Drug	Route of Administration	Side Effects	Comments*
Antiinflammatory Agents
*Corticosteroids*
hydrocortisone (Solu-Cortef)	IV	With long-term use: cushingoid appearance, skin changes (acne, striae, bruising), osteoporosis, increased appetite, obesity, peptic ulcer, hypertension, hypokalemia, cataracts, menstrual irregularities, muscle weakness, immunosuppression, catabolism. With short-term use (e.g., <2 wk): sleep disturbances, increased appetite.	Alternate-day therapy minimizes side effects. Oral dose should be taken in morning with food or milk. When given in high doses, observe for epigastric distress. Long-term corticosteroid therapy requires supplementation with vitamin D and calcium to prevent osteoporosis. Discontinue gradually over time to prevent adrenal insufficiency. If symptoms recur during tapering, notify health care provider.
methylprednisolone (Medrol, Solu-Medrol)	Oral, IV
prednisone	Oral
fluticasone (Flovent HFA, Flovent Diskus)	MDI, DPI	Oral candidiasis (thrush), hoarseness, irritated throat, headache, sinus infection, upper respiratory infection	Not recommended for acute asthma attack. Rinse mouth with water or mouthwash after use to prevent oral fungal infections. Use of spacer device with MDI may decrease incidence of oral candidiasis. With inhaled corticosteroids, may not see effects until after at least 2 wk of regular treatment.
beclomethasone (Qvar)	MDI	Oral candidiasis, hoarseness, irritated throat, dry mouth, cough, few systemic effects except for headache	Same as fluticasone except less oral candidiasis because of very small particle size which is deposited deeper in the airways.
budesonide (Pulmicort Flexhaler)	DPI	Same as above.
mometasone (Asmanex Twisthaler)	DPI	Same as above.
ciclesonide (Alvesco)	MDI	Headache, nasopharyngitis	Oral candidiasis and other localized oropharyngeal effects (e.g., hoarseness). Fewer side effects than other ICSs because of small particle size with minimal activation in oropharynx.
*Phosphodiesterase Inhibitor Type 4 (PDE-4)*
roflumilast (Daliresp)	Oral	GI: diarrhea, nausea, decreased appetite, weight loss. Headache, back pain, influenza, dizziness, insomnia, risk of mental health problems	Only used in severe COPD to reduce exacerbation frequency. Not to be used for acute bronchospasm. GI symptoms occur within 6 months of initiating medication. Patients to report any psychiatric symptoms (e.g., anxiety, depression, suicidal thoughts). Not to be used with theophylline.
Anticholinergics
*Short-Acting*
ipratropium (Atrovent HFA)	Nebulizer, MDI	Drying of oral mucosa, cough, flushing of skin, bad taste	Approved for COPD. May provide additive benefit to SABA in moderate to severe asthma exacerbations (used in emergency department with no benefit beyond that). Use in asthma as alternative to those with intolerable side effects with SABA. Temporary blurred vision if sprayed in eyes. Use cautiously in patients with narrow-angle glaucoma or prostatic enlargement.
aclidinium bromide (Tudorza Pressair)	DPI	Headache, nasopharyngitis, cough	Only approved for COPD. Do not administer with other anticholinergics. Not for acute relief of bronchospasm.
*Long-Acting*
tiotropium (Spiriva HandiHaler)	DPI	Dry mouth, upper respiratory infection	Only approved for COPD. Blurred vision if powder comes in contact with eyes. Must discontinue use of ipratropium while on tiotropium. Patients with COPD must use SABA or short-acting anticholinergics for quick-relief medication. Maximum effect 1 week after initiation of drug.
Anti-IgE
omalizumab (Xolair)	Subcutaneous injection	Injection site reaction (e.g., bruising, redness, warmth, pain)	Only for moderate to severe persistent allergic asthma with symptoms not adequately controlled by ICS. Not for acute bronchospasm. Administer only under direct medical supervision and observe patient for a minimum of 2 hr following administration as anaphylaxis has been reported with use.
