death for people ages 65 and over (Centers for Disease Control and Prevention [CDC], 2018a). In 2016, approximately 154,596 Americans died from COPD and lower respiratory diseases (CDC, 2017a). The CDC (2018b) reports that over 16 million Americans live with COPD. This number does not account for the millions of Americans who have COPD but are not diagnosed. Although the rate of hospitalizations for COPD is slowly decreasing, the Agency for Healthcare Research and Quality (AHRQ) reported in 2016 that there were still 501,849 hospitalizations that had COPD as a primary diagnosis (AHRQ, 2016). The cost of individual hospital admissions for patients with COPD is approximately $6245 more per year than admissions for patients without COPD. COPD’s economic burden goes beyond the direct medical costs. Patients with COPD were 60% more likely to call in sick to work and 2.6 times more likely to incur short-term disability than patients without COPD (Patel, Coutinho, Lunacsek, et al., 2018).

Pathophysiology

People with COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age. Although certain aspects of lung function normally decrease with age—for example, vital capacity and forced expiratory volume in 1 second (FEV1)—COPD accentuates and accelerates these physiologic changes as described later. 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 (GOLD, 2019). Because of the chronic inflammation and the body’s attempts to repair it, changes and narrowing occur in the airways. In the proximal airways (trachea and bronchi greater than 2 mm in diameter), changes include increased numbers of goblet cells and enlarged submucosal glands, both of which lead to hypersecretion of mucus. In the peripheral airways (bronchioles less than 2 mm diameter), inflammation causes thickening of the airway wall, peribronchial fibrosis, exudate in the airway, and overall airway narrowing (obstructive bronchiolitis). Over time, this ongoing injury-and-repair process causes scar tissue formation and narrowing of the airway lumen (GOLD, 2019). Inflammatory and structural changes also occur in the lung parenchyma (respiratory bronchioles and alveoli). Alveolar wall destruction leads to loss of alveolar attachments and a decrease in elastic recoil. Finally, the chronic inflammatory process affects the pulmonary vasculature and causes thickening of the lining of the vessel and hypertrophy of smooth muscle, which may lead to pulmonary hypertension (GOLD, 2019).

Processes related to imbalances of substances (proteinases and antiproteinases) in the lung may also contribute to airflow limitation. When activated by chronic inflammation, proteinases and other substances may be released, damaging the parenchyma of the lung. These parenchymal changes may also occur as a consequence of inflammation or environmental or genetic factors (e.g., alpha1-antitrypsin deficiency).

Chronic Bronchitis

Chronic bronchitis, a disease of the airways, is defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years. Although chronic bronchitis is a clinically and epidemiologically useful term, it does not reflect the major impact of airflow limitation on morbidity and mortality in COPD (GOLD, 2019). In many cases, 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 also become thickened, further narrowing the bronchial lumen (Fig. 20-1). Alveoli adjacent to the bronchioles may become damaged and fibrosed, resulting in altered function of the alveolar macrophages. This is significant because the macrophages play an important role in destroying foreign particles, including bacteria. As a result, the patient becomes more susceptible to respiratory infection. A wide range of viral, bacterial, and mycoplasma infections can produce acute episodes of bronchitis. Exacerbations of chronic bronchitis are most likely to occur during the winter when viral and bacterial infections are more prevalent.

Emphysema

In emphysema, impaired oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli. Emphysema is a pathologic term that describes an abnormal distention of the airspaces beyond the terminal bronchioles and destruction of the walls of the alveoli (GOLD, 2019; Han, Dransfield, & Martinez, 2018). In addition, a 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 (a process accelerated by recurrent infections), the alveolar surface area in direct contact with the pulmonary capillaries continually decreases. This causes an increase in dead space (lung area where no gas exchange can occur) and impaired oxygen diffusion, which leads to hypoxemia. In the later stages of disease, carbon dioxide elimination is impaired, resulting in hypercapnia (increased carbon dioxide tension in arterial blood) leading to respiratory acidosis. As the alveolar walls continue to break down, the pulmonary capillary bed is reduced in size. Consequently, resistance to pulmonary blood flow is increased, forcing the right ventricle to maintain a higher blood pressure in the pulmonary artery. Hypoxemia may further increase pulmonary artery pressures (pulmonary hypertension). Cor pulmonale, one of the complications of emphysema, is right-sided heart failure brought on by long-term high blood pressure in the pulmonary arteries. This high pressure in the pulmonary arteries and right ventricle lead to back up of blood in the venous system, resulting in dependent edema, distended neck veins, or pain in the region of the liver (see Chapter 25 for further discussion).

There are two main types of emphysema, based on the changes taking place in the lung (Fig. 20-2). Both types may occur in the same patient. In the panlobular (panacinar) type of emphysema, there is destruction of the respiratory bronchiole, alveolar duct, and alveolus. All airspaces within the lobule are essentially enlarged, but there is little inflammatory disease. A hyperinflated (hyperexpanded) chest, marked dyspnea on exertion, and weight loss typically occur. To move air into and out of the lungs, negative pressure is required during inspiration, and an adequate level of positive pressure must be attained and maintained during expiration. Instead of being an involuntary passive act, expiration becomes active and requires muscular effort.In the centrilobular (centroacinar) form, pathologic changes take place mainly in the center of the secondary lobule, preserving the peripheral portions of the acinus (i.e., the terminal airway unit where gas exchange occurs). Frequently, there is a derangement of ventilation–perfusion ratios, producing chronic hypoxemia, hypercapnia, polycythemia (i.e., an increase in red blood cells), and episodes of right-sided heart failure. This leads to central cyanosis and respiratory failure. The patient also develops peripheral edema.

Risk Factors

Risk factors for COPD include environmental exposures and host factors (Chart 20-1). The most important environmental risk factor for COPD worldwide is cigarette smoking. A dose–response relationship exists between the intensity of smoking (pack-year history) and the decline in pulmonary function. Other environmental risk factors include smoking other types of tobacco (e.g., pipes, cigars) and marijuana. Secondhand smoke also contributes to respiratory symptoms and COPD (GOLD, 2019). Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary cleansing mechanism, which keeps breathing passages free of inhaled irritants, bacteria, and other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed and air becomes trapped behind the obstruction. The alveoli greatly distend, which diminishes lung capacity. Smoking also irritates the goblet cells and mucous glands, causing an increased accumulation of mucus, which in turn produces more irritation, infection, and damage to the lung (U.S. Department of Health & Human Services [HHS], 2014). In addition, carbon monoxide (a by-product of smoking) combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. Cigarette smoking is the best studied COPD risk factor; however, it is not the only risk factor and studies have demonstrated nonsmokers may also develop chronic airflow obstruction.

Chart 20-1 RISK FACTORS

Chronic Obstructive Pulmonary Disease

•Exposure to tobacco smoke accounts for an estimated 80–90% of cases of chronic obstructive pulmonary disease

•Secondhand smoke

•Increased age

•Occupational exposure—dust, chemicals

•Indoor and outdoor air pollution

•Genetic abnormalities, including a deficiency of alpha1-antitrypsin, an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes

Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2019). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved on 6/23/2019 at: www.goldcopd.org/wp-content/uploads/2018/11/GOLD-2019-v1.7-FINAL-14Nov2018-WMS.pdfOther environmental risk factors for COPD include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution, and outdoor air pollution (GOLD, 2019). Recent studies indicate that the use of electronic nicotine delivery systems (ENDS; e.g., e-cigarettes, e-pens, e-pipes, e-hookahs, e-cigars) could increase the risk for developing COPD, but additional research is needed to better understand how their use causes changes similar to COPD in the lungs (Canistro, Vivarelli, Cirillo, et al., 2017; Evans, Burton, & Schwartz, 2018; Larcombe, Janka, Mullins, et al., 2017). Smoke from ENDS has been shown to trigger lung changes (i.e., airway hyperreactivity and lung tissue destruction) that are normally associated with the development of COPD (Garcia-Arcos, Geraghty, Baumlin, et al., 2016). Further research demonstrated that different flavored e-cigarette fluids, aerosols, and solvents can produce different patterns of cytotoxicity (Behar, Wang, & Talbot, 2018). The Surgeon General reported that more than one third of adults ages 18 to 24 years of age had tried e-cigarettes (HHS, 2016). Young adults who have used e-cigarettes report being attracted to them due to perceptions of low harm, the flavorings/tastes of the product, and curiosity (HHS, 2016).

Host risk factors include a person’s genetic makeup. One well-documented genetic risk factor is a deficiency of alpha1-antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. This deficiency may lead to lung and liver disease. Worldwide, alpha1-antitrypsin deficiency impacts between 1/1500 and 1/3000 people with European ancestry (U.S. National Library of Medicine [NLM], 2019). This genetic risk is uncommon in people of Asian descent (NLM, 2019). Approximately 2% of people with COPD have been diagnosed with this deficiency (Stoller, Barnes, & Hollingsworth, 2018). This deficiency predisposes young people to rapid development of lobular emphysema, even in the absence of smoking. Among Caucasians, alpha1-antitrypsin deficiency is one of the most common genetically linked lethal diseases. COPD may also result from gene–environment interactions (GOLD, 2019). People who are genetically susceptible are sensitive to environmental factors (e.g., smoking, air pollution, infectious agents, allergens) and eventually develop chronic obstructive symptoms. Carriers must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease. Genetic counseling should be offered. Alpha-protease inhibitor replacement therapy, which slows the progression of the disease, is available for patients with this genetic defect and for those with severe disease. However, this infusion therapy is costly and is required on an ongoing basis.

