Introduction

The burdens associated with asthma in the United States—and worldwide—are enormous. Although the precise annual numbers are not known, asthma is clearly linked to a multitude of lost school days, countless missed work days, numerous doctor visits, frequent hospital outpatient visits, and recurrent emergency department visits and hospitalizations. According to the Department of Health and Human Services’ Centers for Disease Control and Prevention, within the United States in 2005 more than 22 million people were diagnosed with asthma, more than 12 million people had experienced an asthma episode in the previous year, and nearly 4000 Americans died of asthma.* The World Health Organization (WHO) estimates that about 180,000 people worldwide die because of asthma each year. Clearly, asthma’s impact on health, quality of life, and the economy is substantial.

A relatively new role of the respiratory care practitioner is that of asthma educator. In this function, the practitioner’s goal is to be sure that the patient and the family are cognizant of their role and functions in the care of this usually chronic and often serious condition. The asthma educator must serve as a “change agent,” and his or her effect as a convincing, empathetic communicator will be tested. Toward this end, we have greatly expanded this chapter from previous editions.

Fortunately, over the past two decades several new and important gains have been made by expert panels in the development of evidence-based clinical guidelines directed toward the education, prevention, diagnosis, and management of asthma. These guidelines are based on an extensive scientific foundation that has provided our current understanding of the pathophysiologic mechanisms, clinical manifestations, and treatment recommendations used to control asthma. Updated clinical guidelines are developed and disseminated on a regular basis by the National Asthma Education and Prevention Program (NAEPP) and the Global Initiative for Asthma (GINA).

National Asthma Education and Prevention Program

The first evidence-based asthma guidelines were published in 1991 by NAEPP, under the coordination of the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH). These guidelines were updated in 1997, 2002, and 2007.^† Today the guidelines are structured around the following four components of care: (1) assessment and monitoring of asthma, (2) patient education, (3) control of factors contributing to asthma severity, and (4) the pharmacologic treatments. The NAEPP “stepwise asthma management charts” have been widely used and now specify optimal treatment for specific age groups 0 to 4 years, 5 to 11 years, and 12 years and older.

Global Initiative for Asthma

GINA^* was launched in 1993 in collaboration with the National Heart, Lung, and Blood Institute of NIH and WHO. GINA works with a network of asthma experts and researchers, health-care professionals, professional organizations, and public health-care officials from around the world. GINA gathers and disseminates asthma-related information while also ensuring that a system is in place to incorporate the results of scientific investigations into asthma care. GINA’s specific goals are the following:

Collectively, by using the evidence-based guidelines provided by NAEPP, along with the extensive information gathered worldwide from asthma experts and researchers, GINA now provides an outstanding—and user-friendly—evidence-based guideline program for the management of asthma. As of this writing, the GINA programs, which are freely available on the internet (www.ginasthma.org), include the following publications:

In this chapter, GINA’s five components of asthma care are presented under the general management of asthma section.

Anatomic Alterations of the Lungs

Asthma is described as a lung disorder characterized by (1) reversible bronchial airway smooth muscle constriction, (2) airway inflammation, and (3) increased airway responsiveness to an assortment of stimuli. During an asthma attack, the smooth muscles surrounding the small airways constrict. Over time the smooth muscle layers hypertrophy and can increase to three times their normal thickness. The airway mucosa becomes infiltrated with eosinophils and other inflammatory cells, which in turn causes airway inflammation and mucosal edema. The goblet cells proliferate, and the bronchial mucous glands enlarge. The airways become filled with thick, whitish, tenacious mucus. Extensive mucous plugging and atelectasis may develop. The cilia are damaged, and the basement membrane of the mucosa is thicker than normal. As a result of smooth muscle constriction, bronchial mucosal edema, and excessive bronchial secretions, air trapping and alveolar hyperinflation develop. If chronic inflammation develops over time, these anatomic alterations become irreversible, resulting in loss of airway caliber. A remarkable feature of bronchial asthma, however, is that many of the pathologic anatomic alterations of the lungs that occur during an asthmatic attack are completely absent between asthmatic episodes (Figure 12-1).