Leukotriene Modifiers
*Leukotriene Receptor Blocker*
zafirlukast (Accolate)	Oral tablets	Headache, dizziness, nausea, vomiting, diarrhea, fatigue, abdominal pain	Take at least 1 hr before or 2 hr after meals. Affects metabolism of erythromycin and theophylline. Not to be used to treat acute asthma episodes.
montelukast (Singulair)	Oral tablets, chewable tablets, oral granules	Well tolerated	Not to be used to treat acute asthma episodes.
*Leukotriene Inhibitor*
zileuton (Zyflo CR)	Oral tablets	↑ Liver enzymes, dyspepsia, pain, headache	Monitor liver enzymes. May interfere with metabolism of warfarin (Coumadin) and theophylline. Not to be used to treat acute asthma episodes.
β₂-Adrenergic Agonists
*Inhaled: Short-Acting (SABA)*
albuterol (Proventil HFA, Ventolin HFA, ProAir HFA, AccuNeb, VoSpire ER [oral only])	Nebulizer, MDI, oral tablets including extended release Note: Oral tablets not for acute use, only long acting	Tachycardia, BP changes, nervousness, palpitations, muscle tremors, nausea, vomiting, vertigo, insomnia, dry mouth, headache, hypokalemia	Use with caution in patients with cardiac disorders as β-agonists may cause ↑ BP and heart rate, CNS stimulation/excitation, and ↑ risk of dysrhythmias. Has rapid onset of action (1-3 min). Duration of action is 4-8 hr.
levalbuterol (Xopenex, Xopenex HFA)	Nebulizer, MDI	Tachycardia, nervousness, tremor (less than albuterol)	Too frequent use can result in loss of effectiveness. Efficacy no better than other SABA.
*Inhaled: Long-Acting (LABA)*		In asthma: Should never be used as monotherapy. Should be used in combination with inhaled corticosteroids. In COPD: Can be used as monotherapy. Not used for rapid relief of dyspnea.
salmeterol (Serevent)	DPI	Headache, throat dryness, tremor, dizziness, pharyngitis	Not to exceed two puffs q12hr. Not to be used for acute exacerbations. Has a counter.
formoterol (Foradil Aerolizer, Perforomist)	DPI, nebulizer Perforomist is for nebulizer	Angina, tachycardia, nervousness, headache, tremor, dizziness	Can affect blood glucose levels. Should be used with caution in patients with diabetes.
arformoterol (Brovana)	Nebulizer	See formoterol	See formoterol. For chronic COPD use.
indacaterol (Arcapta Neohaler)	DPI	Cough, nasopharyngitis, headache, nausea, oropharyngeal pain	Only once daily LABA. For chronic COPD use. Not intended to treat asthma.
Methylxanthines
IV agent: aminophylline (second-line therapy) Oral: theophylline	Oral tablets, IV, elixir, sustained-release tablets	Tachycardia, BP changes, dysrhythmias, anorexia, nausea, vomiting, nervousness, irritability, headache, muscle twitching, flushing, epigastric pain, diarrhea, insomnia, palpitations	Wide variety of response to drug metabolism exists. Half-life is ↓ by smoking and ↑ by heart failure and liver disease. Cimetidine, ciprofloxacin, erythromycin, and other drugs may rapidly ↑ theophylline levels. Taking drug with food or antacids may help GI effects. Use limited usually if other long term bronchodilation not available or not affordable.
Combination Agents		Also see each component of medications for SE.
ipratropium and albuterol (Combivent, DuoNeb, Combivent Respimat)	MDI (only available until late 2013), Nebulizer. Respimat	Chest pain, pharyngitis, diarrhea, nausea	Patients must be careful not to overuse. Must take as prescribed. Respimat has no propellant and is independent of inspiratory flow. Has dose indicator. Respimat totally replaces MDI in 2014.
fluticasone/salmeterol (Advair Diskus or HFA)	DPI, MDI	Headache, pharyngitis, oral candidiasis	See salmeterol and fluticasone. Has a counter. Comes in three different strengths.
budesonide/formoterol (Symbicort)	MDI	Dysrhythmias, hypertension, paradoxic bronchospasm	See budesonide and formoterol. Has a counter.
mometasone furoate/formoterol fumarate (Dulera)	MDI	Nasopharyngitis, sinusitis, headache

