Asthma and COPD Agents




Intermittent – mild

Daytime symptoms ≤2×/week

Short-acting β2 agonist

Nocturnal awakenings ≤2×/month

Use SABA ≤2×/week

FEV1 or PEF ≥80 % predicted

Asymptomatic between exacerbations

0 –1 exacerbations/year requiring steroids

Persistent – mild

Daytime symptoms >2×/week but <1×/day

Inhaled glucocorticoid

Nocturnal awakenings 3–4×/month


Use SABA >2×/week but not daily

Leukotriene receptor antagonist

FEV1 or PEF ≥80 % predicted

Mast cell stabilizer

Persistent – moderate

Normal FEV1 between exacerbations

Inhaled glucocorticoid plus long-acting β2 agonist

≥2 exacerbations/year requiring steroids
Daily symptoms
Nocturnal awakenings >1×/week
Use SABA daily
Some limitation in normal activity


FEV1 or PEF 60–80 % predicted

Leukotriene receptor antagonist or lipoxygenase inhibitor


≥2 exacerbations/year requiring steroids

Oral glucocorticoids (acutely)


Symptoms throughout the day


Frequent nocturnal awakenings
Use SABA multiple times/day

Extreme limitation in normal activity

FEV1 or PEF ≤60 predicted

≥2 exacerbations/year requiring steroids

SABA short-acting β2 agonist, PEF peak expiratory flow


Fig. 18.1
A Venn diagram depicting the three entities of obstructive airway disease and the ways in which they can coexist. Asthma can exist as its own entity or as a bronchospastic component to COPD (chronic bronchitis and emphysema). Alternatively, COPD can exist purely without a reversible bronchospastic/asthmatic component. In addition, each subtype may also contain an element of the other. Asthma and COPD can exist as milder entities without significant airflow obstruction (outside blue box) or with significant obstruction (within blue box) (Modified from Ref. [1])

COPD affects approximately 5 % of the population according to the Centers for Disease Control and Prevention [2] with a mortality of over 120,000 individuals per year [3]. Chronic bronchitis is defined as a chronic productive cough for 3 months over two successive years and emphysema occurs as a result of destruction to alveolar walls causing permanent airspace dilation distal to the terminal bronchioles. The inflammation leading to these two processes is characterized by the infiltration of neutrophils, macrophages, and CD 8+ T lymphocytes [4]. Cigarette use is the most common cause of this inflammation, although inhalational exposures and α-1 antitrypsin deficiency can contribute as well. The diagnosis of COPD is suggested by symptoms of dyspnea with or without exertion, by chronic cough and sputum production, and by spirometric evidence of irreversible airflow limitation during forced expiration, i.e., an FEV1/FVC <70 % and FEV1 <80 % of the predicted value not reversible with bronchodilators.

According to the National Institutes of Health National Asthma Education and Prevention Program, asthma affects approximately 22 million people of all ages in the United States [5]. The inflammation associated with asthma is distinct from that of COPD and involves eosinophils, mast cells, and CD4+ T lymphocytes [4]. This inflammation leads to the destruction of epithelium, the remodeling and thickening of airway walls, airway edema, mucous plugging, and bronchial hyperresponsiveness, all of which can lead to airflow obstruction characterized by wheezing, cough, dyspnea, and chest tightness. The diagnosis of asthma is suggested by episodic symptoms, by triggers such as exercise, cold air, and allergens, and by the presence of a family history of atopy. In contrast to COPD, patients with asthma demonstrate reversibility of their airflow obstruction. Spirometric data suggestive of asthma includes an FEV1/FVC <70 % and an FEV1 <80 % of the predicted value with a post-bronchodilator response demonstrating an increase in FEV1 >12 % from baseline with at least a 200 mL increase in FEV1 [6].

The pharmacologic management of COPD and asthma is very similar with some exceptions. An asthma attack may be acutely managed with short-acting bronchodilators (β2 agonists and anticholinergics) and systemic glucocorticoids. COPD exacerbations, in addition to bronchodilators and systemic glucocorticoids, may also be treated with antibiotics, as approximately 50 % of exacerbations are precipitated by bacterial infections [7]. Depending on the severity, chronic asthma can be controlled with a combination of multiple agents including short- or long-acting β agonists, inhaled corticosteroids, mast cell stabilizers, methylxanthines, leukotriene modifiers (receptor antagonists or lipoxygenase inhibitors), systemic corticosteroids, or immunomodulators. Table 18.1 delineates the recommended therapies according to severity of asthma [5, 8]. Epinephrine, as an intravenous bronchodilator, may be of benefit in severe attacks of asthma where massive bronchoconstriction and restrictive airflow limit the delivery of inhaled bronchodilators to the lungs [9, 10].

COPD may be managed with short- or long-acting β2 agonists, long-acting anticholinergics, and inhaled glucocorticoids (sometimes combined as triple-inhaler therapy), methylxanthines, and PDE-4 inhibitors [11].

Drug Class and Mechanism of Action [5, 8, 1214]

Short-Acting β2 Agonists (SABA)

Albuterol, Levalbuterol, Terbutaline, Bitolterol, Pirbuterol, and Metaproterenol


Binds to the β2 G-protein-coupled adrenergic receptor causing activation of adenyl cyclase, production of cAMP, stimulation of protein kinase A, and inactivation of myosin light-chain kinase leading to smooth muscle relaxation and bronchodilation.


Relief of acute bronchospasm in asthma and COPD. Prophylaxis against exercise-induced asthma.


  • Albuterol: For use in patients >4 years: 1–2 puffs q4–6 h as needed. Two puffs 15 min before exercise to prevent exercise-induced asthma. Maximum: 12 inhalations/day.

