Asthma

Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation (GINA

[Global Initiative for Asthma], 2015). This chronic inflammatory disease of the airways causes airway
hyperresponsiveness, mucosal edema, and mucus production. This inflammation ultimately leads to
recurrent episodes of asthma symptoms: cough, chest tightness, wheezing, and dyspnea (see Fig. 24-6). In
the United States, asthma affects more than 18.7 million adults and accounts for approximately 3,500 deaths
per year (CDC, 2015b). Of these adults, 35.2% have intermittent severity and 64.8% have persistent severity
of asthma symptoms (CDC, 2015c). Twenty-one percent of patients with asthma smoke even though
cigarette smoke is known to trigger an attack, while nearly 17% of people without asthma smoke (CDC
2015c). Asthma accounts for 1.8 million ED visits per year and close to 440,000 hospital admissions (CDC,
2015b). Although asthma is the most common chronic disease of childhood, it can occur at any age. For
most patients, asthma is a disruptive disease, affecting school and work attendance, occupational choices,
physical activity, and general quality of life.
Despite increased knowledge regarding the pathology of asthma and the development of improved
medications and management plans, the death rate from the disease continues to rise. Ethnic and racial
disparities affect morbidity and mortality in asthma, which are higher in inner-city African Americans and
Latinos (CDC, 2015c). Contributing to these disparities are epidemiology and risk factors, genetics and
molecular aspect, inner-city environments, limited community assets, health care access/delivery/and quality,
and insufficient health insurance coverage.
Unlike other obstructive lung diseases, asthma is largely reversible, either spontaneously or with
treatment. Patients with asthma may experience symptom-free periods alternating with acute exacerbations
that last from minutes to hours or days Allergy is the strongest predisposing factor for asthma. Chronic
exposure to airway irritants or allergens also increases the risk of asthma. Common allergens can be
seasonal (e.g., grass, tree, and weed pollens) or perennial (e.g., mold, dust, roaches, animal dander).
Common triggers for asthma symptoms and exacerbations include airway irritants (e.g., air pollutants, cold,
heat, weather changes, strong odors or perfumes, smoke, occupational exposure), foods (e.g., shellfish,
nuts), exercise, stress, hormonal factors, medications, viral respiratory tract infections, and gastroesophageal
reflux. Most people who have asthma are sensitive to a variety of triggers.
Pathophysiology
The underlying pathology in asthma is reversible diffuse airway inflammation that leads to long-term
airway narrowing. This narrowing, which is exacerbated by various changes in the airway, includes
bronchoconstriction, airway edema, airway hyperresponsiveness, and airway remodeling. The interaction of
these factors determines the clinical manifestations and severity of asthma (GINA, 2015). Over the course of
a lifetime, the impact of increasing pathophysiologic changes and environmental susceptibility lead to an
irreversible disease process.
Asthma is a complex disease process that involves numerous inflammatory and structural cells as
well as mediators that lead to the disorder’s effects. Mast cells, macrophages, T lymphocytes, neutrophils,
and eosinophils all play a key role in the inflammation of asthma. When activated, mast cells release several
chemicals called mediators. These chemicals, which include histamine, bradykinin, prostanoids, cytokines,
leukotrienes, and other mediators, perpetuate the inflammatory response, causing increased blood flow,
vasoconstriction, fluid leak from the vasculature, attraction of white blood cells to the area, mucus secretion,
and bronchoconstriction (GINA, 2015).
During acute exacerbations of asthma, bronchial smooth muscle contraction or bronchoconstriction
occurs quickly to narrow the airway in response to an exposure. Acute bronchoconstriction due to allergens
results from an immunoglobulin E (IgE)-dependent release of mediators from mast cells; these mediators
include histamine, tryptase, leukotrienes, and prostaglandins that directly contract the airway. There are also
non– IgE-mediated responses and proinflammatory cytokines (GINA, 2015). In addition, alpha- and beta2-
adrenergic receptors of the sympathetic nervous
system located in the bronchi play a role. When the alpha-adrenergic receptors are stimulated,
bronchoconstriction occurs. The balance between alpha- and beta2-adrenergic receptors is controlled
primarily by cyclic
3′,5′-adenosine monophosphate (cAMP). Beta2-adrenergic stimulation
 results in increased levels of cAMP, which inhibits the release of chemical mediators and causes
bronchodilation.
As asthma becomes more persistent, the inflammation progresses and other factors may be involved
in airflow limitation. These include airway edema, mucus hypersecretion, and the formation of mucus plugs.
In addition, airway “remodeling” (i.e., structural changes) may occur in response to chronic inflammation,
causing further airway narrowing.