CNS, Central nervous system; DPI, dry powder inhaler; HFA, hydrofluoroalkane (propellant); ICSs, inhaled corticosteroids; MDI, metered-dose inhaler.

^*For patient instructions in English and Spanish for the devices, see www.chestnet.org/accp/patient-guides/patient-instructions-inhaled-devices-english-and-spanish.

eTABLE 29-4

MODIFIED MEDICAL RESEARCH COUNCIL (mMRC) DYSPNEA SCALE

A simple grading system is used to assess a patient’s level of dyspnea.
Grade	Description of Breathlessness
0	I only get breathless with strenuous exercise.
1	I get short of breath when hurrying on level ground or walking up a slight hill.
2	On level ground, I walk slower than people of the same age because of breathlessness, or have to stop for breath when walking at my own pace.
3	I stop for breath after walking about 100 yards or after a few minutes on level ground.
4	I am too breathless to leave the house or I am breathless when dressing.

Source: Fletcher CM, Elmes PC, Wood CH: The significance of respiratory symptoms and the diagnosis of chronic bronchitis in a working population, BMJ 2:257, 1959.

eTABLE 29-5

HOME OXYGEN DELIVERY SYSTEMS

Liquid Oxygen

• Portable * unit can be refilled by patient from reservoir (see Fig. 29-13).

• Portable unit holds 6- to 8-hr supply at 2 L/min. Reservoir will last approximately 7 to 10 days at 2 L/min continuously.

• Patients do not use the reservoir continuously because of the high expense. Instead patients use the O₂ concentrator as the cost is much lower.

• Liquid system is strictly for portable and emergency use.

• Not available everywhere; generally limited to urban areas.

Compressed O₂ Cylinders

• Cylinders or tanks of varying sizes (e.g., D, M, E, H, J)

• Duration varies with tank size and liter flow (e.g., J tank at 2 L/min flow lasts about 50 hr). Portability possible with cart, and some of the smaller tanks may be refilled from large cylinders. Smaller tanks weigh about 10 lb and can be carried on shoulder strap, backpack, or fanny pack carried or placed on a portable cart.

Concentrator or Extractor

• Because the O₂ supply is produced from room air, they never need to be “filled.”

• On wheels, movable from room to room, but usually kept centrally located in the dwelling with extension tubing reaching to the furthest area.

• Patients need to be very cautious to prevent falling over the tubing.

• Compact, excellent system for rural or homebound patient.

• Convenient, safe, and reliable.

• Patient will need backup O₂ tank in case electricity fails.

• Concentrator noise may be bothersome; concentrator should be kept in a room other than bedroom.

Portable Oxygen Concentrator

• Lighter-weight devices (8.5 to 17 lb) that are portable via carts or shoulder straps that may provide pulsed or continuous O₂.

• 5 to 6 L/min flow depending on the particular device.

• Batteries provide up to 8 hr of operation with recharging in AC or DC (e.g., car) and are approved by many airlines.

• This combined with another stationary system in the patient’s dwelling provides the patient with exceptional freedom and mobility as the system continuously provides a renewable source of O₂ outside the home.

• Systems are EverGo, Inogen One, and Eclipse Oxygen Generator.

O₂ Conserving or Pulsed Devices

• Delivers a pulse of O₂ only during inhalation to conserve O₂.

• Allows patient increased mobility.

• Devices are relatively lightweight; varying from approximately 3 to 6 lb with a supply of oxygen up to 20 hr.

• System may clip on belt or be contained in a backpack or shoulder bag.

• Audible pulses may be annoying.

• Some devices may require batteries.

• Becomes less efficient at higher O₂ flow rates.

• Usually best for low activity levels.

• Monitor patient’s O₂ saturation during rest and exercise to determine if oxygenation is acceptable.

^*Portable usually refers to units weighing more than 10 lb (4.5 kg); ambulatory units weigh less than 10 lb.

Obstructive pulmonary disease, the most common chronic lung disease, is characterized by increased resistance to airflow as a result of airway obstruction or airway narrowing. Types of obstructive lung diseases include asthma, COPD, cystic fibrosis (CF), and bronchiectasis. Asthma is a chronic inflammatory lung disease that results in variable episodes of airflow obstruction, but it is usually reversible. COPD is an obstructive pulmonary disease with progressive limitation in airflow that is not fully reversible. The patient with asthma has variations in airflow over time, usually with normal lung function between exacerbations, whereas the limitation in expiratory airflow in the patient with COPD is generally more constant. The pathology of asthma and the response to therapy differ from those associated with COPD. However, the patient with a diagnosis of obstructive pulmonary disease may have features of both asthma and COPD. Patients with asthma who have less responsive reversible airflow obstruction are difficult to distinguish from COPD patients.

