Generic and Brand Names
Xanthines: aminophylline (Truphylline), caffeine, dyphylline (Dilor), theophylline (Slo-Bid, Theo-Dur).
Sympathomimetics: albuterol (Proventil), arformoterol (Brovana), ephedrine, epinephrine (Sus-Phrine), formoterol (Foradil), indacaterol (Arcapta), isoetharine, isoproterenol (Isuprel), levalbuterol (Xopenex), metaproterenol (Alupent), pirbuterol (Maxair), salmeterol (Serevent), terbutaline (Brethaire).
Anticholinergics: ipratropium (Atrovent), tiotropium (Spiriva).
Disease Spotlight: Bronchial Asthma
Asthma is reversible bronchospasm, inflammation, and hyperactive airways. Allergens, inhaled irritants, exercise, and emotion trigger it. The early response is an immediate histamine release that produces bronchospasm in about 10 minutes. The late response (3-5 hours) is cytokine-mediated inflammation, mucus, and edema that obstruct airflow. Treatment has to address both. The extreme is status asthmaticus: life-threatening bronchospasm that does not respond to usual treatment and occludes airflow into the lungs.
Current guidelines have moved away from relieving asthma with a short-acting beta-agonist (SABA) alone. The 2024 Global Initiative for Asthma (GINA) strategy recommends that every adult and adolescent with asthma receive inhaled corticosteroid (ICS)-containing treatment, because SABA-only therapy raises the risk of severe exacerbations and death, and its preferred reliever is now as-needed low-dose ICS-formoterol rather than a SABA on its own.
Xanthines
Xanthines come from naturally occurring sources and were once first-line for asthma and bronchospasm. They have a narrow margin of safety and interact with many drugs, so they are no longer first-choice bronchodilators.
They act directly on respiratory smooth muscle in the bronchi and blood vessels, thought to work by mobilizing intracellular calcium and stimulating two prostaglandins, relaxing smooth muscle and increasing vital capacity lost to bronchospasm or air trapping. They also inhibit release of slow-reacting substance of anaphylaxis and histamine, reducing bronchial swelling and narrowing. They are indicated to relieve or prevent bronchial asthma and to reverse COPD-associated bronchospasm. Given orally, they are rapidly absorbed from the GI tract.
Use caution in GI disease, coronary disease, respiratory dysfunction, renal or hepatic disease, alcoholism, or hyperthyroidism, since systemic xanthine effects worsen these. Switch parenteral to oral as soon as possible, because oral effects are less acute and more manageable. Limit use in pregnancy to cases where benefit clearly outweighs fetal risk (animal studies show fetal abnormalities and breathing difficulties at birth), and choose another feeding method during lactation since xanthines enter breast milk. Adverse effects include CNS irritability, restlessness, and dizziness; palpitations and life-threatening arrhythmias; loss of appetite, fever, and flushing; proteinuria; and respiratory arrest. Because xanthines are metabolized in the liver, many drugs interact. Nicotine increases their metabolism, so smokers need a higher dose.
Sympathomimetics
Sympathomimetics mimic the sympathetic nervous system, which dilates the bronchi and increases the rate and depth of respiration. At therapeutic levels most are specific to the beta-receptors in the bronchi, but systemic effects include increased blood pressure and heart rate, vasoconstriction, and decreased renal and GI blood flow. Epinephrine, the prototype, is the drug of choice for acute bronchospasm in adults and children, including anaphylaxis, and is also available for inhalation.
They are indicated for long-acting treatment and prophylaxis of bronchospasm and prevention of exercise-induced bronchospasm in patients 2 years and older, long-term maintenance of bronchoconstriction in COPD, acute bronchospasm in adults and children (though epinephrine is the drug of choice), and treatment and prophylaxis of acute asthma attacks in children more than 6 years old.
Contraindicated or used with caution in conditions aggravated by sympathetic stimulation: cardiac disease, vascular disease, arrhythmias, diabetes, and hyperthyroidism. Use in pregnancy and lactation only if benefit clearly outweighs risk. Adverse effects include headache and restlessness; palpitation and tachycardia; pallor and local burning or stinging; decreased renal formation; rebound congestion with nasal inhalation; and fear or anxiety. Avoid combining with general anesthetics: cyclopropane and halogenated hydrocarbons sensitize the myocardium to catecholamines, risking serious cardiac complications.