Other genetic risk factors may predispose a patient to COPD. Work is ongoing to identify specific variants of genes hypothesized to be involved in the development of COPD. These may include specific phenotypes to several chromosomal regions in families with multiple members developing early-onset COPD (see Chapter 17, Chart 17-8).

Age is often identified as a risk factor for COPD, but it is unclear whether healthy aging is an independent risk or whether the risk is related to cumulative exposures to risks over time (GOLD, 2019). There is a strong inverse relationship between COPD and lower socioeconomic status. However, perhaps it is not the lower socioeconomic status but how the socioeconomic status places the person at risk for increased patterns of exposure (indoor and outdoor pollutants, crowding, poor nutrition, infections, and increased smoking).

Clinical Manifestations

Although the natural history of COPD is variable, it is generally a progressive disease characterized by three primary symptoms: chronic cough, sputum production, and dyspnea (GOLD, 2019). These symptoms often worsen over time. Chronic cough and sputum production often precede the development of airflow limitation by many years. However, not all people with cough and sputum production develop COPD. The cough may be intermittent and may be unproductive in some patients (GOLD, 2019). Dyspnea may be severe and interfere with the patient’s activities and quality of life. It is usually progressive, worse with exercise, and persistent. As COPD progresses, dyspnea may occur at rest. Weight loss is common, because dyspnea interferes with eating and the work of breathing is energy depleting. As the work of breathing increases over time, the accessory muscles are recruited in an effort to breathe. Patients with COPD are at risk for respiratory insufficiency and respiratory infections or COPD exacerbation, which in turn increase the risk of acute and chronic respiratory failure.

In patients 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 (due to hyperinflation) and from loss of lung elasticity (Fig. 20-3). Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward (Fig. 20-4). In advanced emphysema, the abdominal muscles may also contract on inspiration.There are systemic or extrapulmonary manifestations of COPD. These include musculoskeletal wasting (see Chapter 4 for discussion of nutrition assessment and Chapters 39 and 40 for discussion of nutrition therapy), metabolic disturbances, and depression (a frequent comorbidity that accompanies chronic debilitating illnesses). These clinical manifestations beyond the lungs must also be assessed and treated in order to decrease the morbidity and improve the quality of life of the patient with COPD. For example, research has indicated that depression, metabolic syndrome, and diabetes are frequent comorbidities of COPD (Raherison, Ouaalaya, Bernady, et al., 2018). It is speculated that measures to promote healthy eating and activity that may ameliorate metabolic syndrome, diabetes, and depression may also deter the development of COPD.

Assessment and Diagnostic Findings

The nurse obtains a thorough health history from patients with known or potential COPD. Chart 20-2 lists the key factors to assess for patients with known or suspected COPD. Pulmonary function studies are used to help confirm the diagnosis of COPD, determine disease severity, and monitor disease progression. Spirometry is used to evaluate airflow obstruction, which is determined by the ratio of FEV1 to forced vital capacity (FVC). Spirometric results are expressed as an absolute volume and as a percentage of the predicted value using appropriate normal values for gender, age, and height. With obstruction, the patient either has difficulty exhaling or cannot forcibly exhale air from the lungs, reducing the FEV1. Spirometry is also used to determine reversibility of obstruction after the use of bronchodilators (GOLD, 2019). Spirometry is initially performed, the patient is given an inhaled bronchodilator treatment according to a standard protocol, and then spirometry is repeated. The patient demonstrates a degree of reversibility if the pulmonary function values improve after administration of the bronchodilator.Arterial blood gas measurements may also be obtained to assess baseline oxygenation and gas exchange and are especially important in advanced COPD. A chest x-ray may be obtained to exclude alternative diagnoses. A computed tomography (CT) chest scan is not routinely obtained in the diagnosis of COPD, but a high-resolution CT scan may help in the differential diagnosis. Screening for alpha1-antitrypsin deficiency is suggested for all adults who are symptomatic, especially for patients younger than 45 years. Screening in young adults is important for those with a family history of COPD, particularly if they have a family history of blood relatives with alpha1-antitrypsin deficiency or COPD that is primarily emphysematous in nature (Han et al., 2018).

COPD is classified into four grades depending on the severity measured by pulmonary function tests, as shown in Table 20-1 (GOLD, 2019). However, pulmonary function is not the only way to assess or classify COPD; pulmonary function is evaluated in conjunction with symptoms, health status impairment with COPD, and the potential for exacerbations. Factors that determine the clinical course and survival of patients with COPD include history of cigarette smoking, exposure to secondhand smoke, age, rate of decline of FEV1, hypoxemia, pulmonary artery pressure, resting heart rate, weight loss, reversibility of airflow obstruction, and comorbidities.

In diagnosing COPD, several differential diagnoses must be ruled out. The primary differential diagnosis is asthma. It may be difficult to differentiate between a patient 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 (GOLD, 2019). Key factors in determining the diagnosis are the patient’s history, severity of symptoms, and responsiveness to bronchodilators.

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TABLE 20-1

Grades of Chronic Obstructive Pulmonary Disease

Grade

Severity

Pulmonary Function

Grade I

Mild

FEV1/FVC <70%

FEV1 ≥80% predicted

Grade II

Moderate

FEV1/FVC <70%

FEV1 50–79% predicted

Grade III

Severe

FEV1/FVC <70%

FEV1 30–49% predicted

Grade IV

Very severe

FEV1/FVC <70%

FEV1 <30% predicted

FEV1, forced expiratory volume in 1 s; FVC, forced vital capacity.

Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2019). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved on 06/23/2019 at: www.goldcopd.org/wp-content/uploads/2018/11/GOLD-2019-v1.7-FINAL-14Nov2018-WMS.pdf

Complications

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 arterial blood gas values, comorbid conditions, and the severity of other complications of COPD. Respiratory insufficiency and failure may be chronic (with severe COPD) or acute (with severe bronchospasm or pneumonia in a patient with severe COPD). Acute respiratory insufficiency and failure may necessitate ventilatory support until other acute complications, such as infection, can be treated. (See Chapter 19 for the management of the patient requiring ventilatory support.) Other complications of COPD include pneumonia, chronic atelectasis, pneumothorax, and pulmonary arterial hypertension (cor pulmonale).

Medical Management

Therapeutic strategies for the patient with COPD include promoting smoking cessation as appropriate, providing supplemental oxygen therapy as indicated, prescribing medications, and managing exacerbations. Some patients may benefit from surgical interventions; whereas others with advanced COPD may benefit from palliative care.

Risk Reduction

For patients with stable disease, treatment aims to reduce risk and symptoms. The major risk factor associated with COPD is environmental exposure and it is modifiable. The most important environmental exposure is smoking. In 2017, over 34 million people in the United States reported that they were active smokers (CDC, 2018b). Smoking kills more than 480,000 people each year and costs the nation more than $300 billion in health care expenses and lost productivity annually (CDC, 2019a; CDC, 2019b). Smoking cessation is the single most cost-effective intervention to reduce the risk of developing COPD and to stop its progression (GOLD, 2019). However, smoking cessation is difficult to achieve and even more difficult to sustain in the long term. Factors associated with continued smoking vary among patients and may include the strength of the nicotine addiction, continued exposure to smoking-associated stimuli (at work or in social settings), stress, depression, and habit.

Because multiple factors are associated with continued smoking, successful cessation often requires multiple strategies. Health care providers should promote cessation by explaining the risks of smoking and personalizing the “at-risk” message to the patient. After giving a strong warning about smoking, health care providers should work with the patient to set a definite “quit date.” Referral to a smoking cessation program may be helpful. Follow-up within 3 to 5 days after the quit date to review progress and to address any problems is associated with an increased rate of success; this should be repeated as needed. Continued reinforcement with a modality that is individualized to the patient and the patient’s lifestyle (e.g., telephone calls, texting, e-mail, or clinic visits) is beneficial. Relapses should be analyzed, and the patient and health care provider should jointly identify possible solutions to prevent future backsliding. It is important to emphasize successes rather than failures. Nicotine replacement—a first-line pharmacotherapy that reliably increases long-term smoking abstinence rates—comes in a variety of forms (gum, inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge). Bupropion SR and nortriptyline, both antidepressants, may also increase long-term quit rates. Other pharmacologic agents include the antihypertensive agent clonidine; however, its side effects limit its use. Varenicline, a nicotinic acetylcholine receptor partial agonist, may assist in smoking cessation (GOLD, 2019). Patients who are not appropriate candidates for such pharmacotherapy include those with medical contraindications, light smokers (fewer than 10 cigarettes per day), pregnant women, and adolescent smokers.

Smoking cessation can begin in a variety of health care settings—outpatient clinic, nursing center, pulmonary rehabilitation center, community, hospital, and in the home. Regardless of the setting, nurses have the opportunity to educate patients about the risks of smoking and the benefits of smoking cessation. Various materials, resources, and programs developed by several organizations (e.g., AHRQ, CDC, National Cancer Institute, American Lung Association, American Cancer Society) are available to assist with this effort.

General Principles of Oxygen Therapy

Oxygen therapy is the administration of oxygen at a concentration greater than that found in the environmental atmosphere. At sea level, the concentration of oxygen in room air is 21%. The goal of oxygen therapy is to provide adequate transport of oxygen in the blood while decreasing the work of breathing and reducing stress on the myocardium.

Oxygen transport to tissues depends on factors such as cardiac output, arterial oxygen content, concentration of hemoglobin, and metabolic requirements. These factors must be kept in mind when oxygen therapy is considered for use in all patients, regardless of underlying disorders.