The major pathologic or structural changes observed during an asthmatic episode are as follows:

Etiology and Epidemiology

Asthma was first recognized by Hippocrates more than 2000 years ago. It remains one of the most common diseases encountered in clinical medicine. In fact, over the past decade the incidence of asthma has increased dramatically. Today, it is estimated that more than 25 million Americans have asthma. About 500,000 Americans are hospitalized annually for severe asthma, and about 4000 die as a result of asthma annually. According to WHO, about 180,000 people worldwide die because of asthma each year. In the United States, asthma is found in 3% to 5% of adults and 7% to 10% of children. Approximately 50% of people with asthma develop it before age 10. Asthma is the most common chronic illness of childhood. Among young children, asthma is about two times more prevalent in boys than in girls. After puberty, however, asthma is more common in girls.

Risk Factors

Many asthma experts divide asthma into two major types according to its precipitating risk factors: extrinsic asthma, or asthma caused by external or environmental agents, and intrinsic asthma, or asthma that occurs in the absence of (or without clear evidence of) an antigen-antibody reaction. Although some authorities believe that the distinction between these terms is of minimal clinical value, the terms are nevertheless widely used.

According to GINA, the risk factors for asthma can be divided into (1) the risk factors with which one is born that cause the development of asthma (e.g., genetic factors or sex), and (2) the risk factors that trigger asthma symptoms (e.g., domestic mites, furred animals, cockroach allergen, fungi, molds, infections, tobacco smoke). The risk factors for asthma with which the individual is born are primarily genetic in nature; the risk factors that trigger asthma symptoms are usually environmental factors. Regardless of the fact that the various asthma authorities are not in full agreement as to how asthma should be categorized, they are—for the most part—in agreement regarding the following causes, or risk factors, of asthma.

Extrinsic Asthma (Allergic or Atopic Asthma)

When an asthmatic episode can clearly be linked to exposure to a specific allergen (antigen), the patient is said to have extrinsic asthma (also called allergic or atopic asthma). Common indoor allergens include house dust, mites, furred animal dander (e.g., dogs, cats, and mice), cockroach allergen, fungi, molds, and yeast. Outdoor allergens include pollens, fungi, molds, and yeast. In addition, there are a number of occupational substances associated with asthma (see next section).

Extrinsic asthma is an immediate (Type I) anaphylactic hypersensitivity reaction. It occurs in individuals who have atopy, a hypersensitivity condition associated with genetic predisposition and an excessive amount of immunoglobulin E (IgE) antibody production in response to a variety of antigens. From 10% to 20% of the general population are atopic and therefore have a tendency to develop an IgE-mediated allergic reaction such as asthma, hay fever, allergic rhinitis, and eczema. Such individuals develop a wheal-and-flare reaction to a variety of skin test allergens, called a positive skin test result. Extrinsic asthma is family-related and usually appears in children and in adults younger than 30 years old. It often disappears after puberty.

Because extrinsic asthma is associated with an antigen-antibody–induced bronchospasm, an immunologic mechanism plays an important role. As with other organs, the lungs are protected against injury by certain immunologic mechanisms. Under normal circumstances these mechanisms function without any apparent clinical evidence of their activity. In patients susceptible to extrinsic or allergic asthma, however, the hypersensitive immune response actually creates the disease by causing acute and chronic inflammation.

Immunologic mechanism

1. When a susceptible individual is exposed to a certain antigen, lymphoid tissue cells form specific IgE (reaginic) antibodies. The IgE antibodies attach themselves to the surface of mast cells in the bronchial walls (Figure 12-2, A).

2. Reexposure or continued exposure to the same antigen creates an antigen-antibody reaction on the surface of the mast cell, which in turn causes the mast cell to degranulate and release chemical mediators such as histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factors (NCFs), leukotrienes (formerly known as slow-reacting substances of anaphylaxis [SRS-A]), prostaglandins, and platelet-activating factor ([PAP]; Figure 12-2, B).

3. The release of these chemical mediators stimulates parasympathetic nerve endings in the bronchial airways, leading to reflex bronchoconstriction and mucous hypersecretion. Moreover, these chemical mediators increase the permeability of capillaries, which results in the dilation of blood vessels and tissue edema (Figure 12-2, C).