Anticholinergics
For patients who cannot tolerate the sympathetic effects of sympathomimetics, the anticholinergics ipratropium (Atrovent) and tiotropium (Spiriva) offer some relief, though they are less effective. They work on the vagus nerve, blocking acetylcholine at vagal-mediated receptor sites, which relaxes bronchial smooth muscle and produces bronchodilation. They are indicated for maintenance and treatment of bronchospasm in adults with COPD, including long-term once-daily maintenance, and are given by inhaler.
Use caution in anything aggravated by anticholinergic or atropine-like effects: narrow-angle glaucoma, bladder neck obstruction, prostatic hypertrophy, and conditions worsened by dry mouth and throat. Contraindicated with known allergy to the drug or to soy products or peanuts. Although not usually absorbed systemically, use caution in pregnancy and lactation. Adverse effects include dizziness and headache, nausea and GI distress, palpitations, cough, and nervousness.
Nursing Considerations
Assessment
Screen for contraindications and cautions: allergies, cigarette use (it changes drug metabolism), peptic ulcer, gastritis, renal or hepatic dysfunction, coronary disease, and pregnancy or lactation. Establish baseline data: skin color and lesions, blood pressure, pulse, cardiac auscultation, peripheral perfusion, and a baseline ECG. Assess bowel sounds and liver and renal function. Evaluate serum theophylline levels for patients on xanthines. Check urinary output and palpate the prostate as appropriate for anticholinergic effects, and assess orientation, affect, and reflexes for CNS effects.
Nursing Diagnoses
- Acute pain related to headache and GI upset
- Disturbed sensory perception (kinesthetic, visual) related to CNS effects
- Deficient knowledge regarding drug therapy
- Increased cardiac output related to sympathomimetic effects
- Disturbed thought processes related to CNS effects
- Imbalanced nutrition, less than body requirements, related to dry mouth and GI upset
Interventions
Give oral drugs with food or milk if GI upset is a problem. Monitor response (relief of respiratory difficulty, improved airflow) and adjust the dose. Provide rest, a quiet environment, dietary caffeine control, and headache therapy. Arrange periodic followup, including blood tests for serum theophylline levels.
The right sympathomimetic varies by patient, and one may have to try several before finding the most effective. Use the minimal amount for the shortest time to prevent accumulation and adverse effects. For exercise-induced asthma, use the drug 30 to 60 minutes before exercising for peak effect when it is needed. Warn that long-acting adrenergic blockers are slower acting and are not rescue drugs for acute bronchospasm.
Ensure hydration and consider a humidifier. Have the patient void before each dose to avoid urinary retention, and offer small frequent meals and sugarless lozenges for dry mouth and GI upset. Review inhaler technique and caution the patient not to exceed 12 inhalations in 24 hours. Teach the drug name, dose, warning signs, and the need for periodic monitoring.
Evaluation
Monitor for improved airflow and easier breathing, watch for adverse effects (CNS changes, increased pulse or blood pressure, GI upset, dry skin and mucous membranes), and confirm the patient can name the drug, dose, and adverse effects to watch for.
Frequently Asked Questions
What is the difference between a rescue and a maintenance bronchodilator? A rescue drug is a short-acting beta-agonist that opens the airways within minutes during an acute attack. A maintenance drug, such as a long-acting beta-agonist or an inhaled anticholinergic, works slowly to prevent bronchospasm and is not meant for sudden symptoms. Giving the wrong one in an attack costs the patient air.
Are short-acting beta-agonists still used on their own for asthma? Not as the only treatment. The 2024 GINA strategy recommends that all adults and adolescents with asthma receive inhaled-corticosteroid-containing therapy, because relying on a SABA alone increases the risk of severe exacerbations and death.
Why are xanthines like theophylline no longer first-line? Theophylline and other xanthines have a narrow margin of safety, interact with many drugs, and can cause life-threatening arrhythmias, so safer inhaled options have largely replaced them. Patients on a xanthine still need serum-level monitoring.
Why do smokers need a higher dose of theophylline? Nicotine speeds up the liver metabolism of xanthines, so a smoker clears the drug faster and may need a higher dose to stay in the therapeutic range. The dose often has to be revisited if the patient quits.
How should a patient use an inhaler for exercise-induced asthma? Use the prescribed bronchodilator about 30 to 60 minutes before exercise so the peak effect lands when it is needed. This is prevention, not a substitute for a rescue inhaler during an attack.
Why is epinephrine the drug of choice for severe acute bronchospasm? Epinephrine acts fast on bronchial smooth muscle and reverses the airway narrowing of severe bronchospasm and anaphylaxis. Long-acting agents are too slow to rescue an acute attack.