Indications

A change in the patient’s respiratory rate or pattern may be one of the earliest indicators of the need for oxygen therapy. These changes may result from hypoxemia or hypoxia. Hypoxemia, a decrease in the arterial oxygen tension in the blood, is manifested by changes in mental status (progressing through impaired judgment, agitation, disorientation, confusion, lethargy, and coma), dyspnea, increase in blood pressure, changes in heart rate, arrhythmias, central cyanosis (late sign), diaphoresis, and cool extremities. Hypoxemia usually leads to hypoxia, a decrease in oxygen supply to the tissues and cells that can also be caused by problems outside the respiratory system. Severe hypoxia can be life-threatening.

The signs and symptoms signaling the need for supplemental oxygen may depend on how suddenly this need develops. With rapidly developing hypoxia, changes occur in the central nervous system because the neurologic centers are very sensitive to oxygen deprivation. The clinical picture may resemble that of alcohol intoxication, with the patient exhibiting lack of coordination and impaired judgment. With long-standing hypoxia (as seen in patients with COPD as well as in patients with chronic heart failure), fatigue, drowsiness, apathy, inattentiveness, and delayed reaction time may occur. The need for oxygen is assessed by arterial blood gas analysis, pulse oximetry, and clinical evaluation.

Complications

Oxygen is a medication, and except in emergency situations it is given only when prescribed by a health care provider. As with other medications, the nurse administers oxygen with caution and carefully assesses its effects on each patient.

In general, a patient with any type of respiratory disorder is given oxygen therapy only to increase the partial pressure of arterial oxygen (PaO2) back to the patient’s normal baseline, which may vary from 60 to 95 mm Hg. In terms of the oxyhemoglobin dissociation curve (see Chapter 17), arterial hemoglobin at these levels is 80% to 98% saturated with oxygen; higher fraction of inspired oxygen (FiO2) flow values add no further significant amounts of oxygen to the red blood cells or plasma. Instead of helping, increased amounts of oxygen may produce toxic effects on the lungs and central nervous system or may depress ventilation, which is a particularly lethal adverse effect in patients with COPD (see later discussion).

It is important to observe for subtle indicators of inadequate oxygenation when oxygen is given by any method. Therefore, the nurse assesses the patient frequently for confusion, restlessness progressing to lethargy, diaphoresis, pallor, tachycardia, tachypnea, and hypertension. Intermittent or continuous pulse oximetry is used to monitor oxygen levels.

Oxygen toxicity may occur when too high concentration of oxygen is given for an extended period (generally longer than 24 hours) (Kacmarek, Stoller, & Heuer, 2017). It is caused by overproduction of oxygen free radicals, which are by-products of cell metabolism. These free radicals then mediate a severe inflammatory response that can severely damage the alveolar capillary membrane leading to pulmonary edema and progressing to cell death. Clinical manifestations of oxygen toxicity causing lung damage are similar to acute respiratory distress syndrome (ARDS) (see Chapter 19).

Signs and symptoms of oxygen toxicity include substernal discomfort, paresthesias, dyspnea, restlessness, fatigue, malaise, progressive respiratory difficulty, refractory hypoxemia, alveolar atelectasis, and alveolar infiltrates evident on chest x-rays.

Using the lowest amount of oxygen needed to maintain an acceptable PaO2 level and treating the underlying condition aids in the prevention of oxygen toxicity (Kacmarek et al., 2017).

An additional adverse effect of the administration of high concentrations of oxygen (greater than 50%) to patients who are sedated and breathing small tidal volumes of air (volume of air inspired and expired with each breath) is absorption atelectasis. Normally, 79% of room air is comprised of nitrogen. During inhalation, nitrogen, in addition to other gases, fills the alveoli and helps keep the alveoli open. With the administration of high concentrations of oxygen, nitrogen is diluted and replaced with oxygen. Oxygen in the alveoli is absorbed quickly into the bloodstream and not replaced rapidly enough in the alveoli to maintain patency. The alveoli collapse, causing atelectasis (Kacmarek et al., 2017).

Because oxygen supports combustion, there is always a danger of fire when it is used. It is important to post “No Smoking” signs when oxygen is in use. Oxygen therapy equipment is also a potential source of bacterial contamination; therefore, the nurse (or respiratory therapist) changes the tubing according to infection prevention policy, manufacturer’s recommendations, and the type of oxygen delivery equipment.

Gerontologic Considerations

The respiratory system changes throughout the aging process, and it is important for nurses to be aware of these changes when assessing older adult patients who are receiving oxygen therapy. As the respiratory muscles weaken and the large bronchi and alveoli become enlarged, the available surface area of the lungs decreases, resulting in reduced ventilation and respiratory gas exchange. The number of functional cilia is also reduced, decreasing ciliary action and the cough reflex. As a result of osteoporosis and calcification of the costal cartilages, chest wall compliance is decreased. Patients may display increased chest rigidity and respiratory rate and decreased PaO2 and lung expansion. The older adult is at risk for aspiration and infection related to these changes. In addition, patient education regarding adequate nutrition is essential because appropriate dietary intake can help diminish the excess buildup of carbon dioxide and maintain optimal respiratory functioning (Meiner & Yeager, 2019).

Methods of Oxygen Administration

Oxygen is dispensed from a cylinder or a piped-in system. A reduction gauge is necessary to reduce the pressure to a working level, and a flow meter regulates the flow of oxygen in liters per minute (L/min). When oxygen is used at high flow rates, it should be moistened by passing it through a humidification system to prevent it from drying the mucous membranes of the respiratory tract.

The use of oxygen concentrators is another means of providing varying amounts of oxygen, especially in the home setting. These devices are relatively portable, easy to operate, and cost-effective but require more maintenance than tank or liquid systems. These models can deliver oxygen flows from 1 to 10 L/min and provide an FiO2 of about 40% (Cairo, 2018).

Many different oxygen devices are used (Table 20-2). The amount of oxygen delivered is expressed as a percentage concentration (e.g., 70%). The appropriate form of oxygen therapy is best determined by arterial blood gas levels (see Chapter 10), which indicate the patient’s oxygenation status.

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TABLE 20-2

Oxygen Administration Devices

Device Suggested Flow Rate (L/min) O2 Percentage Setting Advantages Disadvantages

Low-Flow Systems

Cannula (nasal and reservoir)

1–2

3–5

6

24–28

32–40

44

Lightweight, comfortable, inexpensive, continuous use with meals and activity

Easily dislodged, from nares, skin breakdown over ears or nares, nasal mucosal and/or pharyngeal mucosal drying, air swallowing, variable FiO2

Nasal (oropharyngeal) catheter

1–6

24–44

Inexpensive, does not require a tracheostomy

Nasal mucosa irritation; catheter should be changed frequently to alternate nostril

Mask, simple

5–8

40–60

Simple to use, inexpensive

Poorly fitting, variable FiO2, must remove to eat

Mask, partial rebreathing

8–11

50–75

Moderate O2 concentration

Warm, poorly fitting, must remove to eat

Mask, nonrebreathing

10–15

80–95

High O2 concentration

Poorly fitting, must remove to eat

High-Flow Systems

Mask, Venturi

4–6

6–8

24, 26, 28

30, 35, 40

Provides low levels of supplemental O2

Precise FiO2, additional humidity available

Must remove to eat

Transtracheal oxygen catheter

¼–4

60–100

More comfortable than other high-flow systems, concealed by clothing, less oxygen liters per minute needed than nasal cannula

Requires frequent and regular cleaning, requires surgical intervention, with associated risk for surgical complications

Mask, aerosol

8–10

28–100

Good humidity, accurate FiO2

Uncomfortable for some

Tracheostomy collar

8–10

28–100

Good humidity, comfortable, fairly accurate FiO2

Requires surgery to place; needs cleaning and suctioning to maintain patency of airway

T-piece

8–10

28–100

Same as tracheostomy collar

Heavy with tubing; no need for surgery for placement

Face tent

8–10

28–100

Good humidity, fairly accurate FiO2

Bulky and cumbersome

Oxygen-Conserving Devices

Pulse dose (or demand)

10–40 mL/breath

Deliver O2 only on inspiration, conserve 50–75% of O2 used

Must carefully evaluate function individually

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Oxygen delivery systems are classified as low-flow systems (variable performance) or high-flow systems (fixed performance). Low-flow systems contribute partially to the inspired gas the patient breathes, which means that the patient breathes some room air along with the oxygen. These systems do not provide a constant or precise concentration of inspired oxygen. The amount of inspired oxygen changes as the patient’s breathing changes. High-flow systems provide the total inspired air. A specific percentage of oxygen is delivered independent of the patient’s breathing. High-flow systems are indicated for patients who require a constant and precise amount of oxygen (Cairo, 2018).

A nasal cannula is used when the patient requires a low to medium concentration of oxygen for which precise accuracy is not essential. This method allows the patient to move about in bed, talk, cough, and eat without interrupting oxygen flow. Although a nasal cannula can deliver up to 6 L/min, flow rates in excess of 4 L/min may lead to swallowing of air or may cause irritation and drying of the nasal and pharyngeal mucosa.

A reservoir cannula stores oxygen in a thin membrane during exhalation. When the patient’s inspiration exceeds the flow rate into the cannula, the patient receives additional gas from the reservoir membrane. This reduces oxygen use because the patient can achieve adequate oxygenation with a lower flow rate than what would be used with a nasal cannula. The patient must exhale through the nose to reopen the reservoir. Any condition, such as pursed lipped breathing, that prevents nasal exhalation would limit the effectiveness of the device.

The nasal (oropharyngeal) catheter delivers low to moderate concentrations of oxygen and is rarely used. This method of delivering low-flow oxygen is usually reserved for use in special procedures, such as those that examine the patient’s airways and lungs (bronchoscopy). When used during long procedures, the catheter should be changed frequently (e.g., every 8 hours), alternating nostrils to prevent nasal irritation and infection.

