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Respiratory Acidosis Medication

  • Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Jul 31, 2015
 

Medication Summary

No drugs are used specifically to treat respiratory acidosis. Medical therapies are directed at the underlying disease or disorder causing hypoventilation and, therefore, respiratory acidosis. The drugs for these various conditions are included in this review.

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Beta2 Agonists

Class Summary

Beta2 agonists, by decreasing muscle tone in both small and large airways in the lungs, increase ventilation. Beta2 agonists activate the beta2 -adrenergic receptors on the surface of smooth muscle cells of the bronchial airways, thereby increasing intracellular cyclic adenosine monophosphate (cAMP). This interaction results in smooth muscle relaxation.

The short-acting beta2 agonists (albuterol, levalbuterol, metaproterenol, and pirbuterol) are used for the treatment or prevention of bronchospasm. These medications are typically delivered to the bronchial smooth muscles through inhalation of aerosolized or nebulized preparations of these medications. Oral preparations of albuterol and metaproterenol are available but are less effective and more prone to complications.

The long-acting beta2 agonists (arformoterol, formoterol, indacaterol, and salmeterol) are typically used in patients with more persistent symptoms. The bronchodilating effects of these drugs last more than 12 hours. Each requires twice-daily dosing, except for indacaterol, which is administered once daily.

Albuterol (Proventil HFA, Ventolin HFA, AccuNeb, ProAir HFA)

 

Albuterol is a beta agonist for bronchospasm that is refractory to epinephrine. This agent relaxes bronchial smooth muscle through its action on beta2 receptors; it has little effect on cardiac muscle contractility.

Salmeterol (Serevent Diskus)

 

By relaxing the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis, salmeterol can relieve bronchospasms. It also may facilitate expectoration. The long-acting bronchodilating effect of salmeterol lasts for more than 12 hours. This agent is used on a fixed schedule, in addition to regular use of anticholinergic agents. When salmeterol is administered at higher or more frequent doses than recommended, the incidence of adverse effects is higher.

Metaproterenol

 

Metaproterenol is a beta2-adrenergic agonist that relaxes bronchial smooth muscle, with little effect on heart rate.

Levalbuterol (Xopenex, Xopenex HFA)

 

Levalbuterol acts on beta2 receptors, causing relaxation of bronchial smooth muscle, with little effect on heart rate.

Pirbuterol (Maxair)

 

Pirbuterol is a beta2-adrenergic agonist with a structure similar to that of albuterol. Binding to beta2-adrenergic receptors causes relaxation of bronchial smooth muscle.

Formoterol (Foradil, Perforomist)

 

Formoterol acts on beta2 receptors, with little effect on the cardiovascular system. It is long acting and relaxes the smooth muscles of the bronchioles, with little effect on heart rate.

Indacaterol (Arcapta Neohaler)

 

Indacaterol acts on beta2 receptors, with little effect on the cardiovascular system. It is long acting and relaxes the smooth muscles of the bronchioles, with little effect on heart rate.

Arformoterol (Brovana)

 

Arformoterol acts on beta2 receptors, with little effect on the cardiovascular system. It is long acting and relaxes the smooth muscles of the bronchioles, with little effect on heart rate.

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Anticholinergics, Respiratory

Class Summary

The anticholinergic medications compete with acetylcholine for postganglionic muscarinic receptors, thereby inhibiting cholinergically mediated bronchomotor tone and resulting in bronchodilatation. These agents effectively block vagally mediated reflex arcs that cause bronchoconstriction. When inhaled, these medications are poorly absorbed systemically and are, therefore, relatively safe.

Compared with beta2 -adrenergic agents, the inhaled short-acting anticholinergic medication ipratropium has equivalent-to-superior bronchodilator activity in stable chronic obstructive pulmonary disease (COPD) patients. When ipratropium is used in combination with beta2 -adrenergic agonists, a synergistic effect on bronchodilatation occurs. This medication has a slower onset of action than the beta2 -adrenergic agents and is, therefore, less suitable for use on an as-needed basis.

Ipratropium (Atrovent HFA)

 

Ipratropium is an anticholinergic bronchodilator that is chemically related to atropine. It inhibits serous and seromucous gland secretions.

Tiotropium (Spiriva)

 

Tiotropium is a quaternary ammonium compound that elicits anticholinergic and antimuscarinic effects with inhibitory effects on M3 receptors on airway smooth muscles, leading to bronchodilation. This agent is available in a capsule form that contains a dry powder for oral inhalation via the HandiHaler inhalation device. Tiotropium helps patients by dilating narrowed airways and keeping them open for 24 hours. It is given once daily.

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Xanthine Derivatives

Class Summary

Xanthine derivatives such as theophylline inhibit phosphodiesterase, resulting in an increase in cAMP. The increase in cAMP causes relaxation of bronchial smooth muscle. Theophylline is dosed orally. Its analogue, aminophylline, can be given intravenously (IV). In addition, theophylline may improve diaphragmatic muscle contractility and stimulate the central nervous system (CNS) respiratory center.

