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.

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.

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.

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.

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).

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:

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).

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.

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.

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

DRUG/USUAL DOSAGE	PURPOSE/ACTION	NURSING INTERVENTIONS	RATIONALE
Bronchodilators
Short-Acting Beta2 Agonist (SABA)
Albuterol (Proventil, Ventolin) 1-2 inhalations every 4-6 hr (90 mcg/inhaled dose)	Causes bronchodilation by relaxing bronchiolar smooth muscle through binding to and activating pulmonary beta2 receptors. Primary use is a fast-acting reliever (rescue) drug to be used either during an asthma attack or just before engaging in activity that usually triggers an attack.	Teach patient to carry with him or her at all times.	The drug can stop or reduce life-threatening bronchoconstriction, which can occur anytime.
		Teach patient to monitor heart rate.	Excessive use causes systemic symptoms, especially tachycardia.
		When taking this drug with other inhaled drugs, teach patient to use this drug at least 5 minutes before the other inhaled drugs.	The bronchodilation effect of the drug allows better penetration of the other inhaled drugs.
		Teach patient the correct technique for using the MDI or DPI, and obtain a return demonstration.	Correct technique is essential to getting the drug to the site of action. Poor technique allows the drug to escape through the nose and mouth.
Long-Acting Beta2 Agonist (LABA)
Salmeterol (Serevent) 2 inhalations every 12 hr (25 mcg/inhalation with MDI) (50 mcg/inhalation with DPI)	Causes bronchodilation by relaxing bronchiolar smooth muscle through binding to and activating pulmonary beta2 receptors. Onset of action is slow with a long duration. Primary use is prevention of an asthma attack.	Teach patient to shake inhaler (MDI) well before using.	Drug separates easily.
		Teach patient to not use this drug with the onset of asthma symptoms or worsening of wheezing.	Drug has slow onset of action and does not relieve or reverse symptoms.
		Teach patient the correct technique for using the MDI or DPI, and obtain a return demonstration.	Correct technique is essential to getting the drug to the site of action. Poor technique allows the drug to escape through the nose and mouth.
Cholinergic Antagonist
Ipratropium (Atrovent, Apo-Ipravent ) 2-4 inhalations 4-6 times daily (18 mcg/inhalation)	Causes bronchodilation by inhibiting the parasympathetic nervous system, allowing the sympathetic system to dominate, releasing norepinephrine that activates beta2 receptors. Purpose is to both relieve and prevent asthma. Drug does not work as well as SABAs but can be used in place of SABAs by patients who cannot tolerate side effects of beta2 agonists.	If patient is to use this as a reliever drug, teach him or her to carry it at all times.	The drug can stop or reduce life-threatening bronchoconstriction, which can occur anytime.
		Teach patient to shake MDI well before using.	Drug separates easily.
		Teach patient to drink at least 4 L of fluid daily unless another health problem requires fluid restriction.	Drug causes mouth dryness.
		Teach patient to observe for and report blurred vision, eye pain, headache, nausea, palpitations, tremors, inability to sleep.	These are systemic symptoms of overdose and require intervention.
		Teach patient the correct technique for using the MDI or DPI, and obtain a return demonstration.	Correct technique is essential to getting the drug to the site of action. Poor technique allows the drug to escape through the nose and mouth.
Anti-Inflammatories
All of these drugs help improve bronchiolar airflow by decreasing the inflammatory response of the mucous membranes in the airways. They do not cause bronchodilation.
Corticosteroids
Fluticasone (Flovent) 50 mcg by MDI twice daily; 100-250 mcg by DPI daily	Disrupts all known production pathways of inflammatory mediators. The main purpose is to prevent an asthma attack caused by inflammation or allergies (controller drug).	Teach patient to use the drug daily, even when no symptoms are present.	Maximum effectiveness requires continued use for 48-72 hr and depends on regular use.
		Teach patient to perform good mouth care and to check the mouth daily for lesions or drainage.	Drug reduces local immunity and increases the risk for local infections, especially Candida albicans (yeast).
		Teach patient to not use this drug with the onset of asthma symptoms or worsening of wheezing.	Drug has slow onset of action and does not relieve or reverse symptoms.
		Teach patient the correct technique for using the MDI or DPI, and obtain a return demonstration.	Correct technique is essential to getting the drug to the site of action. Poor technique allows the drug to escape through the nose and mouth.
Prednisone (Deltasone, Predone) 1-40 mg orally daily	Not recommended unless asthma symptoms cannot be controlled with any other therapy.	Teach patient about the numerous expected side effects (GI ulceration, fat redistribution, weight gain, hyperglycemia).	Knowing the side effects to expect reduces anxiety.
		Teach patient to avoid anyone who has an upper respiratory infection.	Drug reduces all protective inflammatory responses, increasing the risk for infection.
		Teach patient to avoid activities that lead to injury.	Blood vessels become more fragile, leading to bruising and petechiae.
		Teach patient to take drug with food.	The drug increases the risk for GI ulceration; food helps reduce the risk.
		Teach patient not to suddenly stop taking the drug for any reason. If patient cannot take the oral drug because of vomiting, he or she should receive the drug parenterally.	The drug suppresses adrenal production of corticosteroids, which are essential for life.
Cromone
Nedocromil (Tilade) 4 mg by MDI every 6 hr	Stabilizes the membranes of mast cells and prevents the release of inflammatory mediators. Purpose is to prevent asthma attack triggered by inflammation or allergens.	Teach patient to use the drug daily, even when no symptoms are present.	Drug has slow onset of action for asthma prevention and is most effective when taken consistently.
		Teach patient to not use this drug with the onset of asthma symptoms or worsening of wheezing.	Drug does not relieve or reverse symptoms.
		Teach patient the correct technique for using the MDI, and obtain a return demonstration.	Correct technique is essential to getting the drug to the site of action. Poor technique allows the drug to escape through the nose and mouth.
Leukotriene Modifier
Montelukast (Singulair) 10 mg orally daily	Blocks the leukotriene receptor, preventing the inflammatory mediator from stimulating inflammation. Purpose is to prevent asthma attack triggered by inflammation or allergens.	Teach patient to use the drug daily, even when no symptoms are present.	Drug has slow onset of action for asthma prevention and is most effective when taken consistently.
		Teach patient not to decrease the dose of or stop taking any other asthma drugs unless otherwise instructed by the health care professional.	This drug is for long-term asthma control and does not replace other drugs, especially corticosteroids and reliever (rescue) drugs.