When oxygen is given via cannula or catheter, the percentage of oxygen reaching the lungs varies with the depth, rate, and technique of respirations. Anatomic occlusions in the nasal cavity, swollen nasal mucosa, and mouth breathing are examples of conditions that would alter the amount of gas the patient inhales.

Oxygen masks come in several forms. Each is used for different purposes (see Table 20-2). Simple masks, low-flow design, are used to administer low to moderate concentrations of oxygen. The body of the mask itself gathers and stores oxygen between breaths. The patient exhales directly through openings or ports in the body of the mask. If oxygen flow ceases, the patient can draw air in through these openings around the mask edges. Although widely used, these masks cannot be used for controlled oxygen concentrations and must be adjusted for proper fit. They should not press too tightly against the skin, because this can cause a sense of claustrophobia as well as skin breakdown; adjustable elastic bands are provided to ensure comfort and security.

Partial rebreathing masks have a reservoir bag that must remain inflated during both inspiration and expiration. The nurse adjusts the oxygen flow to ensure that the bag does not collapse during inhalation. A moderate concentration of oxygen can be delivered because both the mask and the bag serve as reservoirs for oxygen. Oxygen enters the mask through small-bore tubing that connects at the junction of the mask and bag. As the patient inhales, gas is drawn from the mask, from the bag, and potentially from room air through the exhalation ports. As the patient exhales, the first third of the exhalation fills the reservoir bag. This is mainly dead space and does not participate in gas exchange in the lungs. Therefore, it has a high oxygen concentration. The remainder of the exhaled gas is vented through the exhalation ports. The actual percentage of oxygen delivered is influenced by the patient’s ventilatory pattern (Kacmarek et al., 2017).

Nonrebreathing masks are similar in design to partial rebreathing masks except that they have additional valves. A one-way valve located between the reservoir bag and the base of the mask allows gas from the reservoir bag to enter the mask on inhalation but prevents gas in the mask from flowing back into the reservoir bag during exhalation. One-way valves located at the exhalation ports prevent room air from entering the mask during inhalation. They also allow the patient’s exhaled gases to exit the mask on exhalation. As with the partial rebreathing mask, it is important to adjust the oxygen flow so that the reservoir bag does not completely collapse on inspiration. In theory, if the nonrebreathing mask fits the patient snugly and both side exhalation ports have one-way valves, it is possible for the patient to receive 100% oxygen, making the nonrebreathing mask a high-flow oxygen system. However, because it is difficult to get an exact fit from the mask on every patient, and some nonrebreathing masks have only one one-way exhalation valves, it is almost impossible to ensure 100% oxygen delivery, making it a low-flow oxygen system.

The Venturi mask is the most reliable and accurate method for delivering precise concentrations of oxygen through noninvasive means. The mask is constructed in a way that allows a constant flow of room air blended with a fixed flow of oxygen. It is used primarily for patients with COPD because it can accurately provide appropriate levels of supplemental oxygen, thus avoiding the risk of suppressing the hypoxic drive.

The Venturi mask uses the Bernoulli principle of air entrainment (trapping the air like a vacuum), which provides a high airflow with controlled oxygen enrichment. For each liter of oxygen that passes through a jet orifice, a fixed proportion of room air is entrained. Varying the size of the jet orifice and adjusting the flow of oxygen can deliver a precise volume of oxygen. Excess gas leaves the mask through the two exhalation ports, carrying with it the exhaled carbon dioxide. This method allows a constant oxygen concentration to be inhaled regardless of the depth or rate of respiration.

The mask should fit snugly enough to prevent oxygen from flowing into the patient’s eyes. The nurse checks the patient’s skin for irritation. It is necessary to remove the mask so that the patient can eat, drink, and take medications, at which time supplemental oxygen is provided through a nasal cannula.The transtracheal oxygen catheter requires minor surgery to insert a catheter through a small incision directly into the trachea. It is indicated for patients with chronic oxygen therapy needs. These catheters are more comfortable, less dependent on breathing patterns, and less obvious than other oxygen delivery methods. Because no oxygen is lost into the surrounding environment, the patient achieves adequate oxygenation at lower rates, making this method less expensive and more efficient.

Other oxygen devices include aerosol masks, tracheostomy collars (see Table 20-2), T-pieces, and face tents, all of which are used with aerosol devices (nebulizers) that can be adjusted for oxygen concentrations from 28% to 100% (0.28 to 1.00). If the gas mixture flow falls below patient demand, room air is pulled in, diluting the concentration. The aerosol mist must be available for the patient during the entire inspiratory phase.

Specific Considerations for the Patient with COPD Receiving Oxygen Therapy

Oxygen therapy can be given as long-term continuous therapy, during exercise, or to prevent acute dyspnea during an exacerbation (see later discussion). The goal of supplemental oxygen therapy in the patient with COPD is to increase the baseline resting partial pressure of arterial oxygen (PaO2) to at least 60 mm Hg at sea level, which corresponds with an arterial oxygen saturation (SaO2) of 90% (GOLD, 2019). Long-term oxygen therapy (more than 15 hours per day) has also been shown to improve quality of life, reduce pulmonary arterial pressure and dyspnea, and improve survival (GOLD, 2019). Long-term oxygen therapy is usually introduced in very severe COPD, and indications generally include a PaO2 of 55 mm Hg or less or SaO2 at or below 88% (GOLD, 2019). Other indications for long-term oxygen therapy include evidence of tissue hypoxia and organ damage such as cor pulmonale, secondary polycythemia, edema from right-sided heart failure, or impaired mental status (GOLD, 2019). For patients with exercise-induced hypoxemia, oxygen supplementation during exercise may improve dyspnea but will not diminish breathlessness in daily life (GOLD, 2019). Patients who are hypoxemic while awake are likely to be so during sleep. Therefore, nighttime oxygen therapy is recommended as well, and the prescription for oxygen therapy is for continuous, 24-hour use. Intermittent oxygen therapy is indicated for patients who desaturate (i.e., experience a precipitous drop in hemoglobin molecule saturation with oxygen) only during activities of daily living, exercise, or sleep.

The main objective in treating patients with hypoxemia and hypercapnia is to give sufficient oxygen to improve oxygenation. Patients with COPD who require oxygen may have respiratory failure that is caused primarily by a ventilation–perfusion mismatch. These patients respond to oxygen therapy and should be treated to keep the resting oxygen saturation at or above 90%, which is associated with a PaO2 of 60 mm Hg or higher (GOLD, 2019). Nursing assessments of a patient with COPD on supplemental oxygen must include monitoring the respiratory rate and the oxygen saturation as measured by pulse oximetry (SpO2) so that the patient has an adequate oxygen saturation (90%) on the lowest liter flow of oxygen (GOLD, 2019).

Administering too much oxygen can result in the retention of carbon dioxide. The high O2 levels can then suppress CO2 chemoreceptors, which in turn would depress the respiratory drive and disrupt ventilation–perfusion balance (Kacmarek et al., 2017). The resulting increased O2 tension in the alveoli causes a ventilation–perfusion mismatch that presents as hypercapnia. Monitoring and assessment are essential in the care of patients with COPD on supplemental oxygen due to complications of oxygen supplementation. Although pulse oximetry is helpful in assessing response to oxygen therapy, it does not assess PaCO2 levels. A SaO2 of 88% or less warrants further evaluation with arterial blood gas analysis (GOLD, 2019). The nurse must evaluate for other factors and medications which could further decrease the respiratory drive—neurologic impairment, fluid and electrolyte issues, and opioids or sedatives.Pharmacologic Therapy

Medication regimens used to manage COPD are based on disease severity. For grade I (mild) COPD, a short-acting bronchodilator may be prescribed. For grade II or III (moderate or severe) COPD, a short-acting bronchodilator and regular treatment with one or more long-acting bronchodilators may be used. For grade III or IV (severe or very severe) COPD, medication therapy includes regular treatment with long-acting bronchodilators and/or inhaled corticosteroids (ICSs) for repeated exacerbations.

Bronchodilators

Bronchodilators are key for symptom management in stable COPD (GOLD, 2019). The choice of bronchodilator depends on availability and individual response in terms of symptom relief and side effects. Long-acting bronchodilators are more convenient for patients to use, and combining bronchodilators with different durations of action and different mechanisms may optimize symptom management (GOLD, 2019). Long-acting bronchodilators are typically used for maintenance treatment for long-term symptom control. Short-acting bronchodilators are usually used for acute management of symptomatic flairs. Even patients who do not show a significant response to a short-acting bronchodilator test may benefit symptomatically from long-term bronchodilator treatment.

Bronchodilators relieve bronchospasm by improving expiratory flow through widening of the airways and promoting lung emptying with each breath. These medications alter smooth muscle tone and reduce airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation. Although regular use of bronchodilators that act primarily on the airway smooth muscle does not modify the decline of function or the prognosis of COPD, their use is central in the management of COPD (GOLD, 2019). These agents can be delivered through a pressurized metered-dose inhaler (pMDI), a dry-powder inhaler (DPI), by a small-volume nebulizer (SVN), or via the oral route in pill or liquid form. Bronchodilators are often given regularly throughout the day as well as on an as-needed basis. They may also be used prophylactically to prevent breathlessness by having the patient use them before participating in or completing an activity, such as eating or walking.