Theophylline (Theo-24, Elixophyllin)

 

Theophylline potentiates exogenous catecholamines by stimulating endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation. The popularity of this agent has decreased because of its narrow therapeutic range and its toxicities. Theophylline's therapeutic range is relatively narrow, between 8-15 mg/dL. Unfortunately, bronchodilation may require near-toxic levels (>20 mg/dL). The clinical efficacy of this agent is controversial, especially in the acute setting.

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Corticosteroids

Class Summary

Inflammation plays a significant role in the pathogenesis of asthma. Although the inflammatory pathway mediators differ, inflammation is also important in the pathogenesis of COPD. Accordingly, glucocorticosteroids are used to temper the inflammation in these diseases.

The inhaled glucocorticoids (budesonide, fluticasone, and mometasone) have a direct route to the airways. They are only minimally absorbed systemically and thus have fewer adverse side effects than systemic glucocorticoids do. Inhaled glucocorticoids improve airflow in asthmatic patients by reducing inflammation and, in the long-term, preventing airway remodeling. These medications are less effective in COPD patients. They may slow the rate of progression in patients with COPD.

The systemic glucocorticoids (methylprednisolone, prednisone, and prednisolone) are highly efficacious in the treatment of acute exacerbations of asthma. They are also widely accepted and recommended in the treatment of COPD exacerbations. For long-term use of these medications, the adverse effect profile must be weighed against the potential benefits.

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

 

Budesonide reduces inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing the production of cytokines and other mediators involved in bronchospasm. This agent is available as Pulmicort Flexhaler powder for inhalation (90 µg/actuation and 180 µg/actuation; each actuation delivers 80 µg and 160 µg, respectively) or Pulmicort Respules.

Fluticasone inhaled (Flovent Diskus, Flovent HFA)

 

Fluticasone may decrease the number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. It also has vasoconstrictive activity.

Mometasone (Asmanex Twisthaler)

 

Mometasone reduces inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing the production of cytokines and other mediators involved in bronchospasm.

Methylprednisolone (A-Methapred, Medrol, Solu-Medrol)

 

Methylprednisolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability.

Prednisone

 

The immunosuppressant prednisone is a first-line therapy administered for the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity and CD4 counts.

Prednisolone (Pediapred, Flo-Pred, Orapred)

 

Prednisolone may reduce inflammation by reversing increased capillary permeability and suppressing PMN activity and CD4 counts.

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Benzodiazepine Toxicity Antidotes

Class Summary

Benzodiazepine antagonists are used in reversing the CNS-depressing effects of benzodiazepine overdoses. However, these agents’ ability to reverse the benzodiazepine-induced respiratory depression is less predictable. Care must be taken in reversing the effects of benzodiazepines because patients may have seizures if benzodiazepine reversal is accomplished too vigorously.

Flumazenil (Romazicon)

 

Flumazenil reverses the effects of benzodiazepines in an overdose by selectively antagonizing the gamma-aminobutyric acid (GABA)–benzodiazepine receptor complex. If an overdosed patient has not responded after 5 minutes of administration of flumazenil to a cumulative dose of 5 mg, the cause of the sedation is unlikely to be a benzodiazepine.

Flumazenil is a short-acting agent, with a half-life of 0.7-1.3 hours; however, because most benzodiazepines have longer half-lives, multiple doses should be administered so that patients do not relapse into a sedative state.

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Opioid Antagonists

Class Summary

Opioid abuse, toxicity, and overdose are potential etiologies of hypoventilation and respiratory acidosis. Opioid antagonists can be used to reverse the effects of opiates and to improve ventilation.

Naloxone

 

Naloxone is a pure opioid antagonist that prevents or reverses opioid effects (eg, hypotension, respiratory depression, and sedation), possibly by displacing opiates from their receptors. This agent is used to reverse opioid intoxication.

Naltrexone (Vivitrol, ReVia)

 

Naltrexone is an opioid antagonist that prevents or reverses opioid effects (eg, hypotension, respiratory depression, and sedation), possibly by displacing opiates from their receptors. It shows a higher affinity for mu receptors. This agent may be used to reverse opioid intoxication.

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Contributor Information and Disclosures
Author

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas M Roy, MD Chief, Division of Pulmonary Disease and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, Fellowship Program Director, James H Quillen College of Medicine, East Tennessee State University

Thomas M Roy, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Southern Medical Association, Wilderness Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Wael El Minaoui, MBBS Fellow in Pulmonary/Critical Care Medicine, East Tennessee State University, James H Quillen College of Medicine

Disclosure: Nothing to disclose.

Jackie A Hayes, MD, FCCP Clinical Assistant Professor of Medicine, University of Texas Health Science Center at San Antonio; Chief, Pulmonary and Critical Care Medicine, Department of Medicine, Brooke Army Medical Center

Jackie A Hayes, MD, FCCP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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