The goals of COPD therapy include slowing the progression, initiating a smoking cessation plan, and ensuring the patient is up-to-date on vaccinations including influenza and pneumococcal (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2020). Evidently, patients who received the influenza vaccine showed a significant reduction of exacerbations compared to those who received a placebo, and COPD patients vaccinated had decreased risks of ischemic heart disease (GOLD, 2020). To reduce symptoms of COPD, pharmacological therapy can be utilized, but treatment depends on the severity of symptoms and exacerbations. Short-acting beta-agonists (SABAs) are the first-line treatment in asthma and are commonly used for mild COPD. According to the GOLD guidelines (2020), regular single-dose and PRN use of SABA or short-acting muscarinic antagonists (SAMA) can improve FEV1 and COPD symptoms, and a combination of both have a better outcome than either medication alone. SABA should be utilized as PRN only as frequent usage can potentially lead to paradoxical bronchospasm and worsening the quality of life. In more moderate cases of COPD, LABAs and LAMAs can improve FEV1, reduce exacerbation rates, and improve quality of life (GOLD, 2020).

Levalbuterol is a beta2-receptor agonist that binds to beta-2 adrenergic receptors in bronchial smooth muscle leading to the activation of adenylate cyclase and increasing cyclic-3’,5’-adenosine monophosphate (cAMP) levels (Hsu & Bajaj, 2019). The increase levels of cAMP activate protein kinase A inhibits the phosphorylation of myosin and lower intracellular calcium concentrations; thus, resulting in smooth muscle relaxation and promoting bronchodilatory effects (Hsu & Bajaj, 2019). Beta-2 adrenergic agonists mimic the functions of catecholamines which may stimulate alpha-1, alpha-2, or beta-1 receptors and produce autonomic responses within the cardiac system. This causes a vasodilatory effect decreasing cardiac venous return; however, the body’s compensatory mechanism will result in tachycardia and hypertension (Hsu & Bajaj, 2019). Levalbuterol may cause ECG changes, such as prolongation of the QT interval and ST-segment depression, increasing the risk of arrhythmias. Additionally, beta-2 agonists decrease serum potassium and promote glycogenolysis increasing serum glucose (Levalbuterol, 2019). Other adverse effects of levalbuterol include headache, viral infection, rhinitis, pharyngitis, tremor, nervousness, and asthma. It’s important to consider monitoring FEV1 changes, heart rate, blood pressure, and, in certain patients, serum glucose and potassium. To avoid additive cardiovascular effects, drugs that should be used with caution include atomoxetine, cannabinoid-containing products, haloperidol, linezolid, monoamine oxidase inhibitors, and tricyclic antidepressants (Levalbuterol, 2019). In addition, drugs to avoid during levalbuterol use include beta-blockers as they block beta-adrenergic agonists diminishing the

bronchodilatory effect and loop and thiazide diuretics as they may enhance hypokalemic effects (Levalbuterol, 2019).



Global Initiative for Chronic Obstructive Lung Disease. (2020). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from https://goldcopd.org/wp-content/uploads/2018/11/GOLD-2019-v1.7-FINAL-14Nov2018-WMS.pdf

Hsu, E., Bajaj, T. (2019). Beta 2 agonists. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK542249/

Levalbuterol. (2019). Retrieved from https://www.drugs.com/ppa/levalbuterol.html


In 2007, and expert panel was commissioned by the National Asthma Education and Prevention Program (NAEPP) to develop guidelines for classifying asthma, establishing goals for treating it, and providing a stepwise approach for medication selection (Miller, 2016, p. 913). The panel classified asthma into four groups based on its severity. Those groups are mild intermittent asthma, mild persistent asthma, moderate persistent asthma, and severe persistent asthma. These groups take into account the patients’ need for medication to relieve their symptoms, their nighttime symptoms, and their lung function (Miller, 2016, p. 915). The panel set the goals for therapy to include reducing the patients’ impairment, reducing their risk for recurrent exacerbations, and preventing the loss of lung function. Drug selection is, of course, dependent upon the classification of asthma that the patient falls into. An albuterol inhaler is a short acting inhaled beta-2 adrenergic agonist used in the treatment of mild intermittent asthma. It works by relaxing smooth muscle in the airways and allowing airflow to increase in the lungs. More specifically, it increases the levels of cyclic adenosine monophosphate (cAMP) through the stimulation of beta-2 adrenergic receptors in the smooth muscle, resulting in bronchodilation, which reduces airway resistance (Edmunds et al., 2014, p. 208). The inhaled formulation of albuterol generally exerts its effects locally and after inhalation, it is absorbed over several hours from the respiratory tract. It is the drug of choice for the fast relief of symptoms in asthmatic patients and is primarily used on an as needed basis. It is also used to prevent exercise-induced asthma (Edmunds et al., 2014, p. 208). Some common side effects include palpitations, tachycardia, increased blood pressure, cough, dry throat, chest tightness, GI distress, headache, dizziness, vertigo, and hypersensitivity. Serious adverse effects include arrhythmias, dyspnea, and hypokalemia (Edmunds et al., 2014, p. 219). Because albuterol is a sympathomimetic, its effects are increased when combined with other sympathomimetics. When taken with beta-adrenergic blocking agents, albuterol’s broncodilating effects are decreased. Its effectiveness is also decreased when taken with insulin or oral hypoglycemic agents. When prescribing this medication, one thing to consider is the patient’s cardiovascular history. Albuterol may cause adverse cardiovascular effects in some patients, especially those with coronary insufficiency, cardiac arrhythmias, and hypertension (Edmunds et al., 2014, p. 216).



