Etiology and Genetic Risk

Asthma is classified into different types based on how the attacks are triggered; however, the effect on oxygenation is similar for all types of asthma. Inflammation of the mucous membranes lining the airways is a key event in triggering an asthma attack. Inflammation occurs in response to the presence of specific allergens; general irritants such as cold air, dry air, or fine airborne particles; microorganisms; and aspirin and other NSAIDs. Hyperresponsiveness can occur with exercise, with an upper respiratory illness, and for unknown reasons.

When asthma is well controlled, the airway changes are temporary and reversible. With poor control, chronic inflammation can lead to damage and hyperplasia of the bronchial epithelial cells and of the bronchial smooth muscle (Global Initiative for Asthma [GINA], 2010). When asthma attacks are frequent, even exposure to low levels of the triggering agent or event may stimulate an attack.

Inflammation triggers asthma for some people when allergens bind to specific antibody molecules (especially immunoglobulin E [IgE]). These molecules are attached to tissue cells called mast cells and white blood cells (WBCs) called basophils. These cells are filled with granules containing chemical mediators that can start local inflammatory responses (see Chapters 19 and 22). Some mediators, such as histamine, start an immediate inflammatory response, which can be blocked by drugs like diphenhydramine (Benadryl). Others, such as leukotriene and eotaxin, are slower and cause later, prolonged inflammatory responses, which can be blocked by drugs like montelukast (Singulair), zafirlukast (Accolate), and zileuton (Zyflo). Mediators also attract more WBCs (eosinophils, macrophages, basophils) to the area, which then release even more inflammation-inducing mediators. Inflammation of airway mucous membranes causes blood vessel dilation and capillary leak, leading to tissue swelling with increased secretions and mucus production (McCance et al., 2010). Inflammation can also occur through general irritation rather than allergic responses.

Bronchospasm is a narrowing of the bronchial tubes through constriction of the smooth muscle around and within the bronchial walls. It can occur as a result of hyperresponsive airways when small amounts of pollutants or respiratory viruses stimulate nerve fibers, causing constriction of bronchial smooth muscle. If an inflammatory response is stimulated at the same time, the mediators released during inflammation also trigger constriction. Severe bronchospasm alone, especially in smaller bronchioles, can profoundly limit airflow to the alveoli.

Aspirin and other NSAIDs can trigger asthma in some people, although this response is not a true allergy. It results from increased production of leukotriene when aspirin or NSAIDs suppress other inflammatory pathways.

Gastroesophogeal reflux disease (GERD) is now thought to be a major trigger for asthma in some people, especially in those who have more asthma manifestations at night (GINA, 2010). It does not cause the airway hyperresponsiveness, but the highly acidic stomach contents appear to make the hyperresponsiveness worse when these materials enter the airway.

Incidence/Prevalence

Asthma can occur at any age. About half of adults with asthma also had the disease in childhood. Asthma affects nearly 19 million adults in the United States and Canada (CDC, 2010). It is more common in urban settings than in rural settings.

Patient-Centered Collaborative Care

Assessment

Asthma is classified on the basis of how well controlled the manifestations are, as well as on the patient’s response to asthma drugs. These classes are the basis for current asthma therapy (Charts 32-2 and 32-3).

Chart 32-2 Key Features

Levels of Asthma Control

Chart 32-3 Key Features

The Step System for Medication Use in Asthma Control

History

The patient with asthma usually has a pattern of intermittent episodes of dyspnea (shortness of breath), chest tightness, coughing, wheezing, and increased mucus production. Ask whether the manifestations occur continuously, seasonally, in association with specific activities or exposures, or more frequently at night. Some patients have these manifestations for 4 to 8 weeks after a chest cold or other upper respiratory tract infection. The patient with atopic (allergic) asthma often has other allergic problems such as rhinitis, skin rash, or pruritus. Ask whether any family members have asthma or respiratory problems. Ask about current or previous smoking habits. If the patient smokes, use this opportunity to teach him or her about smoking cessation (Chart 32-4). Wheezing in nonsmokers is an important symptom in the diagnosis of asthma.

Physical Assessment/Clinical Manifestations

The patient with mild to moderate asthma may have no manifestations between asthma attacks. During an acute episode, the most common manifestations are an audible wheeze and increased respiratory rate. At first, the wheeze is louder on exhalation. When inflammation occurs with asthma, coughing may increase.