Several devices are available to deliver medication via the inhaled route. These may be categorized as pMDIs, DPIs, or SVNs, as noted previously (Cairo, 2018; Gregory, Elliott, & Dunne, 2013). The choice of an inhaler device will depend on availability, cost, prescribing provider, insurance coverage, and the skills and ability of the patient (GOLD, 2019). Key aspects of each are described in Table 20-3.

Both pMDIs and DPIs are small handheld devices that may be carried in a pocket or purse (Cairo, 2018; D’Urzo, Chapman, Donohue, et al., 2019). Attention to effective drug delivery and training in proper inhaler technique is essential when using a pMDI or DPI. A respiratory therapist is an excellent health care provider to consult on appropriate inhaler technique. Pressurized metered-dose inhalers (pMDIs) include conventional pMDIs or breath-actuated pMDIs; these may also feature spacer or valved-holding chambers (VHCs). They are pressurized devices that contain aerosolized powder of medications. A precise amount of medication is released with each activation of the pMDI canister. A spacer or VHC may also be indicated to enhance deposition of the medication in the lung and help the patient coordinate activation of the pMDI with inspiration. Spacers come in several designs, but all are attached to the pMDI and have a mouthpiece on the opposite end (Fig. 20-5).

All pMDIs are designed so that they require coordination between the patient’s inspiration and the mechanics of the inhaler. In contrast, dry-powder inhalers (DPIs) (see Fig. 20-5) rely solely on the patient’s inspiration for medication delivery. While DPIs still require the user to press a lever or button to dispense the medication, these inhalers do not require the coordination necessary to administer pMDIs.

Because of the significant relationship between poor inhaler technique and lack of symptom control, issues that could affect proper inhaler use must be considered when assessing the effectiveness of these medications (GOLD, 2019). Conditions such as decreased hand–inhalation coordination, insufficient hand strength, and the inability to generate a sufficient inspiratory flow could impair the delivery of the medication, and thus, impair symptom control (D’Urzo et al., 2019). For example, patients with decreased hand–inhalation coordination could fail to exhale prior to administering pMDIs, which would prevent them from inhaling the proper amount of the medication. While DPIs minimize the need for hand–inhalation coordination, patients with severe COPD may not have the ability to generate a sufficient inspiratory flow necessary to deliver the proper dose (D’Urzo et al., 2019).

TABLE 20-3

Aerosol Delivery Devices

Devices/Drugs

Optimal Technique

Therapeutic Issues

Pressurized metered-dose inhaler (pMDI)

Beta-2-adrenergic agonists

Corticosteroids

Anticholinergics

Actuationa during a slow (30 L/min or 3–5 s) deep inhalation, followed by 10-s breath-hold

Slow inhalation and coordination of actuation may be difficult for some patients. Patients may incorrectly stop inhalation at actuation. Deposition of 50–80% of actuated dose in the oropharynx. Mouth washing and spitting is effective in reducing the amount of drug swallowed and absorbed systemically

Breath-actuated pMDI

Beta-2-adrenergic agonists

Tight seal around mouthpiece and slightly more rapid inhalation than standard pMDI (see above) followed by 10-s breath-hold

May be particularly useful for patients unable to coordinate inhalation and actuation. May also be useful for older patients. Patients may incorrectly stop inhalation at actuation. Cannot be used with currently available spacer/valved-holding chamber (VHC) devices

Spacer or VHC

(Note—this is an accessory to a pMDI)

Slow (30 L/min or 3–5 s) deep inhalation, followed by 10-s breath-hold immediately following actuation. Actuate only once into spacer/VHC per inhalation. Rinse plastic VHCs once a month with low concentration of liquid household dishwashing detergent (1:5000 or 1–2 drops per cup of water) and let drip dry

Indicated for patients who have difficulty performing adequate pMDI technique. May be bulky. Simple tubes do not obviate coordinating actuation and inhalation. VHCs are preferred. Spacers or VHCs may increase delivery of inhalational corticosteroids to the lungs

Dry-powder inhaler (DPI)

Beta-2-adrenergic agonists

Corticosteroids

Anticholinergics

Rapid (1–2 s) deep inhalation. Minimally effective inspiratory flow is device dependent

Dose is lost if patient exhales through device after actuating. Delivery may be greater or lesser than pMDIs, depending on device and technique. Delivery is more flow dependent in devices with highest internal resistance. Rapid inhalation promotes greater deposition in larger central airways. Mouth washing and spitting are effective in reducing amount of drug swallowed and absorbed systemically

Small-volume nebulizer (SVN)

Beta-2-adrenergic agonists

Corticosteroids

Anticholinergics

Slow tidal breathing with occasional deep breaths. Tightly fitting facemask for those unable to use mouthpiece

Less dependent on patient’s coordination and cooperation.

May be expensive, time-consuming, and bulky; output depends on device and operating parameters (fill volume, driving gas flow); internebulizer and intranebulizer output variances are significant. The use of a facemask reduces delivery to lungs by 50%. Choice of delivery system depends on resources, availability, and clinical judgment of clinician caring for patient.

There is potential for infections if device is not cleaned properlyThe small-volume nebulizer (SVN) is a handheld apparatus that is easier to use than a pMDI or a DPI but lacks the convenience of these inhalers as it requires a power source in order to operate. Common SVNs include single-use pneumatic jet nebulizers with reservoir tubes, which are most commonly used in hospitals, and electronic nebulizers, which may be used in the home-based setting (Gregory et al., 2013). SVNs are commonly prescribed when patients are challenged with being able to administer their medications through either a pMDI or a DPI; some reasons why this might happen have been described previously (Cairo, 2018). The SVN may also be a preferred option to other inhalers because the nebulized particles in an SVN are smaller and can better penetrate the airways. Diaphragmatic breathing (see later discussion under “Breathing Retraining”) is a helpful technique to prepare for proper use of the SVN.

Several classes of bronchodilators are used that include beta-adrenergic agonists, muscarinic antagonists (anticholinergics) and combination agents. Beta-adrenergic agonists include short-acting beta-2-adrenergic agonists (SABAs) and long-acting beta-2 adrenergic agonists (LABAs). The anticholinergic agents include short-acting muscarinic antagonists (SAMAs) and long-acting muscarinic antagonists (LAMAs) (GOLD, 2018; GOLD, 2019). ICSs may also be combined with bronchodilators. These medications may be used in combination to optimize bronchodilation. LABA bronchodilators are more convenient for patient use as compared to short-acting beta2-agonist bronchodilators. Examples of these medications are described in Table 20-4.

Fixed dose combinations of LABAs and LAMAs have become the foundation for treating COPD (D’Urzo et al., 2019). Combining these classes of medications in one inhaler has synergistic effects, so that the dosages of each medication may be lesser than if they were each administered separately (i.e., as monotherapy), without diminishing their effectiveness (GOLD, 2019). Furthermore, combination therapy is associated with less adverse reactions and promotes proper medication administration by avoiding the use of multiple inhaler devices (GOLD, 2019).

Corticosteroids

Although inhaled and systemic corticosteroids may improve the symptoms of COPD, they do not slow the decline in lung function. A short trial course of oral corticosteroids may be prescribed for patients to determine whether pulmonary function improves and symptoms decrease. Long-term treatment with oral corticosteroids is not recommended in COPD and can cause steroid myopathy, leading to muscle weakness, decreased ability to function, and, in advanced disease, respiratory failure (GOLD, 2019). ICSs are frequently prescribed in COPD.

Treatment of COPD with combination long-term beta2-agonists plus corticosteroids in one inhaler may improve lung function (GOLD, 2018). Examples of these medications include formoterol/budesonide, vilanterol/fluticasone furoate, and salmeterol/fluticasone.

Other Medications

Other pharmacologic treatments that may be used in COPD include alpha1-antitrypsin augmentation therapy, antibiotic agents, mucolytic agents, antitussive agents, vasodilators, and opioids. Vaccines are also effective in that they prevent exacerbations by thwarting respiratory infections. For instance, influenza vaccines can reduce serious illness and death in patients with COPD (GOLD, 2019). It is recommended that people limit their risk through influenza vaccination and smoking cessation. Pneumococcal vaccination also reduces the incidence of community-acquired pneumonia in the general older adult population (GOLD, 2019).

Management of Exacerbations

An exacerbation of COPD is defined as an event in the natural course of the disease characterized by acute changes (worsening) in the patient’s respiratory symptoms beyond the normal day-to-day variations. An exacerbation also leads to change in medication (GOLD, 2019). During an exacerbation, there is increased dyspnea that is a result of amplified hyperinflation and air trapping (GOLD, 2019). Primary causes of an acute exacerbation are usually related to viral infections, particularly human rhinovirus (i.e., the common cold). However, bacterial infections and environmental factors have also been linked to the development of acute exacerbations (GOLD, 2019). Roflumilast may be used as a treatment to reduce the risk of exacerbations in patients with severe COPD associated with chronic bronchitis and a history of exacerbations. Roflumilast is a selective phosphodiesterase-4 (PDE4) inhibitor and is taken as a tablet once daily.Treatment of an exacerbation requires identifying the primary cause (if possible) and administering the specific treatment. Optimization of bronchodilator medications is first-line therapy and involves identifying the best medication or combinations of medications taken on a regular schedule for a specific patient. Depending on the signs and symptoms, corticosteroids, antibiotic agents, oxygen therapy, and intensive respiratory interventions may also be used. The GOLD (2019) guidelines provide indications for assessment, hospital admission, and possible critical-care admission for patients with exacerbations of COPD. Indications for hospitalization include marked increase in intensity of symptoms, severe underlying COPD, onset of new physical signs (e.g., the use of accessory muscles, paradoxical chest wall movement, worsening or new onset of central cyanosis, peripheral edema, signs of right heart failure, reduced alertness), failure to respond to initial medical management, older age, and insufficient home support. Patients requiring hospitalization for an exacerbation would exhibit severe dyspnea that does not respond adequately to initial therapy, confusion or lethargy, respiratory muscle fatigue, paradoxical chest wall movement, peripheral edema, worsening or new onset of central cyanosis, persistent or worsening hypoxemia, and the need for noninvasive or invasive assisted mechanical ventilation (GOLD, 2019). The outcome from an exacerbation of COPD is closely related to the development of respiratory acidosis, the presence of significant comorbidities, and the need for noninvasive or invasive positive pressure ventilatory support.