  • Levalbuterol: Available in three different 3 mL dose vials: 0.31, 0.63, 1.25 mg. For ages 6–11 years: 0.31 mg three times/day q6–8 h by nebulizer. For patients >12 years: 0.63–1.25 mg three times/day q6–8 h by nebulizer.

  • Terbutaline: May be administered subcutaneously, PO, or inhaled. Subcutaneous dosing has a quick onset of action due to high lipid solubility: Inject 0.25 mg into the lateral deltoid area; additional 0.25 mg dose can be repeated every 15–30 min for a total of three doses. 2.5–5 mg PO q6 h, maximum 15 mg/24 h. 1–2 inhalations q4–6 h.

  • Bitolterol: Two inhalations q8 h. Maximum: Three inhalations q6 h or two inhalations q4 h.

  • Pirbuterol: For use in patients >12 years: Two puffs q4–6 h.

  • Metaproterenol: 2–3 inhalations q3–4 h. Maximum: 12 inhalations/day. Not recommended for children <12 years and in those with cardiac arrhythmias associated with tachycardia.

Side Effects/Drug Interactions

Tachycardia, skeletal muscle tremor, hypokalemia, increased lactic acid, headache, and hyperglycemia. Inhaled route usually causes few systemic side effects. Caution with use in patients with cardiovascular disease.


Ipratropium Bromide, Tiotropium Bromide


Blocks the action of acetylcholine on postsynaptic muscarinic receptors in the lung, thus inhibiting the influx of calcium and reversing vagally mediated bronchoconstriction. Decreases mucus gland secretion.


Ipratropium: Relief of acute bronchospasm in asthma and COPD in conjunction with a β2 agonist. Tiotropium: Long-term maintenance treatment of bronchospasm associated with COPD.


  • Ipratropium bromide: For patients >12 years: Two inhalations q6 h. Maximum: 12 inhalations/day.

  • Tiotropium bromide: Two inhalations of powder contents of one capsule once daily.

Side Effects/Drug Interactions

Increased wheezing, drying of respiratory secretions and mouth, blurred vision if contact with eyes. If used as nebulizer treatment, usually produces less cardiac stimulation compared to SABAs. Reverses only cholinergic-induced bronchospasm, not antigenic or exercise-induced asthma. Treatment of choice for β-blocker-induced bronchospasm. Not proven to be adequate for long-term control method for asthma.

Inhaled Corticosteroids

Beclomethasone Dipropionate, Budesonide, Flunisolide, Fluticasone Propionate, Mometasone Furoate, Triamcinolone Acetonide


Anti-inflammatory. Decreases airway hyperresponsiveness, blocks release of cytokines, and inhibits inflammatory cell migration and activation. Reversal of β2 receptor downregulation.


Long-term prevention of symptoms and reversal of inflammation in asthma and COPD.


  • Beclomethasone dipropionate: Available as a 40 mcg or 80 mcg puff. For children 5–11 years: 40–80 mcg twice daily. For adults: 40–320 mcg twice daily.

  • Budesonide: Available as a 90 mcg or 180 mcg inhaler. For children 6–17 years: 180 mcg twice daily with a maximum dose of 360 mcg twice daily. For patients >18 years: 360 mcg twice daily with a maximum of 720 mcg twice daily. Available as a budesonide/formoterol combination inhaler (80/4.5 and 160/4.5; for patients >12 years – two inhalations twice daily).

  • Flunisolide: 250 mcg/puff. For children >6 years: two inhalations twice daily. For adults: 2–4 inhalations twice daily.

  • Fluticasone propionate: Available as a 44, 110, or 220 mcg inhaler. Dosing varies and must be individualized to patient. Also available as a 50, 100, or 250 mcg Diskus delivery system – 1–2 puffs twice daily. Available as a fluticasone/salmeterol combination inhaler (45/21, 115/21, and 230/21; for patients >12 years – two inhalations twice daily) or Diskus (100/50, 250/50, or 500/50; Diskus with the 100/50 dose for children 4–11 years – one inhalation twice daily for all doses.)

  • Mometasone furoate: Available in 110 and 220 mcg preparations. For children 4–11 years, use of 110 mcg inhaler in the evening recommended. For patients >12 years, 220–880 mcg recommended. Available as a mometasone/formoterol combination in doses of 100/5 and 200/5; in patients >12 years – two puffs twice daily.

  • Triamcinolone acetonide: Available as a 75 mcg inhaler. For children 6–12 years: 2–8 puffs/day in divided doses. For adults: 4–16 puffs/day in divided doses.

Side Effects/Drug Interactions

Oral thrush (candidiasis), dysphonia, cough. In high doses, systemic side effects such as skin thinning, osteoporosis, easy bruising, and adrenal suppression may occur. In low to medium doses, possible suppression of growth velocity observed in children. Spacer/holding chambers and non-breath-activated MDIs with mouth washing after use decrease local side effects. Dexamethasone is not included for long-term inhalation use due to high absorption and suppressive side effects.

Long-Acting Beta Agonists (LABAs)

Formoterol Fumarate, Salmeterol Xinafoate


Binds to the β2 G-protein-coupled adrenergic receptor causing activation of adenyl cyclase, production of cAMP, stimulation of protein kinase A, and inactivation of myosin light-chain kinase leading to smooth muscle relaxation and bronchodilation. Compared to SABAs, formoterol has a similar onset of action (<5 min), while salmeterol has a longer onset (15–30 min). Both salmeterol and formoterol have longer durations of actions of at least 12 h.


Prevention of exercise-induced asthma and maintenance treatment of asthma and COPD. Not indicated for acute exacerbations. The FDA has recommended that LABAs be used only in conjunction with inhaled corticosteroids (see Black Box Warning below).


Sep 18, 2016 | Posted by in ANESTHESIA | Comments Off on Asthma and COPD Agents
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