The patient may use accessory muscles to help breathe during an attack. Observe for muscle retraction at the sternum and the suprasternal notch and between the ribs. The patient with long-standing, severe asthma may have a “barrel chest,” caused by air trapping (Fig. 32-3). The anteroposterior (AP) diameter (diameter between the front and the back of the chest) increases with air trapping, giving the chest a rounded rather than an oval shape. The normal chest is about 1.5 times as wide as it is thick. In the patient with severe, chronic asthma, the AP diameter may equal or exceed the lateral diameter. Compare the AP diameter of the chest with the lateral diameter. Chronic air trapping also flattens the diaphragm and increases the space between the ribs.

FIG. 32-3 A, Normal adult. The thorax has an oval shape with an anteroposterior-to-transverse diameter of 1 : 1.5 or 5 : 7. B, Barrel chest. Note equal anteroposterior-to-transverse diameter and that ribs are horizontal instead of the normal downward slope. This is associated with chronic obstructive pulmonary disease and severe asthma as a result of hyperinflation of the lungs.

Along with an audible wheeze, the breathing cycle is longer with prolonged exhalation and requires more effort. The patient may be unable to speak more than a few words between breaths. Hypoxia occurs with severe attacks. Pulse oximetry shows hypoxemia (poor blood oxygen levels). Examine the oral mucosa and nail beds for cyanosis. Other indicators of hypoxemia include changes in the level of cognition or consciousness and tachycardia.

Laboratory Assessment

Laboratory tests can help determine the type of asthma and the degree of breathing impairment. Arterial blood gas (ABG) levels show how well the patient is obtaining oxygen (see Chapter 14 for discussion of ABGs). The arterial oxygen level (PaO₂) may decrease during an asthma attack. Early in the attack, the arterial carbon dioxide level (PaCO₂) may be decreased as the patient increases respiratory effort. Later in an asthma episode, PaCO₂ rises, indicating carbon dioxide retention. Allergic asthma often occurs with an elevated serum eosinophil count and immunoglobulin E levels. The sputum may contain eosinophils and mucus plugs with shed epithelial cells (Curschmann’s spirals).

Pulmonary Function Tests

The most accurate tests for asthma are the pulmonary function tests (PFTs) measured using spirometry. Baseline PFTs are obtained for all patients diagnosed with asthma. The most important PFTs for a patient with asthma are:

A decrease in either the FEV₁ or the PEF of 15% to 20% below the expected value for age, gender, and size is common for the patient with asthma. An increase of 12% in these values after treatment with bronchodilators is diagnostic for asthma. Airway responsiveness is tested by measuring the PEF and FEV₁ before and after the patient inhales the drug methacholine, which induces bronchospasm in susceptible people.

Interventions

The purposes of asthma therapy are to control and prevent episodes, improve airflow, and relieve symptoms. Adult asthma is best managed when the patient is an active partner in the management plan. Priority nursing actions focus on patient education about proper implementation of a personal asthma action plan, which includes drug therapy and lifestyle management strategies to assist the patient in understanding his or her disease and its treatment (GINA, 2010).

Teaching for Self-Management

Asthma often has intermittent overt symptoms. With guided self-care, patients can co-manage this disease, increasing symptom-free periods and decreasing the number and severity of attacks (Ellis, 2008; Pruitt, 2011). Good management decreases the number of hospital admissions and increases participation in patient-chosen work and leisure activities. Self-care requires extensive education for the patient to be able to self-assess respiratory status, self-treat (including adjusting the frequency and dosage of prescribed drugs), and know when to consult the health care provider.

Ideally, a personal asthma action plan is developed by the health care provider and the patient. This plan is tailored to meet the patient’s personal triggers, asthma manifestation pattern, and drug responses. This plan includes the prescribed daily controller drug(s) schedule and prescribed reliever drug directions, patient-specific daily asthma control assessment questions, directions for adjusting the daily controller drug schedule, when to contact the health care provider (in addition to regularly scheduled visits), and what emergency actions to take when asthma manifestations are not responding to controller and reliever drugs.