Cystic fibrosis, another form of obstructive pulmonary disease, is a genetic disorder that produces airway obstruction because of changes in exocrine glandular secretions, resulting in increased mucus production. Bronchiectasis is an obstructive disease characterized by dilated bronchioles. It most frequently results from untreated or poorly treated pulmonary infections that cause an increase in sputum production.

Gender Differences

Asthma

Men	Women
• Before puberty, more boys are affected than girls.	• After puberty and into adulthood, more women are affected than men. • Women who are admitted to the emergency department are more likely to need hospitalization than men. • Death rate from asthma is greater in women than in men.

Cultural & Ethnic Health Disparities

Obstructive Pulmonary Diseases

Asthma

• Asthma prevalence rates are more than 38% higher among African Americans than whites.

• Puerto Ricans have higher asthma prevalence rates and age-adjusted death rates than all other racial and ethnic subgroups.

• Female African Americans have the highest mortality rates from asthma among all ethnic/gender groups.

Chronic Obstructive Pulmonary Disease (COPD)

• Whites have the highest incidence of COPD in spite of higher rates of smoking among other ethnic groups.

• Hispanics have lower death rates related to COPD than other ethnic groups.

Cystic Fibrosis

• Whites have the highest incidence of cystic fibrosis.

• Cystic fibrosis is uncommon among African Americans, Hispanics, and Asian Americans.

Asthma

Asthma is a chronic inflammatory disorder of the airways. The chronic inflammation leads to recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or in the early morning. These episodes are associated with widespread but variable airflow obstruction that is usually reversible, either spontaneously or with treatment. The clinical course of asthma is unpredictable, ranging from periods of adequate control to exacerbations with poor control of symptoms.³

Asthma affects an estimated 18.8 million adult Americans. Among adults, women are 62% more likely to have asthma than men. Asthma is a public health concern, with more than 14.2 million lost workdays in adults. However, the good news is that after a long period of an increasing incidence of asthma, the mortality and use of health care services are continuing to plateau and/or decrease. Despite the decline in the number of deaths from asthma over the past 10 years, more than 3300 people still die from asthma yearly.¹

Risk Factors for Asthma and Triggers of Asthma Attacks

Risk factors for asthma and triggers of asthma attacks can be related to the patient (e.g., genetic factors) or the environment (e.g., pollen) (Table 29-1). Male gender is a risk factor for asthma in children (but not adults). Obesity is also a risk factor for asthma.⁴ Other factors and triggers are discussed in this section.

TABLE 29-1

TRIGGERS OF ASTHMA ATTACKS

Allergen inhalation

• Animal dander (e.g., cats, mice, guinea pigs)

Inflammation and infection

• Viral upper respiratory tract infection

• Sinusitis, allergic rhinitis

Drugs

• Aspirin

• Nonsteroidal antiinflammatory drugs

• β-Adrenergic blockers

Occupational exposure

• Agriculture, farming

• Paints, solvents

• Laundry detergents

• Metal salts

• Wood and vegetable dusts

• Industrial chemicals and plastics

• Pharmaceutical agents

Food additives

• Sulfites (bisulfites and metabisulfites)

• Beer, wine, dried fruit, shrimp, processed potatoes

• Monosodium glutamate

• Tartrazine

Other factors

• Exercise and cold, dry air

• Stress

• Hormones, menses

• Gastroesophageal reflux disease (GERD)

Occupational asthma is the most common occupational respiratory disorder, with up to 15% of new asthma cases arising from job-related exposures to more than 300 agents.4,5 Irritants cause a change in the responsiveness of the airways. However, the development of symptoms from this alteration may not occur until the patient has had months to years of exposure. Agricultural worker, baker, hospital worker, plastics manufacturer, and beautician are occupations with a high risk of occupational asthma. Characteristically people with occupational asthma give a history of arriving at work feeling well but gradually develop symptoms by the end of the day.

Respiratory Tract Infections.

Respiratory tract infections (i.e., viral and not bacterial) are often the major precipitating factor of an acute asthma attack. Acute infection can increase airway narrowing and airway hyperresponsiveness. Viral-induced alterations of epithelial cells, increased inflammatory cell accumulation, edema of airway walls, and exposure of airway nerve endings contribute to altered airway function. These alterations in airway function may exacerbate asthma.

Nose and Sinus Problems.

Most patients with asthma have a history of allergic rhinitis. Treatment of allergic rhinitis usually improves the symptoms of asthma. Additional information on the relationship of rhinitis and asthma can be found at www.whiar.org.