The patient with extrinsic asthma may demonstrate an early asthmatic (allergic) response, a late asthmatic response, or a biphasic asthmatic response. The early asthmatic response begins within minutes of exposure to an inhaled antigen and resolves in approximately 1 hour. A late asthmatic response begins several hours after exposure to an inhaled antigen but lasts much longer. The late asthmatic response may or may not follow an early asthmatic response. An early asthmatic response followed by a late asthmatic response is called a biphasic response.

Occupational sensitizers (occupational asthma)

Occupational asthma is defined as asthma caused by exposure to an agent encountered in the work environment. More than 300 different substances have been associated with occupational asthma. Occupational asthma is seen predominantly in adults. It is estimated that occupational sensitizers cause about 1 in 10 cases of asthma among adults of working age. High-risk work environments for occupational asthma include farming and agricultural work, painting (including spray painting), cleaning work, and plastic manufacturing. Most occupational asthma is immunologically mediated and has a latency period of months to years after the onset of exposure. Although the cause is not fully understood, it is known that an IgE-mediated allergic reaction and cell-mediated allergic reactions are often involved. Box 12-1 shows additional agents known to cause occupational asthma.

Box 12-1   Agents Associated with Occupational Asthma

Animal and Plant Proteins

• Flour, amylase

• Storage mites

• Bacillus subtilis enzymes (detergent manufacturing)

• Colophony, such as pine resin (electrical soldering)

• Soybean dust

• Midges, parasites (fish food manufacturing)

• Coffee bean dust, meat tenderizer, tea, shellfish, amylase, egg proteins, pancreatic enzymes, papain

• Storage mites, Aspergillus, indoor ragweed, grass (granary workers)

• Psyllium, latex (hospital workers)

• Ispaghula, psyllium (laxative manufacturing)

• Poultry droppings, mites, feathers

• Locusts, dander, urine proteins

• Wood dust, such as western red cedar, oak, mahogany, zebrawood, redwood, Lebanon cedar, African maple, eastern white cedar

• Grain dust, molds, insects, grain

• Silk worm moths and larvae

Inorganic Chemicals

• Persulfate (beauticians)

• Nickel salts

• Platinum salts, vanadium

Organic Chemicals

• Ethanolamine diisocyanate (automobile painting)

• Disinfectants, such as sulfathiazole, chloramines, formaldehyde, and glutaraldehyde; latex (hospital workers)

• Antibiotics, piperazine, methyldopa, salbutamol, cimetidine (manufacturing)

• Ethylene diamine, phthalic anhydride

• Toluene diisocyanate, dephenylene, tetramines, trimellitic anhydride, hexamethyl tetramine, acrylates (plastics industry)

Intrinsic Asthma (Nonallergic or Nonatopic Asthma)

When an asthmatic episode cannot be directly linked to a specific antigen or extrinsic inciting factor, it is referred to as intrinsic asthma (also called nonallergic or nonatopic asthma) (Figure 12-3). The etiologic factors responsible for intrinsic asthma are elusive. Individuals with intrinsic asthma are not hypersensitive or atopic to environmental antigens and have a normal serum IgE level. The onset of intrinsic asthma usually occurs after the age of 40 years, and typically there is no strong family history of allergy.

In spite of the general distinctions between extrinsic and intrinsic asthma, a significant overlap exists. Distinguishing between the two is often impossible in a clinical setting. Precipitating factors known to cause intrinsic asthma are referred to as nonspecific stimuli. Some of the more common nonspecific stimuli associated with intrinsic asthma are discussed in the following paragraphs.

Other Risk Factors

Obesity

Obesity has been shown to be a risk factor for asthma. It is thought that certain mediators, such as leptins, may have an effect on airway function that can lead to the development of asthma.

Sex

Male sex is a risk factor for asthma in children. Up to 14 years of age, the prevalence of asthma is nearly twice as great in boys as in girls. The difference in prevalence of asthma in males and in females progressively narrows through the teenage years. By adulthood, the prevalence of asthma is greater in women than in men. The reason for this sex difference in asthma is unclear. It is suggested that the lung size is smaller in males than in females at birth, but larger in adulthood.