Teach the patient to assess symptom severity at least twice daily with a peak flowmeter (Fig. 32-4) and to adjust drugs according to his or her personal asthma action plan to manage inflammation and bronchospasms to prevent or relieve symptoms. Chart 32-5 describes the correct method to use the meter. Teach the patient to first establish a baseline or “personal best” peak expiratory flow (PEF) by measuring his or her PEF twice daily for 2 to 3 weeks when asthma is well controlled and recording the results. This way, the patient will know when his or her peak flow is reduced to the point that more drugs are needed or that emergency assistance is needed. When the patient has established a “personal best,” all other readings are compared with this value in terms of percent of personal best. Some meters are color-coded to help the patient interpret the results. Green zone readings are at least 80% or above the “personal best.” This is the ideal range for asthma control and indicates that no increases in drug therapy are needed. Yellow is a range between 50% and 80% of personal best. When a patient has a reading in this range, he or she needs to use the prescribed “reliever drug” (formerly called a rescue drug). Within a few minutes after using the reliever drug, another PEF reading should be made to determine whether the reliever drug is working. Frequent readings in the yellow zone or increasing use of reliever drugs is a warning that indicates the need to reassess the asthma plan for a temporary or permanent change in controller (preventive) drugs. Red is a range below 50% of the patient’s personal best and indicates serious respiratory obstruction.

FIG. 32-4 A typical peak flowmeter. This model will show faster exhalation rates in green, reduced exhalation rates in yellow, and seriously reduced exhalation rates in red.

Teach the patient to keep a symptom and intervention diary to learn specific triggers of asthma symptoms, early cues for impending attacks, and personal response to drugs. Stress the importance of proper use of his or her personal asthma action plan for any severity of asthma (Corbridge & Corbridge, 2010). Chart 32-6 lists areas to emphasize when teaching the patient with asthma.

Drug Therapy

Pharmacologic management of adult patients with asthma is based on the step category for severity and treatment (see Charts 32-2 and 32-3) (GINA, 2010). Control therapy drugs (formerly called preventive drugs) are drugs used to reduce airway responsiveness to prevent asthma attacks from occurring. They are used every day, regardless of symptoms. Reliever drugs are those used to actually stop an attack once it has started. Some patients may need drug therapy only during an asthma episode. For others, daily drugs are needed to keep asthma episodic rather than a more frequent problem. This therapy involves the use of bronchodilators and various drug types to reduce inflammation. Some drugs reduce the asthma response, and other drugs actually prevent the response. Combination drugs are two agents from different classes combined together for better response. Chart 32-7 lists the most common preferred drugs in each class for control (prevention) and relief (rescue) therapy of asthma. The actions, interventions, and rationales for most drugs within a single class are similar although drug dosages may differ. Be sure to consult a pharmacology text or drug handbook for more information on a specific drug.

Chart 32-7 Common Examples of Drug Therapy

Asthma Prevention and Treatment

Bronchodilators

Bronchodilators increase bronchiolar smooth muscle relaxation. They have no effect on inflammatory processes. Thus when a patient with asthma has airflow obstruction by both bronchospasm and inflammation, at least two types of drug therapy are needed. Some bronchodilators work by stimulating the beta₂-adrenergic receptors on bronchial smooth muscle in much the same way that the sympathetic nervous system transmitters epinephrine and norepinephrine do; others work by blocking the parasympathetic nervous system. Bronchodilators include beta₂ agonists and cholinergic antagonists.

Beta₂ agonists bind to the beta₂-adrenergic receptors and cause an increase in the intracellular level of a substance called cyclic adenosine monophosphate (cAMP). This substance sets pathways into motion that trigger smooth muscle relaxation.

Short-acting beta₂ agonists (SABAs) provide rapid but short-term relief. These inhaled drugs are most useful when an attack begins (as relief) or as premedication when the patient is about to begin an activity that is likely to induce an attack (GINA, 2010). Such agents include albuterol (Proventil, Ventolin), bitolterol (Tornalate), levalbuterol (Xopenex), pirbuterol (Maxair), and terbutaline (Brethaire). When inhaled from either a metered dose inhaler (MDI) or a dry powder inhaler (DPI), the drug is delivered directly to the site of action and systemic effects are minimal (unless the agent is overused). Teach the patient the correct technique for using an inhaled drug to achieve the greatest benefit. Chart 32-8 describes the proper way to use an MDI. Fig. 32-5 shows a patient using a “spacer” with an MDI. Spacer use increases the amount of drug delivered to the lungs. Chart 32-9 describes the proper care and use of a DPI. Fig. 32-6 shows a patient using a DPI.