When the patient with an exacerbation of COPD arrives in an ED, the first line of treatment is supplemental oxygen therapy and rapid assessment to determine if the exacerbation is life-threatening (GOLD, 2019). A short-acting inhaled bronchodilator may be used to assess response to treatment. Oral or intravenous (IV) corticosteroids, in addition to bronchodilators, are recommended in the hospital management of a COPD exacerbation. The administration of antibiotics remains controversial, but in general, they should be administered when the patient has three cardinal symptoms of an exacerbation: increase in dyspnea, increase in sputum volume, and sputum purulence (GOLD, 2019).

Surgical Management

Surgical options might be appropriate for patients who do not demonstrate symptom improvement with nonsurgical therapies.

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Bullectomy

A bullectomy is a surgical option for select patients with bullous emphysema. Bullae are enlarged airspaces that do not contribute to ventilation but occupy space in the thorax; these areas may be surgically excised. These bullae compress areas of the lung and may impair gas exchange. Bullectomy may help reduce dyspnea and improve lung function. It can be performed via a video-assisted thoracoscope or a limited thoracotomy incision (GOLD, 2019).

Lung Volume Reduction Surgery

Treatment options for patients with advanced or end-stage COPD (grade IV) with a primary emphysematous component are limited, although lung volume reduction surgery is a palliative surgical option. This includes patients with homogenous disease or disease that is focused in one area and not widespread throughout the lungs. Lung volume reduction surgery involves the removal of a portion of the diseased lung parenchyma. This reduces hyperinflation and allows the functional tissue to expand, resulting in improved elastic recoil of the lung and improved chest wall and diaphragmatic mechanics. This type of surgery does not cure the disease but may improve health status, exercise tolerance, and the patient’s overall quality of life (GOLD, 2019).

Bronchoscopic lung volume reduction therapies are under investigation in clinical research protocols. These bronchoscopic procedures were developed to collapse areas of emphysematous lung and thus improve aeration of the functional lung tissue. Techniques include endobronchial placement of a one-way valve that allows air and mucus to exit the treated area but does not allow air to reenter. Another technique achieves biologic lung volume reduction through bronchoscopic instillation of nitinol coils into the airway of the hyperinflated lung tissue of patients with advanced emphysema. Because air can no longer enter the airway, the lung tissue beyond the sealed airway collapses over time. Patients receiving this procedure reported increased quality of life. However, there is insufficient evidence to determine the benefit–risk ratios, cost-effectiveness, and possible roles of these procedures in care of the patient with severe emphysema (GOLD, 2019).

Lung Transplantation

Lung transplantation is a viable option for definitive surgical treatment of severe COPD in select patients. It has been shown to improve quality of life and functional capacity in some patients with COPD. Limited not only by the shortage of donor organs, it is also a costly procedure with financial implications for months to years because of complications and the need for costly immunosuppressive medication regimens (GOLD, 2019).

Pulmonary Rehabilitation

Pulmonary rehabilitation, one of the most cost-effective treatment strategies, is a holistic intervention aimed at improving physical and psychological health of patients with COPD (GOLD, 2019). The primary goals of rehabilitation are to reduce symptoms, improve quality of life, and increase physical and emotional participation in everyday activities (GOLD, 2019). The benefits of this therapy include improvement of exercise capacity, reduction in the perceived intensity of breathlessness, improvement in health-related quality of life, reduction in the number of hospitalizations and days in the hospital, and reduction in the anxiety and depression associated with COPD (GOLD, 2019). Pulmonary rehabilitation services are multidisciplinary and include assessment, education, smoking cessation, physical reconditioning, nutritional counseling, skills training, and psychological support. Patients are taught methods to alleviate symptoms. Breathing exercises, as well as retraining and exercise programs, are used to improve functional status.

Pulmonary rehabilitation is appropriate for most patients with COPD, particularly those with moderate or severe COPD (GOLD, 2019). Optimum benefits are achieved in programs that are 6 to 8 weeks in length (GOLD, 2019). Programs vary in duration and may be conducted in inpatient, outpatient, or home settings. Program selection depends on the patient’s physical, functional, and psychosocial status; insurance coverage; availability of programs; and preference. Pulmonary rehabilitation may also be used therapeutically in other disorders besides COPD, including asthma, CF, lung cancer, interstitial lung disease, thoracic surgery, and lung transplantation. Despite their proven efficacy, comprehensive programs for patients with moderate to severe COPD are covered by Medicare only for those who meet specific criteria.

Patient Education

Nurses play a key role in identifying potential candidates for pulmonary rehabilitation and in facilitating and reinforcing the material learned in the rehabilitation program. Not all patients have access to a formal rehabilitation program. However, nurses can be instrumental in educating patients and families as well as facilitating specific services, such as respiratory therapy education, physical therapy for exercise and breathing retraining, occupational therapy for conserving energy during activities of daily living, and nutritional counseling. Patient education is a major component of pulmonary rehabilitation and includes a broad variety of topics. (See Chart 20-3, Nursing Research Profile: Managing Anxiety among Patients with Advanced COPD.)

Depending on the length and setting of the educational program, topics may include normal anatomy and physiology of the lung, pathophysiology and changes with COPD, medications and home oxygen therapy, nutrition, respiratory therapy treatments, symptom alleviation, smoking cessation, sexuality and COPD, coping with chronic disease, communicating with the health care team, and planning for the future (advance directives, living wills, informed decision making about health care alternatives). Education, including that relating to smoking cessation, should be incorporated into all aspects of care for COPD and in many settings (primary providers’ offices, clinics, hospitals, home and community health care settings, and comprehensive rehabilitation programs).

Nutritional Therapy

Nutritional assessment and counseling are important for patients with COPD. Nutritional status is reflected in severity of symptoms, degree of disability, and prognosis. Significant weight loss is often a major problem; however, excessive weight can also be problematic, although it occurs less often. Most patients with COPD have difficulty gaining and maintaining weight. A thorough assessment of caloric needs and counseling about meal planning and supplementation is part of the rehabilitation process. Continual monitoring of weight and interventions as necessary are important parts of the care of patients with COPD.Palliative Care

Palliative care is integral for the patient with advanced COPD. Unfortunately, palliative care is often not considered until the disease is far advanced. The overall goals of palliative care are to manage symptoms and improve the quality of life for patients and families with advanced disease (GOLD, 2019). Areas addressed in palliative care include effective and empathetic communication with patients and families; close attention to pain, dyspnea, panic, anxiety, depression and other symptoms; psychosocial, spiritual and bereavement support; and coordination of the wide range of medical and social services required with this disease (GOLD, 2019). Palliative, hospice care, and end-of-life care are fundamental components of treatment for patients with advanced COPD (GOLD, 2019) (see Chapter 13).

An overview of the nursing care of the patient with COPD is provided in Chart 20-4. Additional nursing considerations with regard to assessing the patient with COPD and promoting optimal nursing and collaborative outcomes are specified as follows.

Assessing the Patient

Assessment involves obtaining information about current symptoms as well as previous disease manifestations. See Chart 20-2 for sample questions that may be used to obtain a clear history of the disease process. In addition to the history, the nurse reviews the results of diagnostic tests.

Achieving Airway Clearance

Bronchospasm, which occurs in many pulmonary diseases, reduces the caliber of the small bronchi and may cause dyspnea, static secretions, and infection. Bronchospasm can sometimes be detected on auscultation with a stethoscope when wheezing or diminished breath sounds are heard. Increased mucus production, along with decreased mucociliary action, contributes to further reduction in the caliber of the bronchi and results in decreased airflow and decreased gas exchange. This is further aggravated by the loss of lung elasticity that occurs with COPD (GOLD, 2019). These changes in the airway require that the nurse monitor the patient for dyspnea and hypoxemia. The relief of bronchospasm is confirmed by measuring improvement in expiratory flow rates and volumes (the force of expiration, how long it takes to exhale, and the amount of air exhaled) as well as by assessing the dyspnea and making sure that it has lessened.

Diminishing the quantity and viscosity of sputum can clear the airway and improve pulmonary ventilation and gas exchange. All pulmonary irritants should be eliminated or reduced, particularly cigarette smoke, which is the most persistent source of pulmonary irritation. The nurse instructs the patient in directed or controlled coughing, which is more effective and reduces the fatigue associated with undirected forceful coughing. Directed coughing consists of a slow, maximal inspiration followed by breath-holding for several seconds and then two or three coughs. “Huff” coughing may also be effective. The technique consists of one or two forced exhalations (huffs) from low to medium lung volumes with the glottis open.

Chest physiotherapy (CPT), increased fluid intake, and bland aerosol mists (with normal saline solution or water) may be useful for some patients with COPD. The use of these measures must be based on the response and tolerance of each patient. Chest physiotherapy (CPT) includes postural drainage, chest percussion and vibration, and breathing retraining. The goals of CPT are consistent with improved airway clearance as they are to remove bronchial secretions, improve ventilation, and increase the efficiency of the respiratory muscles.