Infections

Although bacterial infections may cause asthma, viral upper airway infections are more likely to contribute to asthma. For example, intrinsic asthma is commonly seen in children after respiratory syncytial virus (RSV), parainfluenza virus, or rhinovirus infection. These conditions often produce a pattern of symptoms that parallel many features of childhood asthma. For example, it is estimated that about 40% of children with RSV infection will continue to wheeze or have asthma into later childhood.

Exercise-induced asthma

Asthma is sometimes associated with vigorous exercise. The asthmatic episode typically occurs 3 to 10 minutes after the exercise. The asthmatic episode usually resolves in about 1 hour. Although the precise mechanism is not understood, it is believed that the heat loss, water loss, and increased osmolarity of the lower airways causes the release of certain mediators from the basophils and tissue mast cells. The release of the mediators, in turn, causes bronchospasm. Exercise in cold, dry air (e.g., jogging, ice skating, cross-country skiing) also may provoke an asthmatic response in susceptible individuals.

Outdoor and indoor air pollution

Outbreaks of asthma exacerbations have been reported in areas of increased levels of air pollution. The role of outdoor air pollution in causing asthma remains controversial. Similar associations have been reported in relation to indoor pollutants, such as smoke and fumes from gas and biomass fuels used for heating and cooling, molds, and cockroach infestation. These conditions are not IgE mediated.

Drugs, food additives, and food preservatives

Asthma is associated with the ingestion of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). As much as 20% of the asthmatic population may be sensitive to aspirin and NSAIDs. Various beta-adrenergic blocking agents used to treat hypertension and some cardiac disorders (e.g., propranolol, metoprolol) also may provoke an asthmatic episode. The yellow food-coloring agent tartrazine may provoke an asthmatic episode. The ingestion of tartrazine especially is contraindicated in patients sensitive to aspirin. Bisulfites and metabisulfites, commonly used as preservatives and antioxidants in restaurant food (e.g., salad bars, certain wines, beers, dried fruits), are known to provoke bronchoconstriction. About 5% of the asthmatic population is sensitive to foods and drinks that contain sulfites.

Gastroesophageal reflux

Gastroesophageal reflux disease (GERD), or regurgitation, appears to contribute significantly to bronchoconstriction in some patients. The precise mechanism of this relationship is not known. The patient may complain of burning, substernal pain, belching, and a bitter, acid taste, particularly when lying down.

Sleep (nocturnal asthma)

Patients with asthma often have more difficulty late at night or in the early morning. Precipitating factors associated with nocturnal asthma include gastroesophageal reflux, retained airway secretions (caused by a suppressed cough reflex during sleep), exposure to irritants or allergens in the bedroom, and prolonged time between medication doses. Eradication of nocturnal asthma is one measure of good asthma control.

Emotional stress

In some patients the exacerbation of asthma appears to correlate with emotional stress and other psychologic factors.

Perimenstrual asthma (catamenial asthma)

The clinical manifestations associated with asthma often worsen in women during the premenstrual and menstrual periods. The peak of worsening symptoms generally occurs 2 to 3 days before menstruation begins. Perimenstrual asthma correlates with the late luteal phase of ovarian activity, the phase during which circulating progesterone and estrogen levels are at their lowest.

Diagnosis of Asthma

The diagnosis of asthma can often be challenging. For example, the diagnosis of asthma in early childhood is based primarily on the assessment of the child’s symptoms and physical findings—and good clinical judgment. In the older child and the adult, a complete history and physical examination—along with the demonstration of reversible and variable airflow obstruction—will in most cases confirm the diagnosis of asthma. In the elderly patient, asthma is often undiagnosed because of the presence of comorbid diseases that complicate the diagnosis.

Furthermore, the diagnosis of asthma is often missed in the patient who acquires asthma in the workplace. This form of asthma is called occupational asthma (see Box 12-1). Because occupational asthma usually has a slow and insidious onset, the patient’s asthma is often misdiagnosed as chronic bronchitis or COPD. As a result, the asthma is either not treated at all or treated inappropriately. Finally, even though asthma can usually be distinguished from COPD, in some patients—those who have chronic respiratory clinical manifestations and fixed airflow limitations—it is often very difficult to differentiate between the two disorders—that is, asthma or COPD.