Chart 32-8 Patient And Family Education: Preparing For Self-Management: How to Use an Inhaler Correctly*

With a Spacer (Preferred Technique)

1. Before each use, remove the caps from the inhaler and the spacer.

2. Insert the mouthpiece of the inhaler into the non-mouthpiece end of the spacer.

3. Shake the whole unit vigorously three or four times.

4. Place the mouthpiece into your mouth, over your tongue, and seal your lips tightly around it.

5. Press down firmly on the canister of the inhaler to release one dose of medication into the spacer.

6. Breathe in slowly and deeply. If the spacer makes a whistling sound, you are breathing in too rapidly.

7. Remove the mouthpiece from your mouth, and, keeping your lips closed, hold your breath for at least 10 seconds and then breathe out slowly.

8. Wait at least 1 minute between puffs.

9. Replace the caps on the inhaler and the spacer.

10. At least once a day, clean the plastic case and cap of the inhaler by thoroughly rinsing in warm, running tap water; at least once a week, clean the spacer in the same manner.

Without a Spacer (Primary Method)

1. Before each use, remove the cap and shake the inhaler according to the instructions in the package insert.

2. Tilt your head back slightly, and breathe out fully.

3. Open your mouth, and place the mouthpiece 1 to 2 inches away.

4. As you begin to breathe in deeply through your mouth, press down firmly on the canister of the inhaler to release one dose of medication.

5. Continue to breathe in slowly and deeply (usually over 3-5 sec).

6. Hold your breath for at least 10 seconds to allow the medication to reach deep into the lungs, and then breathe out slowly.

7. Wait at least 1 minute between puffs.

8. Replace the cap on the inhaler.

9. At least once a day, remove the canister and clean the plastic case and cap of the inhaler by thoroughly rinsing in warm, running tap water.

Without a Spacer (Alternative Method)

1. Follow steps 1 and 2 of the primary method for using an inhaler without a spacer.

2. Place the mouthpiece into your mouth, over your tongue, and seal your lips tightly around it.

3. Follow steps 4 to 9 of the primary method for using an inhaler without a spacer.

^* Avoid spraying in the direction of the eyes.

FIG. 32-5 Patient using an aerosol inhaler with a spacer.

Chart 32-9 Patient And Family Education

Preparing For Self-Management: How to Use a Dry Powder Inhaler (DPI)

For Inhalers Requiring Loading

• First load the drug by:

• Turning the device to the next dose of drug, or

• Inserting the capsule into the device, or

• Inserting the disk or compartment into the device

After Loading the Drug and for Inhalers That Do Not Require Drug Loading

• Read your doctor’s instructions for how fast you should breathe for your particular inhaler.

• Place your lips over the mouthpiece, and breathe in forcefully (there is no propellant in the inhaler; only your breath pulls the drug in).

• Remove the inhaler from your mouth as soon as you have breathed in.

• Never exhale (breathe out) into your inhaler. Your breath will moisten the powder, causing it to clump and not be delivered accurately.

• Never wash or place the inhaler in water.

• Never shake your inhaler.

• Keep your inhaler in a dry place at room temperature.

• If the inhaler is preloaded, discard the inhaler after it is empty.

• Because the drug is a dry powder and there is no propellant, you may not feel, smell, or taste it as you inhale.

FIG. 32-6 Patient using a dry powder inhaler (DPI).

 Nursing Safety Priority

Action Alert

Teach the patient with asthma to always carry the relief drug inhaler with him or her and to ensure that enough drug remains in the inhaler to provide a quick dose when needed.

Dry powder inhalers indicate the amount of remaining drug; however, aerosol inhalers (MDIs) do not. Demonstrate how to check approximate aerosol inhaler drug levels by placing the inhaler in water (Fig. 32-7). Full inhalers sink to the bottom. An empty inhaler floats on its side. This technique is controversial because it is only a general approximation. The more recommended technique is for the patient to count the number of doses as they are used; however, many patients have difficulty keeping the dose count accurate.

FIG. 32-7 Checking the approximate drug level in an aerosol inhaler by placing it in water.

Long-acting beta₂ agonists (LABAs) are also delivered by inhaler directly to the site of action—the bronchioles. Proper use of the long-acting agonists can decrease the need to use reliever (rescue) drugs as often. Unlike short-acting agonists, long-acting drugs need time to build up an effect but the effects are longer lasting. Thus these drugs are useful in preventing an asthma attack but have no value during an acute attack. Therefore teach patients not to use LABAs alone to relieve (rescue) them during an attack or when wheezing is getting worse but, instead, to use a SABA. Relying on LABAs during an attack can lead to worsening of symptoms and death (Aschenbrenner, 2010). Examples of LABAs include formoterol (Foradil) and salmeterol (Serevent). These drugs are never prescribed as the only drug therapy for asthma. Teach the patient to use these control drugs daily as prescribed, even when no symptoms are present.