Acute and chronic sinusitis may worsen asthma. Some patients with asthma have chronic sinus problems that cause inflammation of the mucous membranes. Sinusitis must be treated and large nasal polyps removed for an asthma patient to have good control. (Sinusitis is discussed in Chapter 27.)

Drugs and Food Additives.

Sensitivity to specific drugs may occur in some people, especially those with nasal polyps and sinusitis. Some people with asthma have what is termed the asthma triad: nasal polyps, asthma, and sensitivity to aspirin and nonsteroidal antiinflammatory drugs (NSAIDs). Salicylic acid can be found in many over-the-counter (OTC) drugs and some foods, beverages, and flavorings. Some asthmatics who use aspirin or NSAIDs (e.g., ibuprofen [Motrin]) develop wheezing within 2 hours. In addition, there is usually profound rhinorrhea, congestion, tearing, and even angioedema. Avoidance of aspirin and NSAIDs is required. However, patients with aspirin sensitivity under the care of an allergist can be desensitized by daily administration of the drug.

β-Adrenergic blockers in oral form (e.g., metoprolol [Toprol]) or topical eyedrops (e.g., timolol) may trigger asthma because they can cause bronchospasm. Angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril [Prinivil]) may produce cough in susceptible individuals, thus making asthma symptoms worse.

Other agents that may precipitate asthma in the susceptible patient are tartrazine (yellow dye no. 5, found in many foods) and sulfiting agents widely used in the food and pharmaceutical industries as preservatives and sanitizing agents. Sulfiting agents are commonly found in fruits, beer, and wine and used extensively in salad bars to protect vegetables from oxidation. Asthma exacerbations have been reported after the use of sulfite-containing preservatives found in topical ophthalmic solutions, IV corticosteroids, and some inhaled bronchodilator solutions.

Food allergies triggering asthma reactions in adults are rare. Avoidance diets are not recommended until an allergy has been demonstrated, usually by oral challenges.

Gastroesophageal Reflux Disease.

Gastroesophageal reflux disease (GERD) is more common in people with asthma than in the general population. GERD may worsen asthma symptoms. Reflux may trigger bronchoconstriction and cause aspiration. On the other hand, asthma medications may worsen GERD symptoms. β₂-Agonists (especially given orally), which are used to treat asthma, relax the lower esophageal sphincter, thus allowing stomach contents to reflux into the esophagus and possibly be aspirated into the lungs. Medications used to treat GERD usually do not reduce asthma symptoms in most people.4,6 (GERD is discussed in Chapter 42.)

Psychologic Factors.

Asthma is not a psychosomatic disease. However, many people with asthma report that symptoms worsen with stress. Certainly psychologic factors cause bronchoconstriction via stimulation of the cholinergic reflex pathways. Extreme emotional expressions (e.g., crying, laughing, anger, fear) can lead to hyperventilation and hypocapnia, which can cause airway narrowing.⁴

An asthma attack caused by any triggering event can produce panic, stress, and anxiety. However, it varies from patient to patient and in the same patient from episode to episode.

Pathophysiology

The primary pathophysiologic process in asthma is persistent but variable inflammation of the airways. The airflow is limited because the inflammation results in bronchoconstriction, airway hyperresponsiveness (hyperreactivity), and edema of the airways. Exposure to allergens or irritants initiates the inflammatory cascade (Fig. 29-1). A variety of inflammatory cells are involved, including mast cells, macrophages, eosinophils, neutrophils, T and B lymphocytes, and epithelial cells of the airways.³

As the inflammatory process begins, mast cells (found beneath the basement membrane of the bronchial wall) degranulate and release multiple inflammatory mediators (Fig. 29-2). IgE antibodies are linked to mast cells, and the allergen cross-links the IgE. Then inflammatory mediators such as leukotrienes, histamine, cytokines, prostaglandins, and nitric oxide are released. Some inflammatory mediators have effects on the blood vessels, causing vasodilation and increasing capillary permeability. Some mediators result in the airways being infiltrated by eosinophils, lymphocytes, and neutrophils. The resulting inflammatory process causes vascular congestion, edema, production of thick and tenacious mucus, bronchial muscle spasm, thickening of airway walls, and increased bronchial hyperresponsiveness (Fig. 29-3). This whole process is sometimes referred to as the early-phase response in asthma. Clinically it can occur within 30 to 60 minutes after exposure to an allergen or irritant.