GINA provides a general guideline to help in the clinical diagnosis of asthma, which is based on the patient’s symptoms and medical history. There are many signs and symptoms that should increase the suspicion of asthma. This includes wheezing and a history of any of the following:

Other indicators are if the symptoms occur or worsen at night or in a seasonal pattern. The presence of eczema, hay fever or a family history of asthma or atopic disease may also be an indicator. Another sign is if an individual has colds that “go to the chest” or that take more than 10 days to clear up. There are also situations in which asthma related symptoms may worsen, such as exposure to:

These symptoms often respond to appropriate antiasthma therapy.

Diagnostic and Monitoring Test for Asthma

There are several tests used to diagnose and monitor asthma. These tests measure the severity, reversibility, and variability of airflow limitations. Common tests used to for diagnostic and monitoring asthma include the following:

Spirometry measures airflow limitation and its reversibility. An increase in FEV₁ of ≥ 12% (or ≥ 200 ml) after administration of a bronchodilator indicates reversible airflow limitation consistent with asthma.

Peak expiratory flow (PEF) measurements are used to diagnose and monitor asthma. An improvement of 60 L/min (or ≥ 20% of the prebronchodilator [PEF] after inhalation of a bronchodilator), or diurnal variation in PEF of more than 20% (with twice-daily readings, more than 10%), suggests a diagnosis of asthma.

Other tests include measurements of airway responsiveness to methacholine, histamine, mannitol, or exercise in order to diagnose. The presence of allergies (including a positive skin test with allergens or measurement of specific IgE in serum) increases the probability of a diagnosis of asthma, and can help identify risk factors that cause asthma symptoms in individual patients.

Classification of Asthma Severity

GINA provides a general classification of asthma severity based on the clinical features before treatment. The four categories of symptoms include intermittent, mild persistent, moderate persistent, and severe persistent.

Although the classification of asthma based on severity is useful when decisions are being made about treatment plans during the initial assessment of the patient, GINA points out that this classification model has the following limitations:

General Management of Asthma

Using the scientific evidence-based information developed by the National Asthma Education and Prevention Program (NAEPP), and the extensive research and input provided by leading asthma experts from around the world, the Global Initiative for Asthma (GINA) now provides an excellent—and user friendly—clinical guideline program for the management and prevention of asthma. The complete GINA documents are available at the following web site: http://www.ginasthma.org. The five major components of asthma care described by GINA are:

Component 1: Develop Patient-Doctor Partnership

If a patient establishes and maintains a good working relationship with their doctor, he or she will learn to avoid risk factors, take medication correctly, understand the differences between the types of asthma medication, monitor symptoms and take action and seek medical help when appropriate.

Component 2: Identify and Reduce Exposure to Risk Factors

Reducing the exposure to risk factors can improve control of asthma and reduce medication needs. It is important to develop strategies to avoid the risk factors such as staying away from tobacco smoke as well as foods, drugs and additives that may trigger symptoms. Also reduce or avoid exposure to occupational sensitizers.

Component 3: Assess, Treat, and Monitor Asthma

Evaluating a patient is necessary before successful treatment can begin. Once a patient has been assessed and the level of control has been established, a patient can be properly treated. Many drugs can be used in the treatment of asthma. The following is a list of inhaled glucocorticosteroids commonly used in the treatment of asthma:

• beclomethasone dipropionate

• budesonide

• ciclesonide

• flunisolide

• fluticasone

• mometasone furoate

• triamcinolone acetonide

Common controller medications used in the treatment of asthma are presented in Table 12-1. Table 12-2 provides an overview of common reliever medications used to manage acute exacerbations of asthma.

Table 12-1

Controller Medications Commonly Used to Treat Asthma

Generic Name	Brand Name	Dose and Administration
Inhaled Corticosteroids (ICSs)
Beclomethasone dipropionate	QVAR	MDI: 2 puffs, 40 µg/puff or 80 µg/puff, bid
Triamcinolone acetonide	Azmacort	MDI: 2 puffs, 100 µg/puff, tid, qid
Flunisolide	Aerobid, Aerobid-M	MDI: 2 puffs, 250 µg/puff, bid
Flunisolide hemihydrate	Aerospan	MDI: 2 puffs, 80 µg/puff, bid
Fluticasone propionate	Flovent HFA Flovent Diskus