 Nclex Examination Challenge

Health Promotion and Maintenance

A client reaches for the salmeterol (Serevent) inhaler with the onset of an asthma attack. What is the nurse’s best action?

A. Instruct the client to use the albuterol (Proventil) inhaler instead.

B. Assist the client to use oxygen for three breaths between the two puffs of the inhaled drug.

C. Instruct the client to attach the spacer to the inhaler before using it and inhale as rapidly as possible.

D. Remind the client to take a deep breath, hold it for 15 seconds, and then exhale before using the inhaler.

Cholinergic antagonists, also called anticholinergic drugs, are similar to atropine and block the parasympathetic nervous system. This blockade allows the sympathetic nervous system to dominate, resulting in increased bronchodilation and decreased pulmonary secretions. The most common drug in this class is ipratropium (Atrovent), which is used as an inhalant. Most cholinergic antagonists are short acting and must be used several times a day, although long-acting agents such as tiotropium (Spiriva) are available for use once a day. These drugs are not as effective as beta₂ agonists and are recommended as first-line asthma control therapy only for those patients who cannot tolerate the side effects of beta₂ agonists.

Xanthines, such as theophylline and aminophylline, are used only when other types of management are ineffective. These drugs are given systemically, and the dosage that is effective is close to the dosage that produces many dangerous side effects. Blood levels must be monitored closely to ensure the drug level is within the therapeutic range.

Exercise/Activity

Regular exercise is a recommended part of asthma therapy (Holcomb, 2008). Aerobic exercise assists in maintaining cardiac health, enhancing skeletal muscle strength, and promoting ventilation and perfusion. Teach patients with asthma to examine the conditions that trigger an attack and adjust the exercise routine as needed. Some may need to premedicate with inhaled SABAs before beginning activity. For others, adjusting the environment may be needed (e.g., changing from outdoor ice-skating in cold, dry air to indoor ice-skating).

Oxygen Therapy

Supplemental oxygen is often used during an acute asthma attack. Oxygen is delivered by mask, nasal cannula, or endotracheal tube. High flow rates or concentrations may be needed when bronchospasms are severe and limit flow of oxygen through the bronchiole tubes. Heliox, a mixture of helium and oxygen (often 50% helium and 50% oxygen), can help improve oxygen delivery to the alveoli. This gas mixture is lower in density than oxygen alone or room air and flows even when airway resistance is high.

Status Asthmaticus

Status asthmaticus is a severe, life-threatening acute episode of airway obstruction that intensifies once it begins and often does not respond to usual therapy. The patient arrives in the emergency department with extremely labored breathing and wheezing. Use of accessory muscles for breathing and distention of neck veins are observed. If the condition is not reversed, the patient may develop pneumothorax and cardiac or respiratory arrest. IV fluids, potent systemic bronchodilators, steroids (to decrease inflammation), epinephrine, and oxygen are administered immediately to reverse the acute condition. Prepare for emergency intubation. Sudden absence of wheezing may indicate complete airway obstruction and require a tracheotomy. When breathing improves and wheezing decreases, management is similar to that for any patient with asthma.

Emphysema

The two major changes that occur with emphysema are loss of lung elasticity and hyperinflation of the lung (see Fig. 32-1). These changes result in dyspnea and the need for an increased respiratory rate.

In the healthy lung, protein degrading enzymes called proteases are present to destroy and eliminate particulates and organisms inhaled during breathing. If these proteases are present in higher-than-normal levels, they damage the alveoli and the small airways by breaking down elastin. High protease levels cause the alveolar sacs to lose their elasticity and the small airways to collapse or narrow. Some alveoli are destroyed, and others become large and flabby, with decreased area for effective gas exchange.

An increased amount of air is trapped in the lungs. Causes of air trapping are loss of elastic recoil in the alveolar walls, overstretching and enlargement of the alveoli into air-filled spaces called bullae, and collapse of small airways (bronchioles). These changes greatly increase the work of breathing. The hyperinflated lung flattens the diaphragm (Fig. 32-9), weakening the effect of this muscle. As a result, the patient with emphysema needs to use additional muscles (accessory muscles) in the neck, chest wall, and abdomen to inhale and exhale. This increased effort increases the need for oxygen, making the patient work harder and have an “air hunger” sensation. Often, inhalation starts before exhalation is completed, resulting in an uncoordinated pattern of breathing.