FIG. 29-2 Allergic asthma is triggered when an allergen cross-links IgE receptors on mast cells, which are then activated to release histamine and other inflammatory mediators (early-phase response). A late-phase response may occur due to further inflammation.

Symptoms can recur 4 to 6 hours after the early response because of the influx of many inflammatory cells, which are set in motion by the initial response. At this later time the patient may develop symptoms again or worsening of symptoms. This is called the late-phase response, which occurs in about 50% of individuals with asthma. In this late-phase response, more inflammatory cells are recruited and activated, with continuing inflammation of the airways. Thus bronchoconstriction with symptoms persists for 24 hours or more. Corticosteroids are effective in treating this inflammation.

Alterations in the neural control of the airways also occur in asthma. The autonomic nervous system, consisting of the parasympathetic and sympathetic systems, innervates the bronchi. Airway smooth muscle tone is regulated by the parasympathetic nervous system. In asthma the parasympathetic nervous system is overactive. When airway nerve endings are stimulated by mechanical or chemical stimuli (e.g., air pollution, cold air, dust, allergens), increased release of acetylcholine results in increased smooth muscle contraction and mucus secretion, ultimately leading to bronchoconstriction.

Chronic inflammation may result in structural changes in the bronchial wall known as remodeling. A progressive loss of lung function occurs that is not prevented or fully reversed by therapy. The changes in structure may include fibrosis of the subepithelium, smooth muscle hypertrophy of the airways, mucus hypersecretion, continued inflammation, and angiogenesis (proliferation of new blood vessels). Remodeling is thought to explain why some individuals have persistent asthma and limited response to therapy.3,4

Hyperventilation occurs during an asthma attack as lung receptors respond to increased lung volume from trapped air and airflow limitation. Decreased perfusion and ventilation of the alveoli and increased alveolar gas pressure lead to ventilation-perfusion abnormalities in the lungs. The patient is hypoxemic early on with decreased PaCO₂ and increased pH (respiratory alkalosis) because he or she is hyperventilating. As the airflow limitation worsens with air trapping, the patient works much harder to breathe. The PaCO₂ normalizes as the patient tires, and then it increases to produce respiratory acidosis, which is an ominous sign of respiratory failure.⁶

Clinical Manifestations

Asthma is characterized by an unpredictable and variable course, with a person’s asthma attacks ranging from seemingly minor interferences in breathing to life-threatening episodes. Depending on an individual’s response, asthma can rapidly progress from normal breathing to acute severe asthma. Recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning, are typical in asthma.

An attack of asthma may have an abrupt onset, but usually symptoms occur more gradually. Attacks may last for a few minutes to several hours. Between attacks the patient may be asymptomatic with normal or near-normal pulmonary function, depending on the severity of disease. However, in some people, compromised pulmonary function may result in a state of continuous symptoms and chronic debilitation characterized by irreversible airway disease.

The characteristic clinical manifestations of asthma are wheezing, cough, dyspnea, and chest tightness after exposure to a precipitating factor or trigger. Expiration may be prolonged. Instead of a normal inspiratory-expiratory ratio of 1:2, it may be prolonged to 1:3 or 1:4. Normally the bronchioles constrict during expiration. However, as a result of bronchospasm, edema, and mucus in the bronchioles, the airways become narrower than usual. Thus it takes longer for the air to move out of the bronchioles. This produces the characteristic wheezing, air trapping, and hyperinflation.

Wheezing is an unreliable sign to gauge the severity of an attack. Many patients with minor attacks wheeze loudly, whereas others with severe attacks do not wheeze. The patient with severe asthma attacks may have no audible wheezing because of the marked reduction in airflow. For wheezing to occur, the patient must be able to move enough air to produce the sound. Wheezing usually occurs first on exhalation. As asthma progresses, the patient may wheeze during inspiration and expiration. The term wheezing may also be used to describe sounds arising from the nose and upper airways.⁷

In some patients with asthma, cough is the only symptom, and this is termed cough variant asthma. The bronchospasm may not be severe enough to cause airflow obstruction, but it can increase bronchial tone and cause irritation with stimulation of the cough receptors. The cough may be nonproductive. Secretions may be thick, tenacious, white, gelatinous mucus, which makes their removal difficult.