MDI: 2 puffs, 44 µg/puff, 110 µg/puff, 220 µg/puff, bid

DPI: 50 µg, 100 µg, 250 µg, 100-1000 µg, bid

Ciclesonide Alvesco MDI: 1-2 puffs, 80 µg/puff abd 160 µg/puff, daily Budesonide Mometasone furoate Asmanex Twisthaler DPI: 220 µg/actuation, 220-880 µg, q day Systemic Corticosteroids Prednisone Deltasone Tablets and syrups: For acute attacks 40-60 mg daily in 1 or 2 divided doses for adults or 1-2 mg/kg daily in children Methylprednisolone Hydrocortisone Solu-Cortef Prednisolone Orapred Long-Acting Beta₂ Agents (LABAs) Salmeterol Serevent DPI: 50 µg/inhalation, bid Formoterol Foradil DPI: 12 µg/inhalation, bid Arformoterol Brovana SVN: 15 µg/2 mL unite dose, bid Inhaled Corticosteroids and Long-Acting Beta₂ Agents Fluticasone propionate and salmeterol Budesonide and formoterol fumarate Symbicort MDI: 80 µg and 160 µg budesonide with 4.5 µg formoterol, 1-2 inhalations bid Mast Cell–Stabilizing Agents Cromolyn sodium Intal Nedocromil sodium Tilade MDI: 2 puffs, 1.75 mg/puff, qid Leukotriene Inhibitors (Antileukotrienes) Zafirlukast Accolate Montelukast Singulair Zileuton Zyflo Monoclonal Anti–Immunoglobulin E (IgE) Antibody Omalizumab Xolair Adults and children ≥12 yr: Subcutaneous injection every 4 weeks; dose dependent on weight and serum immunoglobulin E (IgE) level Xanthine Derivatives Theophylline Slo-phyllin, Theolair, Quibron-T/SR Dividose, Bronkodyl, Elixophyllin, Theo-Dur, Uniphyl Oxtriphylline Choledyl SA Aminophylline Aminophylline Dyphylline Dylix, Lufyllin

Component 4: Manage Asthma Exacerbations

Asthma exacerbation (also called an asthma attack or asthma episode) is defined as a progressive increase in shortness of breath, cough, wheezing, or chest tightness or a combination of these symptoms. A severe asthma exacerbation is life threatening. Table 12-3 provides a clinical scale to classify the severity of asthma exacerbations. The table categorizes the signs, symptoms and assessment into four categories: mild, moderate, severe and respiratory arrest imminent.

Absence suggests respiratory muscle fatigue Functional Assessment PEF (% predicted or % personal best) 80% ~50%-80% <50% predicted or personal best or response lasts <2 h   Pao₂ (on air) Normal (test not usually necessary) >60 mm Hg (test not usually necessary) <60 mm Hg: possible cyanosis   and/or Pco₂ <42 mm Hg (test not usually necessary) <42 mm Hg (test not usually necessary) ≥42 mm Hg: possible respiratory failure   Sao₂ % (on air) at sea level >95% (test not usually necessary) 91%-95% <91%     Hypercapnia (hypoventilation) develops more readily in young children than in adults and adolescents.

Component 5: Special Considerations in Managing Asthma

Special considerations to consider when managing asthma are:

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in asthma is usually caused by the hypoventilation and shuntlike effect associated with bronchospasm and increased airway secretions. Hypoxemia caused by a shuntlike effect can at least partly be corrected by oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Bronchopulmonary Hygiene Therapy Protocol

Because of the excessive mucous production and secretion accumulation associated with asthma, a number of bronchial hygiene treatment modalities may be used to enhance the mobilization of bronchial secretions (see Bronchopulmonary Hygiene Therapy Protocol, Protocol 9-2).

Aerosolized Medication Protocol

Both sympathomimetic and parasympatholytic agents commonly are used in the treatment of asthma to induce bronchial smooth muscle relaxation (see Aerosolized Medication Protocol, Protocol 9-4).

