Hypoventilation Syndromes Medication

Updated: Sep 22, 2016
  • Author: Jazeela Fayyaz, DO; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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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.

Long-acting beta-2 agonists and long-acting anticholinergics such as tiotropium can also be helpful. Inhaled steroids might help, for short-term treatment.


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.

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.


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

Ipratropium (Atrovent)

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

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


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.


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.


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.

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.


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.

Acetazolamide (Diamox Sequels)

Acetazolamide improves symptomatic periodic breathing and hypoxia.



Class Summary

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

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.