FIG. 32-9 Diaphragm shape and lung inflation in the normal patient and in the patient with chronic airflow limitation (CAL), especially chronic obstructive pulmonary disease (COPD).

Oxygenation is affected by the increased work of breathing and the loss of alveolar tissue. Although some alveoli enlarge, the curves of alveolar walls decrease and less surface area is available for gas exchange. Often the patient adjusts by increasing the respiratory rate, so arterial blood gas (ABG) values may not show gas exchange problems until the patient has advanced disease. Then carbon dioxide is produced faster than it can be eliminated, resulting in carbon dioxide retention and chronic respiratory acidosis (see Chapter 14). The patient with late-stage emphysema also has a low arterial oxygen (PaO₂) level, because it is difficult for oxygen to move from diseased alveoli into the blood.

Emphysema is classified as panlobular, centrilobular, or paraseptal depending on the pattern of destruction and dilation of the gas-exchanging units (acini) (see Fig. 32-1). Each type can occur alone or in combination in the same lung. Most are associated with smoking or chronic exposure to other inhalation irritants.

Chronic Bronchitis

Bronchitis is an inflammation of the bronchi and bronchioles caused by exposure to irritants, especially cigarette smoke. The irritant triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm. Bronchitis affects only the airways, not the alveoli.

Chronic inflammation increases the number and size of mucous glands, which produce large amounts of thick mucus. The bronchial walls thicken and impair airflow. This thickening, along with excessive mucus, blocks some of the smaller airways and narrows larger ones. Smaller airways are involved first. In addition, the increased mucus provides a breeding ground for microorganisms and leads to chronic low-grade infection.

Chronic bronchitis hinders airflow and gas exchange because of mucus plugs and infection narrowing the airways. As a result, the PaO₂ decreases (hypoxemia) and the arterial blood carbon dioxide (PaCO₂) level increases (respiratory acidosis).

Etiology and Genetic Risk

Cigarette smoking is the greatest risk factor for COPD. The patient with an 8–pack-year history usually has obstructive lung changes but no manifestations of disease. The patient with a 20–pack-year history or longer often has early-stage COPD with changes in pulmonary function tests (PFTs).

The harmful effects of tobacco occur because inhaled smoke triggers the release of excessive amounts of the proteases from cells in the lungs. These enzymes break down elastin, the major component of alveoli. By impairing the action of cilia, smoking also inhibits the cilia from clearing the bronchi of mucus, cellular debris, and fluid.

In addition to the increased risk for COPD from active smoking, passive smoking (or secondhand smoke), as well as smoke that clings to hair and clothing (sometimes called “thirdhand” smoke), contributes to upper and lower respiratory problems. The risk is greater when exposure occurs in small, confined spaces.

Alpha₁-antitrypsin deficiency is a less common but important risk factor for COPD. A special enzyme, alpha₁-antitrypsin (AAT), is normally present in the lungs. One purpose of AAT is to regulate the proteases that are present to break down inhaled pollutants and organisms. AAT, a protease inhibitor, prevents the proteases from working on lung structures.

The production of normal amounts of AAT depends on the inheritance of a pair of normal gene alleles for this protein. The AAT gene is recessive. Thus if one of the pair of alleles is faulty and the other allele is normal, the person makes enough AAT to prevent COPD unless there is significant exposure to cigarette smoke and other precipitating factors. This person, however, is a carrier for AAT deficiency. If both alleles are faulty, COPD develops at a fairly young age even when the person is not exposed to cigarette smoke or other irritants.

About 100,000 Americans have severe AAT deficiency, and many more have mild to moderate deficiencies (Nussbaum et al., 2007). Although an AAT deficiency also can cause problems in the skin and liver, lung diseases are more common.

Incidence/Prevalence

The prevalence of chronic bronchitis and emphysema in the United States has been estimated at about 13.5 million (for chronic bronchitis) and 2 million (for emphysema). Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of morbidity and mortality in the United States (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2009).

Complications

COPD affects oxygenation of all tissues. Complications can result in tissue anoxia and death. Major problems occur, such as hypoxemia, acidosis, respiratory infection, cardiac failure, and dysrhythmias.

Hypoxemia and acidosis occur because the patient with COPD has reduced gas exchange, leading to decreased oxygenation and increased carbon dioxide levels. These problems reduce cellular function.