Mechanical Ventilation Protocol

Because acute ventilatory failure is associated with status asthmaticus, continuous mechanical ventilation may be required to maintain an adequate ventilatory status. Status asthmaticus is defined as a severe asthmatic episode that does not respond to conventional pharmacologic therapy. When the patient becomes fatigued, the ventilatory rate decreases. Clinically, the patient demonstrates a progressive decrease in Pao₂ and pH and a steady increase in Paco₂ (acute ventilatory failure). If this trend is not reversed, mechanical ventilation becomes necessary (see Mechanical Ventilation Protocols, Protocols 9-5, 9-6, and 9-7).

CASE STUDY

Asthma

Admitting History and Physical Examination

A 8-year-old girl was admitted to the emergency department (ED) in severe respiratory distress. Her respiratory symptoms dated to age 6 months, when she first developed wheezing. She was hospitalized in different hospitals on a number of occasions and was usually managed satisfactorily with aerosolized albuterol, intravenous (IV) steroids, and aminophylline. She developed a cough and wheezing the night before admission and became progressively worse during the night. Her cough was nonproductive. At 8 am, she was brought to the ED.

Physical examination revealed an extremely anxious, well-developed female child in acute respiratory distress. She stated, “It is very hard for me to breathe.” Her vital signs were as follows: blood pressure 152/115, pulse 220/min, and respiratory rate 62/min. Her temperature was 100° F. Her extremities appeared cyanotic, and her tonsils were enlarged. She was using her accessory muscles of respiration. On auscultation, rhonchi and wheezing could be heard throughout both lung fields. Her PEFR was 70 L/min. (Her personal best was about 200 to 250 L/min.) Arterial blood gases on 2 L/min nasal cannula oxygen were pH 7.17, Paco₂ 71, 22, and Pao₂ 47. A chest x-ray examination was ordered but not performed. The physician ordered a respiratory care consultation and stated that she did not want to commit the patient to a ventilator at this time if possible. The physician asked that aggressive noninvasive pulmonary care be tried first. At this time the respiratory care practitioner documented the following.

Respiratory Assessment and Plan

S Patient stated, “It is very hard for me to breathe”

O Vital signs: BP 152/115, HR 220, RR 62, T 100°. Cyanotic and using accessory muscles. Wheezing and rhonchi over both lungs. PEFR: 70 L/min. ABGs pH 7.17, Paco₂ 71, 22, and Pao₂ 47. No CXR yet.

A

• Severe exacerbation of asthma

• Respiratory distress (increased heart rate, blood pressure, respiratory rate)

• Bronchospasm (wheezing, decreased PEFR, history)

• Excessive airway secretions (rhonchi)

• Acute ventilatory failure (acute respiratory acidosis) with moderate to severe hypoxemia (ABG)

• Metabolic acidosis also likely (both pH and are both lower than expected for a Paco₂ of 71). Likely caused by lactic acid (low Pao₂ of 47)

P Oxygen Therapy Protocol (Fio₂ 80%-100% via oxygen nonrebreather mask). Monitor Spo₂ with oximeter. Aerosolized Medication Therapy Protocol (med. neb. every 30 minutes with albuterol 0.15 mL in 2.0 mL normal saline via nebulizer). Monitor PEFR and breath sounds. Bronchopulmonary Hygiene Therapy Protocol (cough and deep breathe as tolerated). Monitor breath sounds. Place endotracheal tube and mechanical ventilator on standby. Repeat ABG in 30 minutes. Respiratory care practitioner to remain in ED.

In addition to this plan, the patient was treated vigorously with IV aminophylline, steroids, and a beclomethasone inhaler (2 puffs every 30 minutes × 4 per emergency room standing orders for asthma) over the next 2 hours. After 2 hours of therapy, her aminophylline blood level was therapeutic at 12 mg/L. Although the patient seemed to improve slightly, her next arterial blood gas reading showed that her Paco₂ had increased slightly to 79.

The respiratory therapist notified the doctor immediately. After this, the patient was lightly sedated, paralyzed (with vecuronium [Norcuron]), intubated, and placed on a mechanical ventilator. The ventilator parameters were set per the Mechanical Ventilation Protocol. The next morning, on an Fio₂ of 0.4 and a mechanical ventilator in SIMV mode at a backup rate of 12 breaths per minute, her arterial blood gases were pH 7.38, Paco₂ 37, 23, and Pao₂ 124. Her vital signs were blood pressure 122/87, heart rate 93, temperature 98.8° F. Her wheezes and rhonchi had diminished but were still present. At this point, the following information was recorded.