The person with asthma has difficulty with air movement in and out of the lungs, which creates a feeling of suffocation. Patients may express, “I can’t get a deep breath.” Therefore during an acute attack, the person with asthma usually sits upright or slightly bent forward using the accessory muscles of respiration to try to get enough air. The more difficult the breathing becomes, the more anxious the patient feels.

Examination of the patient during an acute attack usually reveals signs of hypoxemia, which may include restlessness, anxiety, inappropriate behavior, and increased pulse and blood pressure (BP). As the patient worsens, it becomes difficult to speak in complete sentences. The respiratory rate is significantly increased (greater than 30 breaths/minute) with the use of accessory muscles. Percussion of the lungs indicates hyperresonance, and auscultation indicates inspiratory or expiratory wheezing. As the episode resolves, coughing produces thick, stringy mucus.

Diminished or absent breath sounds may indicate a significant decrease in air movement resulting from exhaustion and an inability to generate enough muscle force to ventilate. Severely diminished breath sounds, often referred to as the “silent chest,” are an ominous sign, indicating severe obstruction and impending respiratory failure.

Classification of Asthma

Asthma can be classified as intermittent, mild persistent, moderate persistent, or severe persistent (Table 29-2). The classification system is used to determine the treatment. Patients may move to different asthma classifications over the course of their disease.

TABLE 29-2

CLASSIFICATION OF ASTHMA SEVERITY

FEV₁, Forced expiratory volume in 1 sec; FVC, forced vital capacity; SABA, short-acting β₂-adrenergic agonist.

*Percent predicted values for FEV₁ or ratio of FEV₁/FVC. Normal FEV₁/FVC: 8-19 yr, 85%; 20-39 yr, 80%; 40-59 yr, 75%; 60-80 yr, 70%.

†Consider short-term corticosteroid therapy.

Source: Adapted from National Asthma Education and Prevention Program, National Heart, Lung, and Blood Institute: Expert Panel Report 3: guidelines for the diagnosis and management of asthma, NIH pub no 08-4051, Bethesda, Md, 2007, National Institutes of Health. Retrieved from www.nhlbi.nih.gov/guidelines.

Complications

Severe and Life-Threatening Asthma Exacerbations.

Severe asthma exacerbations occur when the patient is dyspneic at rest and the patient speaks in words, not sentences, because of the difficulty of breathing. The patient is usually sitting forward to maximize the diaphragmatic movement with prominent wheezing, a respiratory rate higher than 30 breaths/minute, and pulse greater than 120 beats/minute. Accessory muscles in the neck are straining to lift the chest wall, and the patient is often agitated. The peak flow (peak expiratory flow rate [PEFR]) is 40% of the personal best or less than 150 L/minute. Arterial blood gas (ABG) changes are listed in Table 29-3. Neck vein distention may result. These patients usually are seen in emergency departments (EDs) or hospitalized.⁶

TABLE 29-3

COMPARISON OF ASTHMA AND COPD *

	Asthma	COPD
Clinical Features
Age	Usually <40 yr (onset).	Usually 40-50 yr (onset).
Smoking history	Not causal.	Often long history (>10-20 pack-years).
Health and family history	Presence of allergy, rhinitis, eczema. Family history of asthma.	Infrequent allergies. May have exposure to environmental pollutants. With α₁-antitrypsin deficiency, family history of lung or liver disease without smoking history.
Clinical symptoms	Intermittent, vary day to day, at night or early morning.	Slowly progressive and persistent.
Dyspnea	Absent except in exacerbations or poor control.	Dyspnea during exercise.
Sputum	Infrequent.	Often.
Disease course	Stable (with exacerbations).	Progressive worsening (with exacerbations).
Diagnostic Study Results
ABGs	Normal between exacerbations.	Between exacerbations in advanced COPD • Often low-normal pH and PaO₂ • High-normal PaCO₂ with high HCO₃⁻ (compensated respiratory acidosis)
pH	↑ Early in exacerbation, then ↓ if prolonged or severe exacerbation.	N→↓
PaO₂	↓	N→↓
PaCO₂	↓ Early in exacerbation, then ↑ if prolonged or severe exacerbation.	N→↑
Chest x-ray	May reveal hyperinflation.	Hyperinflation. May have cardiac enlargement, flattened diaphragm.
Lung volumes	Often normalizes.	Never normalizes.
• Total lung capacity	Increased.	Increased.
• Residual volume	Increased.	Increased.
• FEV₁	Decreased.	Decreased.
• FEV₁/FVC	Normal to decreased.	Decreased (<70%).