Hypoventilation Syndromes Medication

  • Author: Jazeela Fayyaz, DO; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Apr 20, 2012
 

Medication Summary

Several drugs may be used to treat hypoventilation syndromes. Most produce the desired effect by stimulating the central respiratory drive, by reversing the effects of other medications that can depress the central respiratory drive, or by inducing bronchial dilatation.

For example, bronchodilators such as beta agonists (eg, albuterol), anticholinergic agents (eg, ipratropium bromide), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive lung disease and severe bronchospasm. Additionally, theophylline may improve diaphragm muscle contractility and stimulate the respiratory center.

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Beta2 Agonists

Class Summary

Bronchodilators act to decrease the muscle tone in small and large airways in the lungs, thereby increasing ventilation. These drugs include beta adrenergic agonists, methylxanthines, and anticholinergic agonists.

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Albuterol (Proventil HFA, Ventolin HFA, ProAir HFA)

 

Albuterol is a beta agonist for the reversal of bronchospasm. It relaxes bronchial smooth muscle by its action on beta2 receptors, with little effect on cardiac muscle contractility.

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Metaproterenol

 

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

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Ipratropium (Atrovent)

 

Ipratropium is an anticholinergic bronchodilator that is chemically related to atropine.

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Theophylline (Elixophyllin Elixir, Theo-24)

 

Theophylline potentiates exogenous catecholamines, stimulates endogenous catecholamine release, and stimulates diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation.

The drug's popularity has decreased because of theophylline's narrow therapeutic range and frequent toxicity. The therapeutic range is 10-20 mg/dL, but bronchodilation may require near-toxic (>20 mg/dL) levels. The clinical efficacy is controversial, especially in an acute setting

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Opioid Reversal Agents

Class Summary

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

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Naloxone

 

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

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Benzodiazepine Toxicity Antidotes

Class Summary

These drugs are used to reverse the CNS-depressant effects of benzodiazepine overdose. Their ability to reverse benzodiazepine-induced respiratory depression is less predictable.

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Flumazenil (Romazicon)

 

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

Flumazenil is short acting, with a half-life of 0.7-1.3 hours. However, because most benzodiazepines have longer half-lives, multiple doses should be administered to avoid relapse into a sedative state.

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Pulmonary, Other

Class Summary

These agents inhibit the enzyme carbonic anhydrase, which, in turn, increases HCO3 excretion and causes metabolic acidosis. The metabolic acidosis subsequently stimulates ventilation.

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Acetazolamide (Diamox Sequels)

 

Acetazolamide improves symptomatic periodic breathing and hypoxia.

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Progestins

Class Summary

These agents stimulate the central respiratory drive and may be beneficial in patients with hypoventilation.

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Medroxyprogesterone acetate (Provera, Depo-Provera)

 

Medroxyprogesterone acetate increases the central respiratory drive and stimulates ventilation. It may increase upper airway muscular tone. For the treatment of hypoventilation, higher doses than usual of medroxyprogesterone acetate are required to induce significant reductions in hypercapnia.

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Contributor Information and Disclosures
Author

Jazeela Fayyaz, DO  Pulmonologist, Department of Pulmonology, Unity Hospital

Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Klaus-Dieter Lessnau, MD, FCCP  Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

Ryland P Byrd Jr, MD Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, East Tennessee State University, James H Quillen College of Medicine; Medical Director of Respiratory Therapy, James H Quillen Veterans Affairs Medical Center

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

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.

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

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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