Respiratory Assessment and Plan

S N/A (patient sedated and paralyzed on ventilator)

O Sedated, paralyzed, fewer wheezes and rhonchi. Vital signs: BP 122/87, HR 93, T 98.8° F. ABG: pH 7.38, Paco₂ 37, 23, Pao₂ 124 (on mechanical ventilator in SIMV mode at a ventilatory rate of 12 and an Fio₂ of 0.4)

A

• Less bronchospasm (decreased wheezing, normal ABGs)

• Less bronchial secretions (decreased rhonchi)

• Adequately ventilated and oxygenated on present ventilator settings (ABG)

P Discuss with physician: D/C Norcuron. Continue in-line med. nebs. IMV wean and O₂ wean as per Mechanical Ventilation Protocol. Continue to monitor O₂ saturation.

The patient remained intubated for another 24 hours, at which time her lungs were clear and when suctioned returned scant but clear secretions. She was weaned from the ventilator with ease and was extubated shortly thereafter. The patient was discharged the following day, after review of the Asthma Action Plan with her parents.

Discussion

Asthma is a potentially fatal disease—largely because its severity is often unrecognized in the home or outpatient setting. The clinical manifestations presented in this case can all be easily traced back through the Bronchospasm clinical scenario (see Figure 9-11) and Excessive Airway Secretions clinical scenario (see Figure 9-12). For example, the patient’s increased blood pressure, heart rate, and respiratory rate can all be followed back to the hypoxemia caused by the decreased ratio, pulmonary shunting, and venous admixture activated by bronchospasm and Excessive Bronchial Secretions (see Figure 9-11 and 9-12). The patient’s anxiety and previous use of beta₂-agonists also may have contributed to her abnormal vital signs (tachycardia).

In addition, the decreased PEFR, use of accessory muscles, diminished breath sounds, rhonchi, and wheezing reflect the increased airway resistance and air trapping caused by the Bronchospasm (see Figure 9-11) and Excessive Airway Secretions (see Figure 9-12). The fact that the patient’s arterial blood gas values showed acute ventilatory failure confirmed that the patient was in the severe stages of an asthmatic episode and that mechanical ventilation was justified, although vigorous routine respiratory care was first tried to prevent this.

After the initial assessment, the respiratory care practitioner chose a fairly aggressive approach to both the Oxygen Therapy Protocol (Protocol 9-1) and the Aerosolized Medication Therapy Protocol (Protocol 9-4). Use of a nonrebreather oxygen therapy mask at initially high Fio₂ levels (0.8 to 1.0) allowed him to adjust the Fio₂ in small, precise concentration changes while not risking rebreathing of expired air. Frequent monitoring of ABGs and Spo₂ levels was appropriate. Note also the frequency with which he chose to administer inhaled bronchodilators (every 30 minutes) in the Aerosolized Medication Therapy Protocol. An alternative approach, often used in pediatric patients, would be to use continuous bronchodilator or aerosol therapy.

The manner in which any therapy modality is up-regulated may be (1) a different aerosolized drug or procedure, (2) a larger dose of a drug or therapy, or (3) more frequent use of such drugs or therapy. In this case, he chose the last course, only to see it fail (the patient required intubation).

Among the lessons to be learned here is that some asthmatic episodes worsen despite vigorous therapy. This patient received optimal emergent treatment of her resistant asthma but required intubation and mechanical ventilation nonetheless. Almost continuous assessment by the respiratory care practitioner is necessary if more aggressive therapy (including induced sedation, paralysis, and mechanical ventilation) is to be effective.

The use of IV aminophylline in the emergency treatment of acute asthma in the emergency department is controversial. Care must be taken to avoid theophylline toxicity, and symptoms of toxicity often do not reflect serum concentrations of the drug. The acutely ill asthmatic requires almost continuous monitoring and frequent SOAP notes if the patient care team is to be constantly apprised of the patient’s progress. The two such notes recorded here are but a small portion of the more than 14 notes that we found on analysis of the patient’s medical record after her ED discharge alone.