Postural Drainage (Segmented Bronchial Drainage)

Postural drainage allows the force of gravity to assist in the removal of bronchial secretions. The secretions drain from the affected bronchioles into the bronchi and trachea and are removed by coughing or suctioning. Because the patient usually sits in an upright position, secretions are likely to accumulate in the lower parts of the lungs. Several other positions (Fig. 20-6) are used so that the force of gravity helps move secretions from the smaller bronchial airways to the main bronchi and trachea. Each position contributes to effective drainage of a different lobe of the lungs; lower and middle lobe bronchi drain more effectively when the head is down, whereas the upper lobe bronchi drain more effectively when the head is up. The secretions then are removed by coughing.

The nurse should keep in mind the medical diagnosis, the lung lobes or segments involved, the cardiac status, and any structural deformities of the chest wall and spine. Auscultation of the chest before and after the procedure is used to identify the areas that need drainage and assess the effectiveness of treatment. The nurse educates family members who will assist the patient at home to evaluate breath sounds before and after treatment. The nurse explores strategies that will enable the patient to assume the indicated positions at home. This may require the creative use of objects readily available at home, such as pillows, cushions, or cardboard boxes.

Postural drainage is usually performed two to four times daily, before meals (to prevent nausea, vomiting, and aspiration) and at bedtime. Prescribed bronchodilators, mucolytic agents, water, or saline may be nebulized and inhaled before postural drainage to dilate the bronchioles, reduce bronchospasm, decrease the thickness of mucus and sputum, and combat edema of the bronchial walls. The recommended sequence starts with positions to drain the lower lobes, followed by positions to drain the upper lobes.

The patient is made as comfortable as possible in each position and provided with an emesis basin, sputum cup, and paper tissues. The nurse instructs the patient to remain in each position for 10 to 15 minutes and to breathe in slowly through the nose and out slowly through pursed lips to help keep the airways open so that secretions can drain. If a position cannot be tolerated, the nurse helps the patient assume a modified position. When the patient changes position, instructions for how to cough and remove secretions are provided.

If the patient cannot cough, the nurse may need to suction the secretions mechanically. It also may be necessary to use chest percussion and vibration or a high-frequency chest wall oscillation (HFCWO) vest to loosen bronchial secretions and mucus plugs that adhere to the bronchioles and bronchi and to propel sputum in the direction of gravity drainage (see later discussion). If suctioning is required at home, the nurse instructs caregivers in safe suctioning technique and care of the suctioning equipment.

After the procedure, the nurse or family caregivers note the amount, color, viscosity, and character of the expelled sputum. The nurse evaluates the patient’s skin color and pulse the first few times the procedure is performed. It may be necessary to administer oxygen during postural drainage.

If the sputum is foul smelling, postural drainage is performed in a room away from other patients or family members. Deodorizers may be used to counteract the odor. However, because aerosol sprays can cause bronchospasm and irritation, deodorizers should be used sparingly and with caution. After the procedure, the patient may find it refreshing to brush the teeth and use a mouthwash before resting.

Chest Percussion and Vibration

Thick secretions that are difficult to cough up may be loosened by percussing (tapping) and vibrating the chest or through the use of an HFCWO vest. Chest percussion and vibration help dislodge mucus adhering to the bronchioles and bronchi. A scheduled program of coughing and clearing sputum, together with hydration, reduces the amount of sputum in most patients.

Chest percussion is carried out by cupping the hands and lightly striking the chest wall in a rhythmic fashion over the lung segment to be drained. The wrists are alternately flexed and extended so that the chest is cupped or clapped in a painless manner (Fig. 20-7). A soft cloth or towel may be placed over the segment of the chest that is being cupped to prevent skin irritation and redness from direct contact. Percussion, alternating with vibration, is performed for 3 to 5 minutes for each position. The patient uses diaphragmatic breathing during this procedure to promote relaxation (see later discussion on Breathing Retraining). As a precaution, percussion over chest drainage tubes and the sternum, spine, liver, kidneys, spleen, or breasts (in women) is avoided. Percussion is performed cautiously in older adult patients because of their increased incidence of osteoporosis and risk of rib fracture.

Vibration is the technique of applying manual compression and tremor to the chest wall during the exhalation phase of respiration (see Fig. 20-7). This helps increase the velocity of the air expired from the small airways, thus freeing mucus. After three or four vibrations, the patient is encouraged to cough, contracting the abdominal muscles to increase the effectiveness of the cough.

The number of times the percussion and coughing cycle is repeated depends on the patient’s tolerance and clinical response. The nurse evaluates breath sounds before and after application of these techniques.

An inflatable HFCWO vest (Fig. 20-8) may be used to provide chest therapy. The vest uses air pulses to compress the chest wall 8 to 18 times/sec, causing secretions to detach from the airway wall and enabling the patient to expel them by coughing. Patients prescribed vest therapy are generally more satisfied with this mode of treatment delivery than patients who receive manual CPT. Furthermore, research suggests that the vest is equally effective to manual CPT; however, the mode of therapy selected should consider the patient’s specific needs and preferences (Hanlon, 2015; Powner, Nesmith, Kirkpatrick, et al., 2019). Technologic advances to the HFCWO vest include portable versions, the AffloVest® and Monarch®, which allow users to move about freely during therapy, thus improving patient adherence and satisfaction. In addition, CPT may also be delivered using specialized beds. These beds feature programmable mattresses that deliver vibropercussion and may rotate the upper torso up to 45 degrees to help mobilize pulmonary secretions.

To increase the effectiveness of coughing, a flutter valve may be used, which is especially useful for patients who have CF (see later discussion). The flutter valve looks like a pipe but has a cap covering the bowl, which contains a steel ball. When the patient exhales actively into the device, movement of the ball causes pressure oscillations, thereby decreasing viscosity of the mucus, facilitating mucous clearance (Fig. 20-9).

When performing CPT, the nurse ensures that the patient is comfortable, is not wearing restrictive clothing, and has not just eaten. The nurse gives medication for pain, as prescribed, before applying the techniques of percussion and vibration, splints any incision, and provides pillows for support as needed. The positions are varied, but focus is placed on the affected areas. On completion of the treatment, the nurse assists the patient to assume a comfortable position.

If an HFCWO vest is being used, the patient may assume whatever position is most comfortable and may even continue to perform light activity during therapy, such as household chores (e.g., folding laundry) or engaging in hobbies (e.g., playing the guitar). The patient does not need to assume specific positions for the vest to be effective.

Treatment should be stopped if any of the following occur: increased pain, increased shortness of breath, weakness, lightheadedness, or hemoptysis. Therapy is indicated until the patient has normal respirations, can mobilize secretions, and has normal breath sounds, and until the chest x-ray findings are normal.

Nursing management of the patient using flutter valve therapy includes ensuring that the patient assumes the proper position, educating the patient on the technique for using the flutter valve, and setting realistic goals for the patient.

Improving Breathing Patterns

The breathing pattern of most people with COPD is shallow, rapid, and inefficient; the more severe the disease, the more inefficient the breathing pattern. Impaired breathing patterns and shortness of breath are due to the modified respiratory mechanics of the chest wall and lung resulting from air trapping (i.e., incomplete emptying of alveoli during expiration), ineffective diaphragmatic movement, airway obstruction, the metabolic cost of breathing, and stress. Breathing retraining may help improve breathing patterns. Training in diaphragmatic breathing reduces the respiratory rate, increases alveolar ventilation, and sometimes helps expel as much air as possible during expiration. Pursed-lip breathing helps slow expiration, prevent collapse of small airways, and control the rate and depth of respiration. It also promotes relaxation, which allows patients to gain control of dyspnea and reduce feelings of panic.Breathing Retraining

Breathing retraining consists of exercises and breathing practices that are designed to achieve more efficient and controlled ventilation and to decrease the work of breathing. These exercises promote maximal alveolar inflation and muscle relaxation; relieve anxiety; eliminate ineffective, uncoordinated patterns of respiratory muscle activity; and slow the respiratory rate (Kacmarek et al., 2017). Slow, relaxed, rhythmic breathing also helps to control the anxiety that occurs with dyspnea. Specific breathing exercises include diaphragmatic and pursed-lip breathing (Chart 20-5).

Diaphragmatic breathing can become automatic with sufficient practice and concentration. Pursed-lip breathing, which improves oxygen transport, helps induce a slow, deep breathing pattern and assists the patient to control breathing, even during periods of stress. Breathing exercises should be practiced in several positions because air distribution and pulmonary circulation vary with the position of the chest.

Promoting Self-Care

As gas exchange, airway clearance, and the breathing pattern improve, the patient is encouraged to assume increasing participation in self-care activities. The patient is taught to coordinate diaphragmatic breathing with activities such as walking, bathing, bending, or climbing stairs. The patient should bathe, dress, and take short walks, resting as needed to avoid fatigue and excessive dyspnea. Fluids should always be readily available for the patient to promote adequate hydration. Patient education should address self-regulation of fluid intake. This could include the use of fluid diaries and using premeasured water containers to help patients become more cognizant of their fluid intake.

If management of secretions is a problem and some type of postural drainage or airway clearance maneuver is to be performed at home, the nurse or respiratory therapist instructs and supervises the patient before discharge or in an outpatient setting.

Improving Activity Tolerance

People with COPD have decreased exercise tolerance during specific periods of the day, especially in the morning on arising, because bronchial secretions have collected in the lungs during the night while the patient was lying down. The patient may have difficulty bathing or dressing and may become fatigued. Activities that require the arms to be supported above the level of the thorax may produce fatigue or respiratory distress but may be tolerated better after the patient has been up and moving around for an hour or more. The nurse can help the patient reduce these limitations by planning self-care activities and determining the best times for bathing, dressing, and other daily activities.

