MED/SURG
ASTHMA
INTRODUCTION
Chronic reactive airway disorder involving episodic, reversible airway obstruction
resulting from bronchospasms, increased mucus secretions, and mucosal edema
Characterized by airway inflammation, intermittent airflow obstruction, and
bronchial hyperresponsiveness
Involving signs and symptoms of bronchial airway obstruction that may persist
between acute episodes and that range from mild wheezing, coughing, chest
tightness, and dyspnea to life-threatening respiratory failure
Comorbidities, when coupled with asthma, can exacerbate its course; such
comorbidities include gastroesophageal reflux diseases, chronic rhinosinusitis,
smoking, obesity, and obstructive sleep apnea
Pathophysiology
Tracheal and bronchial linings overreact to various stimuli, causing episodic
smooth-muscle spasms and swelling that severely constrict the airways.
Mucosal edema and thickened secretions further block the airways.
Immunoglobulin (Ig)E antibodies, attached to histamine-containing mast cells and
receptors on cell membranes, initiate allergic asthma attacks.
When exposed to an antigen such as pollen, the IgE antibody combines with the
antigen. On subsequent exposure to the antigen, mast cells degranulate and release
mediators.
The mediators cause the bronchoconstriction and edema of an asthma attack.
Exudates of serum proteins and cell debris lead to mucous plug formation.
During an asthma attack, expiratory airflow decreases, trapping gas in the airways
and causing alveolar hypoinflation.
Causes
Sensitivity to specific external allergens (leading cause)
Internal nonallergenic factors, such as genetic factors and stress
Risk Factors
Family history(Atopic triad - atopic dermatitis, atopic rhinitis & asthma)
Smoking or exposure to secondhand smoke
History of another allergy condition
Food additives containing sulfites and any other sensitizing substance
Perennial allergens, such as house dust, mold, and animal dander
Kapok or feather pillows
Seasonal allergens, such as pollen from grass, trees, or weeds
Exposure to pollution or occupational chemicals
Being overweight
Emotional stress
Infection
Exercise
Cold or dry air
Senter`s triad (Aspirin sensitivity , nasal polyps & asthma)
Beta-adrenergic blockers
Incidence
Incidence is highest with chronic exposure to an allergen.
Asthma is estimated to affect approximately 26 million Americans.
The disorder can occur at any age.
Adult onset occurs more commonly in females than in males.
Signs and symptoms
Visible dyspnea
Use of accessory respiratory muscles
Diaphoresis
Increased anteroposterior thoracic diameter
Hyperresonance
Tachycardia, tachypnea, mild systolic hypertension, and pulsus
paradoxus (possibly as exacerbation progresses)
Inspiratory and expiratory wheezes
Wheezing and cough, which may be exercise-induced
Prolonged expiratory phase of respiration
Cyanosis, confusion, and lethargy, indicating the onset of life-
threatening acute severe asthma (status asthmaticus) and respiratory
failure
Diagnosis
The amount and depth of diagnostic testing will be variable and unique for each
patient.
Laboratory
ABG the best indication of an attack's severity and may reveal
hypoxemia during an acute attack. In acutely severe asthma, the
partial pressure of arterial oxygen is less than 60 mm Hg, the
partial pressure of arterial carbon dioxide (Paco2) is 40 mm Hg or
more, and pH is usually decreased. A normal Paco2 during an
acute attack may be a sign of impending respiratory failure.
Radioallergosorbent test shows increased serum IgE levels as the
result of an allergic reaction.
Complete blood count (CBC) with differential shows increased
eosinophil count in acute phases; an increased white blood cell
count and differential can also indicate infection.
Total serum IgE levels may be elevated.
Imaging
Chest radiography may show hyperinflation, flattened diaphragms, areas of focal
atelectasis, pneumothorax, or pneumomediastinum.
High-resolution computed tomography scanning (thorax) reveals bronchial wall
thickening, bronchial dilation, mucoid impaction, opacities, and air trapping (for
patients with chronic or recurring symptoms or possible complications).
Sinus computed tomography scanning helps rule out acute or chronic sinusitis.
Magnetic resonance imaging measures the amount of lung edema.
Diagnostic procedures
Pulmonary function tests commonly show decreased peak flow rates and
forced expiratory volume in 1 second, low-normal or decreased vital
capacity, and increased total lung and residual capacities. However,
pulmonary function tests may be normal between attacks.
Skin testing may identify specific allergens.
Bronchial challenge testing shows the clinical significance of allergens
identified by skin testing.
Peak flow monitoring reveals a result of 50% to 79% of personal best and
indicates that asthma may be worsening; a reading below 50% of personal
best indicates a severe exacerbation requiring immediate medical
intervention.
Medical management
Generally, two categories of asthma medications: quick-acting medications to
relieve and long-acting medications to control the underlying inflammation (See
Stepwise approach for asthma management.)
Quick-relief bronchodilators, such as albuterol sulfate inhaler, as needed
Quick-relief anticholinergics, such as ipratropium bromide, for relief of
bronchospasm
Corticosteroids, such as systemic methylPREDNISolone, prednisoLONE, and
prednisone, to prevent exacerbation progression during moderate or severe
exacerbations
Corticosteroids for persistent asthma, such as an inhaled corticosteroid of
fluticasone furoate, beclomethasone dipropionate (inhalation), budesonide
(inhalation, intranasal), or mometasone furoate inhaled
Long-acting beta2-adrenergic agonist or combination drug, such as salmeterol
xinafoate inhaled, formoterol fumarate inhaled, fluticasone furoate, and salmeterol
xinafoate inhaled, or budesonide–formoterol fumarate dihydrate
Leukotriene antagonists (antileukotrienes) such as montelukast sodium
Anticholinergic bronchodilators such as tiotropium bromide inhaled
Anti-inflammatory drugs, such as nedocromil sodium, inhaled before exercise to
reduce bronchospasm
Low-flow oxygen
Antibiotics, as indicated, if infection is present
Nursing management
Serve prescribed asthma medications and inhalers via metered-dose
inhalation or nebulizer therapy. Tell the patient to rinse the mouth after using
inhaled corticosteroids.
Auscultate lungs before and after administering inhaled medications.
Inspect the oral cavity for irritation, redness, and signs of fungal infection
when administering inhaled corticosteroids.
Place the patient in the high Fowler position or encourage leaning forward
on a table to ease the work of breathing.
Observe the color of the skin and mucous membranes for changes.
Encourage pursed-lip and diaphragmatic breathing.
Administer prescribed humidified oxygen.
Adjust oxygen according to the patient's vital signs, pulse oximetry, and
arterial blood gas (ABG) values.
Assist with intubation and mechanical ventilation, if appropriate. Ensure a
patent airway.
Perform postural drainage and chest percussion, if tolerated. Encourage
respiratory hygiene measures.
Suction an intubated patient, as needed. Perform endotracheal tube care
according to your facility's guidelines.
Treat the patient's dehydration with IV or oral fluids, as tolerated.
Encourage frequent rest periods and cluster activities to provide for them.
Emphasize energy-conservation measures.
Offer small, frequent meals to prevent tiring.
Assist the patient in identifying measures to relieve anxiety.
Obtain specimens for laboratory testing, such as ABGs.
Apply antiembolism or sequential compression stockings (if the patient is
hospitalized) to prevent VTE.
Monitor vital signs, Intake and output and response to treatment
Complications
Acute, severe asthma (formerly known as status asthmaticus)
Respiratory failure
Pneumonia
Atelectasis
Air-leak syndrome (such as pneumothorax)