Respiratory infection risk increases because of the increased mucus and poor oxygenation. Bacterial infections with Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis are common. Acute lung infections make COPD manifestations worse by increasing inflammation and mucus production and inducing more bronchospasm. Airflow becomes even more limited, the work of breathing increases, and dyspnea results.

Cardiac failure, especially cor pulmonale (right-sided heart failure caused by pulmonary disease), occurs with bronchitis or emphysema. Air trapping, airway collapse, and stiff alveolar walls increase the lung tissue pressure, making blood flow through lung vessels more difficult. The increased pressure creates a heavy workload on the right side of the heart, which pumps blood into the lungs. As the disease progresses, the amount of oxygen in the blood decreases, causing major blood vessels in the lung to constrict. To pump blood through these narrowed vessels, the right side of the heart generates high pressures. In response to this heavy workload, the right chambers of the heart enlarge and thicken, causing right-sided heart failure with backup of blood into the general venous system. Chart 32-10 lists key features of cor pulmonale.

Cardiac dysrhythmias are common in patients with COPD. They result from hypoxemia (from decreased oxygen to the heart muscle), other cardiac disease, drug effects, or acidosis.

History

Ask about risk factors such as age, gender, occupational history, and ethnic-cultural background. COPD is seen more often in older men. Some types of emphysema occur in families, especially those with alpha₁-antitrypsin (AAT) deficiency.

Obtain a thorough smoking history, because tobacco use is a major risk factor. Ask about the length of time the patient has smoked and the number of packs smoked daily. Use these data to determine the pack-year smoking history.

Ask the patient to describe his or her breathing problems. Assess whether the patient has any difficulty breathing while talking. Can he or she speak in complete sentences, or is it necessary to take a breath between every one or two words? Ask about the presence, duration, or worsening of wheezing, coughing, and shortness of breath. Determine what activities trigger these problems. Assess the patient’s cough, and ask whether sputum is clear or colored and how much is produced each day. Ask about the time of day when sputum production is greatest. Smokers often have a productive cough when they get up in the morning; nonsmokers generally do not. Ask whether sputum production has increased or changed during the past year.

Check the relationship between activity tolerance and dyspnea by asking the patient to compare the activity level and shortness of breath now with those of a month ago and a year ago. Ask about any difficulty with eating and sleeping. Many patients sleep in a semi-sitting position because breathlessness is worse when lying down (orthopnea). Ask about usual daily activities and any difficulty with sleeping, bathing, dressing, or sexual activity. Document this initial assessment to personalize the intervention plan.

Weigh the patient, and compare this weight with previous weights. Unplanned weight loss is likely when COPD severity increases, because the work of breathing increases metabolic needs. Dyspnea and mucus production often result in poor food intake and inadequate nutrition. Ask the patient to recall a typical day’s meals and fluid intake. When heart failure is present with COPD, general edema with weight gain may occur.

Physical Assessment/Clinical Manifestations

General appearance can provide clues about the patient’s respiratory status and energy level. Observe weight in proportion to height, posture, mobility, muscle mass, and overall hygiene. The patient with increasingly severe COPD is thin, with loss of muscle mass in the extremities, although the neck muscles may be enlarged. He or she tends to be slow moving and slightly stooped. Usually the person sits with a forward-bending posture, sometimes with the arms held forward, a position known as the orthopneic or tripod position (Fig. 32-10). When dyspnea becomes severe, activity intolerance may be so great that bathing and general grooming are neglected.

FIG. 32-10 Orthopnea positions that patients with chronic obstructive pulmonary disease (COPD) often assume to ease the work of breathing.

Respiratory changes occur as a result of obstruction, changes in chest size, and fatigue. Inspect the chest to assess the breathing rate and pattern. The patient with respiratory muscle fatigue breathes with rapid, shallow respirations, and may have an abnormal breathing pattern in which the abdominal wall is sucked in during inspiration, or may use accessory muscles in the abdomen or neck. The respiratory rate could be as high as 40 to 50 breaths/min. The breathing patterns often seen with respiratory muscle fatigue use abdominal muscles and the intercostal muscles more than the diaphragm. Respiratory movement is jerky and appears uncoordinated.

Check the patient’s chest for abnormal retractions and for asymmetric chest expansion. The patient with emphysema has limited diaphragmatic movement (excursion) because the diaphragm is flattened and below its usual resting state. Chest vibration (fremitus) is often decreased and the chest sounds hyperresonant on percussion because of trapped air.

