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Pediatric Respiratory Failure Medication

  • Author: Shelley C Springer, JD, MD, MSc, MBA, FAAP; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Apr 27, 2014
 

Medication Summary

The use of medications in the treatment of respiratory failure depends on the underlying disorder. For example, corticosteroids and beta-agonist medications treat an asthma exacerbation, whereas antibiotics treat bacterial pneumonia. Patients with pulmonary edema from myocardial dysfunction improve with diuretics and inotropic support.

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Pulmonary Vasodilators

Class Summary

Inhaled nitric oxide (NO) is a pulmonary vasodilator indicated to treat pulmonary hypertension. NO is also being studied for severe hypoxemia in acute respiratory distress syndrome (ARDS).

Nitric oxide, inhaled (INOmax)

 

NO is produced endogenously from the action of the enzyme NO synthetase on arginine. It relaxes vascular smooth muscle by binding to the heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cyclic guanosine monophosphate (cGMP), which then leads to vasodilation. When inhaled, NO decreases pulmonary vascular resistance and improves lung blood flow.

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Lung Surfactants

Class Summary

Exogenous surfactant can be helpful in the treatment of airspace disease. After inhalation, surface tension is reduced and alveoli are stabilized, decreasing the work of breathing and increasing lung compliance. These drugs are indicated for the prevention and treatment of neonatal RDS. They are also being investigated for the treatment of hypoxemia secondary to ARDS.

Calfactant (Infasurf)

 

This is a natural bovine calf lung extract containing phospholipids, fatty acids, and surfactant-associated proteins B (260 mcg/mL) and C (390 mcg/mL). Surfactant is an endogenous complex of lipids and proteins that lines alveolar walls and promotes alveolar stability by reducing surface tension. Relative surfactant deficiency is variably present in many lung diseases.

Poractant alfa (Curosurf)

 

Poractant alfa lines the alveolar walls and promotes alveolar stability against collapse by reducing surface tension at the air-liquid interface of the alveoli.

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Contributor Information and Disclosures
Author

Shelley C Springer, JD, MD, MSc, MBA, FAAP Professor, University of Medicine and Health Sciences, St Kitts, West Indies; Clinical Instructor, Department of Pediatrics, University of Vermont College of Medicine; Clinical Instructor, Department of Pediatrics, University of Wisconsin School of Medicine and Public Health

Shelley C Springer, JD, MD, MSc, MBA, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD Associate Professor of Clinical Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia

Margaret A Priestley, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Jimmy W Huh, MD Associate Professor of Anesthesiology, Critical Care and Pediatrics, Department of Anesthesiology and Critical Care Medicine, Perelman School of Medicine, University of Pennsylvania and Children's Hospital of Philadelphia

Jimmy W Huh, MD is a member of the following medical societies: American Academy of Pediatrics, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

G Patricia Cantwell, MD Clinical Professor, Department of Pediatrics, Miller School of Medicine, University of Miami; Director of Pediatric Critical Care Medicine, Holtz Children's Hospital/Jackson Memorial Hospital

G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress syndrome that resulted in respiratory failure.
Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting.
A Bilevel positive airway pressure support machine is shown here. This could be used in spontaneous mode or timed mode (backup rate could be set).
Table 1. Survival Statistics from CHA, 2005-2009[17]
YearCHA (US)International
200558%54%
200647%53%
200771%56%
200857%54%
200975%55%
Table 2. 2009 Top 5 Diagnoses for ECMO and Survival Rates[17]
DiagnosisCHA (US)International
Bacterial pneumonia74%57%
Viral pneumonia78%63%
Aspiration pneumonia92%66%
Non-ARDS acute respiratory failure62%51%
Other65%52%
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