Patients with COPD of all grades may benefit from exercise training programs. These benefits may include increased exercise tolerance and decreased dyspnea and fatigue (GOLD, 2019). Physical conditioning techniques include breathing exercises and general exercises intended to conserve energy and increase pulmonary ventilation. Graded exercises and physical conditioning programs using treadmills, stationary bicycles, and measured level walks can improve symptoms and increase work capacity and exercise tolerance. Any physical activity that can be performed regularly is helpful. Walking aids may be beneficial (GOLD, 2019). Lightweight portable oxygen systems are available for ambulatory patients who require oxygen therapy during physical activity. Education is focused on rehabilitative therapies to promote independence in executing activities of daily living. These may include pacing activities throughout the day or using supportive devices to decrease energy expenditure. The nurse evaluates the patient’s activity tolerance and limitations and uses education strategies to promote independent activities of daily living. Other health care professionals (rehabilitation therapist, occupational therapist, physical therapist) may be consulted as additional resources.

Encouraging Effective Coping

Any factor that interferes with normal breathing quite naturally induces anxiety, depression, and changes in behavior. Constant shortness of breath and fatigue may make the patient irritable and apprehensive to the point of panic. Restricted activity (and reversal of family roles due to loss of employment), the frustration of having to work to breathe, and the realization that the disease is prolonged and unrelenting may cause the patient to become angry, depressed, and anxious. Sexual function may be compromised, which also diminishes self-esteem. The nurse should provide education and support to spouses or significant others and families, because the caregiver role in end-stage COPD can be challenging.

Monitoring and Managing Potential Complications

The nurse must assess for various complications of COPD, such as life-threatening respiratory insufficiency and failure, as well as respiratory infection and chronic atelectasis, which may increase the risk of respiratory failure. The nurse monitors for cognitive changes (personality and behavioral changes, memory impairment), increasing dyspnea, tachypnea, and tachycardia, which may indicate increasing hypoxemia and impending respiratory failure.

The nurse monitors pulse oximetry values to assess the patient’s need for oxygen and administers supplemental oxygen as prescribed. The nurse also instructs the patient about signs and symptoms of respiratory infection that may worsen hypoxemia and reports changes in the patient’s physical and cognitive status to the primary provider.

Bronchopulmonary infections must be controlled to diminish inflammatory edema and to permit recovery of normal ciliary action. Minor respiratory infections that are of no consequence to people with normal lungs can be life-threatening to people with COPD. Infection compromises lung function and is a common cause of respiratory failure in people with COPD. In COPD, infection may be accompanied by subtle changes. The nurse instructs the patient to report any signs of infection, such as a fever or change in sputum color, character, consistency, or amount. Any worsening of symptoms (increased tightness of the chest, increased dyspnea, fatigue) also suggests pneumonia and must be reported. Viral infections are hazardous to the patient because they are often followed by pneumonia caused by bacterial organisms, such as Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae (Bartlett & Sethi, 2018).

To prevent pneumonia, the nurse encourages the patient with COPD to be immunized against influenza and pneumococcal pneumonia, because the patient is prone to respiratory infection. In addition, because each patient reacts differently to external exposures (significant air pollution, high or low temperatures, high humidity, strong smells), the nurse must assess the patient’s actual and potential triggers that cause bronchospasm so that avoidance or a treatment plan can be established.

Pneumothorax is a potential complication of COPD and can be life-threatening in patients with COPD who have minimal pulmonary reserve. Patients with severe emphysematous changes can develop large bullae, which may rupture and cause a pneumothorax. Development of a pneumothorax may be spontaneous or related to an activity such as severe coughing or large intrathoracic pressure changes. If a rapid onset of shortness of breath occurs, the nurse should quickly evaluate the patient for potential pneumothorax by assessing the symmetry of chest movement, differences in breath sounds, and a decrease in pulse oximetry.

Over time, pulmonary hypertension may occur as a result of chronic hypoxemia, which causes the pulmonary arteries to constrict and leads to this complication. Pulmonary hypertension may be prevented by maintaining adequate oxygenation through an adequate hemoglobin level, improved ventilation–perfusion of the lungs, or continuous administration of supplemental oxygen (if needed).

Promoting Home, Community-Based, and Transitional Care

Referral for home, community-based, or transitional care is important. These referrals assess the patient’s home environment in relation to their physical and psychological status and the patient’s ability to adhere to a prescribed therapeutic regimen. These assessments include evaluating the patient’s ability to cope with changes in lifestyle and physical status so that their medical management can be tailored to their specific needs. Once home care is set up, the visits provide an opportunity to reinforce the information and activities learned in the inpatient or outpatient pulmonary rehabilitation program and to have the patient and family demonstrate correct administration of medications and oxygen, if indicated, and performance of exercises. If the patient does not have access to a formal pulmonary rehabilitation program, the nurse provides the education and breathing retraining necessary to optimize the patient’s functional status.

Educating Patients About Self-Care

When providing education about self-management, the nurse must assess the knowledge of patients and family members about self-care and the therapeutic regimen. The nurse should also consider whether they are comfortable with this knowledge. Familiarity with potential side effects of prescribed medications is essential. In addition, patients and family members need to learn the early signs and symptoms of infection and other complications so that they seek appropriate health care promptly. Nurses are key in promoting smoking cessation and educating patients about its importance. Patients diagnosed with COPD who continue to smoke must be encouraged and assisted to quit.

A major area of patient education involves setting and accepting realistic short-term and long-range goals. If the COPD is mild (e.g., grade I), the objectives of treatment are to increase exercise tolerance and prevent further loss of pulmonary function. If the COPD is severe (e.g., grade III), the objectives are to preserve current pulmonary function and relieve symptoms as much as possible. It is important to plan and share the goals and expectations of treatment with the patient. Both the patient and the care provider need patience to achieve these goals.The nurse instructs the patient to avoid extremes of heat and cold. Heat increases the body temperature, thereby raising oxygen requirements, and cold tends to promote bronchospasm. Air pollutants such as fumes, smoke, dust, and even talcum, lint, and aerosol sprays may initiate bronchospasm. High altitudes aggravate hypoxemia.

A patient with COPD should adopt a lifestyle of moderate activity, ideally in a climate with minimal shifts in temperature and humidity. As much as possible, the patient should avoid emotional disturbances and stressful situations that might trigger a coughing episode. Self-management also includes getting sufficient rest and sleep. The medication regimen can be quite complex; patients receiving aerosol medications by a pMDI or other type of inhaler may be particularly challenged. The nurse must review educational information and have the patient demonstrate correct pMDI use before discharge, during follow-up visits to a caregiver’s office or clinic, and during home visits (Chart 20-6).

Smoking cessation goes hand in hand with lifestyle changes, and reinforcing the patient’s efforts is a key nursing activity. Smoking cessation is the single most important therapeutic intervention for patients with COPD. There are many strategies, including prevention, cessation with or without oral or topical patch medications, and behavior modification techniques.

At times, the patient will need oxygen at home. The nurse instructs the patient or family in the methods for administering oxygen safely and informs the patient and family that oxygen is available in gas, liquid, and concentrated forms. The gas and liquid forms come in portable devices so that the patient can leave home while receiving oxygen therapy. Humidity must be provided while oxygen is used (except with portable devices) to counteract the dry, irritating effects of compressed oxygen on the airway (Chart 20-7). To help the patient adhere to the oxygen prescription, the nurse explains the proper flow rate and required number of hours for oxygen use as well as the dangers of arbitrary changes in flow rate or duration of therapy. The nurse also reassures the patient that oxygen is not “addictive” and explains the need for regular evaluations of blood oxygenation by pulse oximetry or arterial blood gas analysis.Numerous educational materials are available to assist nurses in educating patients with COPD (see Resources at the end of the chapter).

Continuing and Transitional Care

Home visits by a nurse or respiratory therapist may be arranged based on the patient’s status and needs. It is important to assess the patient’s home environment, the patient’s physical and psychological status, and the need for further education. The nurse reinforces educational points on how to use oxygen safely and effectively, including fire safety tips. To maintain a consistent quality of care and to maximize the patient’s financial reimbursement for home oxygen therapy, the nurse ensures that the prescription given by the primary provider includes the diagnosis, the prescribed oxygen flow, and conditions for use (e.g., continuous use, nighttime use only). Because oxygen is a medication, the nurse reminds the patient receiving long-term oxygen therapy and the family about the importance of keeping follow-up appointments with the patient’s primary provider. The patient is instructed to see the primary provider every 6 months or more often, if indicated. Arterial blood gas measurements and laboratory tests are repeated annually or more often if the patient’s condition changes.

The nurse directs patients to community resources, such as pulmonary rehabilitation programs and smoking cessation programs, to help improve patients’ ability to cope with their chronic condition and the therapeutic regimen and to provide a sense of worth, hope, and well-being. In addition, the nurse reminds the patient and family about the importance of participating in general health promotion activities and health screening.

Patients with COPD have indicated that information about their end-of-life needs is limited. Areas to discuss regarding end-of-life care may include symptom management, quality of life, satisfaction with care, information/communication, use of care professionals, use of differing care facilities, hospital admission, and place of death. It is crucial that patients know what to expect as the disease progresses. In addition, they should have information about their role in decisions regarding aggressiveness of care near the end of life and access to specialists who may help them and their families. As the disease course progresses, a holistic assessment of physical and psychological needs should be undertaken at each hospitalization, clinic visit, or home visit. This helps gauge the patient’s assessment of the progression of the disease and its impact on quality of life and guides planning for future interventions and management (see Chapter 13 for additional information).