Clinical Manifestations
The three most common symptoms of asthma are cough, dyspnea, and wheezing. In some
instances, cough may be the only symptom. An asthma attack often occurs at night or early in the morning,
possibly because of circadian variations that influence airway receptor thresholds.
An asthma exacerbation may begin abruptly but most frequently is preceded by increasing symptoms
over the previous few days. There is cough, with or without mucus production. At times, the mucus is so
tightly wedged in the narrowed airway that the patient cannot cough it up. There may be generalized
wheezing (the sound of airflow through narrowed airways), first on expiration and then possibly during
inspiration as well. Generalized chest tightness and dyspnea occur. Expiration requires effort and becomes
prolonged. As the exacerbation progresses, diaphoresis, tachycardia, and a widened pulse pressure may
occur along with hypoxemia and central cyanosis (a late sign of poor oxygenation). Although severe, life-
threatening hypoxemia can occur in asthma, it is relatively uncommon. The hypoxemia is secondary to a
ventilation– perfusion mismatch and readily responds to supplemental oxygenation.
Symptoms of exercise-induced asthma include maximal symptoms during exercise, absence of
nocturnal symptoms, and sometimes only a description of a “choking” sensation during exercise.

Assessment and Diagnostic Findings

To establish the diagnosis, the clinician must determine that episodic symptoms of airflow obstruction
are present, airflow is at least partially reversible, and other causes have been excluded. A positive family
history and environmental factors, including seasonal changes, high pollen counts, mold, pet dander, climate
changes (particularly cold air), and air pollution, are primarily associated with asthma. In addition, asthma is
associated with a variety of occupation-related chemicals, foods, and compounds. Comorbid conditions that
may accompany asthma include viral infections, gastroesophageal reflux disease, drug-induced asthma, and
allergic bronchopulmonary aspergillosis. Other possible allergic reactions that may accompany asthma
include eczema, rashes, and temporary edema. Specific in the assessment that may help to evaluate the
patient’s asthma control include:

• Have your symptoms awakened you at night or in the early morning? Have you needed your
quick-acting relief medication more than usual?
• Have you needed unscheduled care for your asthma—a call to the primary provider’s office,
office visit, ED?
• Have your symptoms impacted your normal activities at school/work/sports?
 During acute episodes, sputum and blood tests may disclose eosinophilia (elevated levels of
eosinophils). Serum levels of IgE may be elevated if allergy is present. Arterial blood gas analysis and pulse
oximetry reveal hypoxemia during acute attacks. Initially, hypocapnia and respiratory alkalosis are present.
As the patient’s condition worsens and he or she becomes more fatigued, the PaCO2 may increase. Because
carbon
dioxide is 20 times more diffusible than oxygen, it is rare for PaCO2 to be normal or elevated in a
person who is breathing very rapidly. During an exacerbation, the FEV1 and FVC are markedly decreased
but improve with bronchodilator administration (demonstrating reversibility). Pulmonary function is usually
normal between exacerbations. The occurrence of a severe, continuous reaction is referred to as status
asthmaticus and is considered life threatening (see later discussion).
Asthma severity is considered in the selection of the initial type, amount, and schedule of treatments
(GINA, 2015; National Heart Lung and Blood Institute [NHLBI], 2012). Disease severity is classified by current
impairment and future risk of adverse events. Impairment is defined by the following factors: nighttime
awakenings, the need for short- acting bronchodilators for symptom relief, work/school days missed, ability
to engage in normal activities, and quality of life. Lung function is evaluated by spirometry. Assessment of
risk of future adverse events is evaluated by numbers of exacerbations, the need for ED care or
hospitalizations in the past year, demographic data (gender, ethnicity, nonuse of prescribed inhaled
corticosteroid therapy, existing smoking), psychosocial factors and attitudes, and beliefs about taking
medication (GINA, 2015; NHLBI, 2012).