DPI, Dry powder inhaler; MDI, metered dose inhaler.

From National Institutes of Health. (2007). Guidelines for the diagnosis and management of asthma. Expert panel report 3. Bethesda, MD: U.S. Department of Health and Human Services.

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.

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.

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.

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.

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.

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.

Anti-Inflammatory Agents.

Anti-inflammatory agents decrease the inflammatory responses in the airways. Those given systemically have more side effects. Others are used as inhalants and have fewer systemic side effects.

Corticosteroids decrease inflammatory and immune responses in many ways, including by preventing the synthesis of mediators. Inhaled corticosteroids (ICSs) can be helpful in controlling (preventing) the manifestations of asthma. Newer high-potency steroid inhalers, such as fluticasone (Flovent), budesonide (Pulmicort), and mometasone (Asmanex), may be used once per day for maintenance. Systemic corticosteroids, because of severe side effects, are avoided for mild to moderate intermittent asthma and are used on a short-term basis for moderate asthma. For some patients with severe asthma, daily oral corticosteroids may be needed. Both inhaled corticosteroids and those taken orally are control drugs (preventive). They are not effective in reversing symptoms during an asthma attack and should not be used as reliever (rescue) drugs. Teach patients the difference between ICSs and relief drug inhalers. Control drugs must be used on a scheduled basis, even when asthma symptoms are not present.

Cromones, both those that are inhaled and those that are taken orally, are useful as preventive asthma therapy when taken on a scheduled basis. These agents have different mechanisms of action to reduce airway inflammation. Nedocromil (Tilade) inhibits the release of inflammatory mediators from respiratory cells and WBCs. Mast cell stabilizers, such as cromolyn sodium (Intal), prevent mast cell membranes from opening when an allergen binds to IgE. Thus these drugs help prevent atopic asthma attacks but are not useful during an acute episode. The inhaled cromones are not effective in reversing symptoms during an asthma attack and should not be used as reliever (rescue) drugs.

Leukotriene modifiers are oral drugs that work in several ways to prevent an asthma episode when taken on a scheduled basis. Montelukast (Singulair) and zafirlukast (Accolate) block the leukotriene receptor. Zileuton (Zyflo) prevents leukotriene synthesis. These drugs do not reverse symptoms during an asthma attack and should not be used as reliever (rescue) drugs.

Anti-IgE agents are monoclonal antibodies directed against part of the immunoglobulin E (IgE) structure. When these agents bind to IgE molecules that have allergens attached to them, the complex cannot bind to mast cells and basophils. This action prevents the IgE-allergen complex from triggering the release of mediators from mast cells and basophils. Thus these drugs help prevent atopic asthma attacks but are not useful during an acute episode. Omalizumab (Xolair) is currently the only drug in this class and is used only for people with asthma who have high blood levels of IgE. It is injected subcutaneously every 2 to 3 weeks.

Nursing Safety Priority

Drug Alert

There is a high risk for anaphylaxis from omalizumab. Administer it only in a setting capable of managing this type of reaction.

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).

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.

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.

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.

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).

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.