Edmunds, M. W., Mayhew, M. S., & Setter, S. M. (2014). Asthma and chronic obstructive pulmonary disease medications. In Pharmacology for the primary care provider (4th ed., pp. 204-224). Mosby.

Miller, B. J. (2016). Asthma and chronic obstructive pulmonary disease. In T. M. Woo & M. V. Robinson, Pharmacotherapeutics for advanced practice nurse prescribers (4th ed., pp. 913-942). F A Davis Company.


Anticholinergics antagonize the parasympathetic effects of acetylcholine, which is a parasympathetic neurotransmitter in the airways that is involved in the pathophysiology of obstructive airway diseases, such as asthma. Tiotropium bromide (Spiriva) is an anticholinergic medication that reduces the acetylcholine-induced inflammatory response by inhibiting the release of chemokines and the recruitment of inflammatory cells. These long-acting muscarinic antagonists (LAMA) give clinicians and patients an additional tool to manage asthma as add-on therapy to inhaled corticosteroids (ICS) and a long-acting beta-adrenoceptor agonist (LABA) (Bonini & Scichilone, 2017).

Dosage is 2.5 mcg inhaled orally for once daily maintenance in patients ages 6 years and older. Common side effects include dry mouth, runny nose, tachycardia, upper respiratory tract infection, shortness of breath and headache. Severe side effects may include angioedema, blurred vision, hypertension, worsening bronchospasm, and QT prolongation (Gosens & Gross, 2018). It should also cautiously be used in patients with moderate to severe renal impairment. Tiotropium is contraindicated in patients with hypersensitivity to ipratropium and to milk protein. Due to this drug’s anticholinergic properties, it is known to worsen conditions such as narrow-angle glaucoma, benign prostatic hyperplasia, and bladder neck obstruction. Drug interactions with tiotropium include benztropine mesylate, dimenhydrinate, donepezil, tacrine, scopolamine, and dicyclomine. Cannabinoid containing products may enhance the tachycardic effect of tiotropium (Chari & McIvor, 2018).

Bonini and Scichilone (2017) provide evidence from several clinical trials in adult and pediatric populations showing that tiotropium is well tolerated and significantly improves symptoms as an add-on treatment. The first study showed that tiotropium added on to ICS and LABA therapy in adult patients with poorly controlled symptomatic asthma resulted in an improvement of up to 154 mL in peak FEV1, with a 21 percent risk reduction for severe asthma exacerbation. The second study showed that tiotropium had a comparable safety profile to placebo in adolescents and children, as well as demonstrated it as a well-tolerated treatment improving lung function and asthma control regardless of severity. Overall, these data show that tiotropium is efficacious and has a favorable safety profile across a range of asthma severity in adults, adolescents, and children.


 Bonini, M., & Scichilone, N. (2017). Tiotropium in asthma: back to the future of anticholinergic treatment. Clinical & Molecular Allergy, 15, 1–11. https://doi-org.lopes.idm.oclc.org/10.1186/s12948-017-0076-1

 Chari, V. M., & McIvor, R. A. (2018). Tiotropium for the Treatment of Asthma: Patient Selection and Perspectives. Canadian respiratory journal, 2018, 3464960. https://doi.org/10.1155/2018/3464960

 Gosens, R., & Gross, N. (2018). The mode of action of anticholinergics in asthma. The European respiratory journal, 52(4), 1701247. https://doi.org/10.1183/13993003.01247-2017