Prevention
Patients with recurrent asthma should undergo tests to identify the substances that precipitate the
symptoms. Possible causes are dust, dust mites, roaches, certain types of cloth, pets, horses, detergents,
soaps, certain foods, molds, and pollens. If the attacks are seasonal, pollens can be strongly suspected.
Patients are instructed to avoid the causative agents whenever possible. Knowledge is the key to quality
asthma care. Evaluation of impairment and risk are primary methods that help ensure control.
Occupational asthma refers to asthma induced by exposure in the work environment to dusts,
vapors, or fumes, with or without a preexisting diagnosis of asthma. An estimated 15% of new asthma cases
in the United States are related to workplace exposures (American Academy of Allergy, Asthma and
Immunology [AAAAI], 2016a; GINA, 2015). Work-related asthma should be part of the differential diagnosis
of every case of adult- onset asthma. A detailed work history evaluation is key to identifying occupational
asthma. Immediate treatment is aimed at removing or decreasing the exposure in the patient’s environment
and following the patient on an ongoing basis. Standard asthma medications may be prescribed to minimize
bronchoconstriction and airway inflammation. In certain cases, patients may be impaired or disabled from the
disease. Compensation systems are in place to protect a worker; however, these systems are often slow and
complex to navigate.

Complications
 Complications of asthma may include status asthmaticus, respiratory failure, pneumonia, and
atelectasis. Airway obstruction, particularly during acute asthmatic episodes, often results in hypoxemia,
requiring the administration of oxygen and the monitoring of pulse oximetry and arterial blood gases. Fluids
are given because people with asthma are frequently dehydrated from diaphoresis and insensible fluid loss
with hyperventilation.

Medical Management
Immediate intervention may be necessary because continuing and progressive dyspnea leads to
increased anxiety, aggravating the situation. The NHLBI (2012) and GINA (2015) recommendations are
based on the concept of severity and control of asthma along with the domains of reducing impairment and
reducing risk as keys to improving care. Primary treatment concerns are impairment of lung function and
normal life and risk of exacerbations, decline in lung function, and adverse effects from medications (NHLBI,
2012).

Self-Care and Management

To effectively manage your asthma, here are some critical practices:

Inhalation Technique:
Ensure you know how to use your inhaler correctly. Proper technique is vital for the medication to work
effectively. This will help you make sure you’re using it correctly.

1. Prepare the Inhaler: Before you use it, shake the inhaler well. This ensures the medication
is mixed properly.
2. Remove the Cap: Take off the cap from the mouthpiece. Check for any debris or dust inside.
3. Prime the Inhaler (if needed): If this is the first time you're using it or if you haven't used it in
a while, you might need to prime it. Follow the instructions on the inhaler for how many
sprays to do.
4. Positioning: Hold the inhaler upright. You can either hold it with your thumb on the bottom
and your index and middle fingers on the top or use a spacer if you have one.
5. Exhale: Before you take a puff, breathe out gently to empty your lungs. This helps the
medication go deeper into your lungs.
6. Inhale the Medication: Place the mouthpiece in your mouth.
7. Start to inhale slowly and deeply through your mouth.
8. As you do this, press down on the inhaler to release the medication.
9. Hold Your Breath: After inhaling the medication, try to hold your breath for about 10 seconds.
This allows the medication to settle in your lungs.
10. Exhale Slowly: After holding your breath, exhale gently through your mouth or nose.
 11. Rinse Your Mouth (if using a corticosteroid inhaler): If your inhaler contains a steroid, it’s a
good idea to rinse your mouth with water afterward to prevent any irritation or infection.
12. Replace the Cap: Don’t forget to put the cap back on the inhaler to keep it clean.

Peak Flow Monitoring:

Learn how to use a peak flow meter to measure your lung function. This will help you recognize when
your asthma is worsening.

Asthma Action Plan:

Work with your healthcare provider to develop a personalized asthma action plan. This plan outlines
what to do daily, how to manage worsening symptoms, and when to seek help.

Ongoing Education and Support

Patient education is an ongoing process. Resources from the NHLBI and GINA provide excellent
materials to help you stay informed about managing your asthma effectively.

Partnering with Healthcare Providers

Establish a partnership with your healthcare team. Regular check-ins and open communication are
essential for adjusting your management plan as needed.

REFERENCE: Hinkle, J. L., & Cheever, K. H. (Eds.). (2021). Suddarth's medical-surgical nursing (11th ed.).
Wolters Kluwer.