Auscultate the chest to assess the depth of inspiration and any abnormal breath sounds. Wheezes and other abnormal sounds occur with emphysema and chronic bronchitis, often on inspiration and expiration, although crackles are usually not present. Reduced breath sounds are common, especially with emphysema. Note the pitch and location of the sound and the point in the respiratory cycle at which the sound is heard. A silent chest may indicate serious airflow obstruction or pneumothorax.

Assess the degree of dyspnea using an assessment tool called a Visual Analog Dyspnea Scale (VADS). The VADS is a straight line with verbal anchors at the beginning and end of a 100-mm line. Ask the patient to place a mark on the line to indicate his or her perceived breathing difficulty (Fig. 32-11). Document the response, and use this scale to assess dyspnea, determine the therapy effectiveness, and pace the patient’s activities.

FIG. 32-11 A visual analog scale to assess dyspnea.

Examine the patient’s chest for the presence of a “barrel chest” (see Fig. 32-3). With a barrel chest, the ratio between the anteroposterior (AP) diameter of the chest and its lateral diameter is 2 : 2 rather than the normal ratio of 1 : 1.5. This shape change results from lung overinflation and diaphragm flattening.

The patient with chronic bronchitis often has a cyanotic, or blue-tinged, dusky appearance and has excessive sputum production. Assess for cyanosis, delayed capillary refill, and finger clubbing (Fig. 32-12), which indicate chronically decreased arterial oxygen levels.

FIG. 32-12 Late digital clubbing (on left) compared with a normal digit (on right).

Cardiac changes occur as a result of the anatomic changes associated with COPD. Assess the patient’s heart rate and rhythm. Check for swelling of the feet and ankles (dependent edema) or other manifestations of right-sided heart failure. Examine nail beds and oral mucous membranes. The patient with later-stage emphysema may have pallor or frank cyanosis.

Psychosocial Assessment

COPD affects all aspects of a person’s life. Socialization may be reduced when friends and family avoid the patient with COPD because of annoying coughs, excessive sputum, or dyspnea. The patient may be isolated because dyspnea causes fatigue or because of embarrassment from coughing and excessive sputum production.

Ask the patient about interests and hobbies to assess whether socialization has decreased or whether hobbies cause exposure to irritants. Ask about home conditions for exposure to smoke or crowded living conditions that promote transmission of respiratory infections.

Economic status may be affected by the disease through changes in income and health insurance coverage. Severe COPD may require role changes that have a negative impact on self-image. Drugs, especially the metered dose inhalers (MDIs) and dry powder inhalers (DPI), are expensive, and many patients with limited incomes may use them only during exacerbations and not as prescribed on a scheduled basis.

Anxiety and fear related to dyspnea and feelings of breathlessness may reduce the patient’s ability to participate in a full life. Work, family, social, and sexual roles can be affected. Encourage the patient and family to express their feelings about the limitations on lifestyle and disease progression. Assess their awareness and use of support groups and services.

Laboratory Assessment

Arterial blood gas (ABG) values identify abnormal oxygenation, ventilation, and acid-base status. Compare serial or repeated ABG values to assess changes in the patient’s respiratory status. Once baseline ABG values are obtained, pulse oximetry can gauge the response to treatment. As COPD worsens, the amount of oxygen in the blood decreases (hypoxemia) and the amount of carbon dioxide in the blood increases (hypercarbia). Chronic respiratory acidosis (increased arterial carbon dioxide [PaCO₂]) then results; metabolic alkalosis (increased arterial bicarbonate) occurs as compensation by kidney retention of bicarbonate. This change is seen on ABGs as an elevation of , although pH remains lower than normal. Not all patients with COPD are carbon dioxide retainers, even when hypoxemia is present. Carbon dioxide diffuses more easily across lung membranes than does oxygen. Hypercarbia is a problem in advanced emphysema (because the alveoli are affected) rather than in bronchitis (wherein the airways are affected). For more detailed information about acidosis, see Chapter 14.

Sputum samples are obtained for culture from hospitalized patients with an acute respiratory infection. The infection is treated on the basis of manifestations and the common bacterial organisms. A WBC count helps confirm the presence of infection.

Other blood tests include hemoglobin and hematocrit to determine polycythemia (a compensatory increase in red blood cells [RBCs] in the chronically hypoxic patient). Serum electrolyte levels are examined because acidosis can change electrolyte values. Low phosphate, potassium, calcium, and magnesium levels reduce muscle strength. In patients with a family history of COPD, serum AAT levels may be drawn.