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Pediatric Respiratory Acidosis Treatment & Management

  • Author: Mithilesh K Lal, MBBS, MD, MRCP, FRCPCH; Chief Editor: Timothy E Corden, MD  more...
Updated: Jun 05, 2014

Approach Considerations

The goals of therapy are to remove the underlying cause and return the arterial partial pressure of carbon dioxide (Pa CO2) to baseline. Patients with acute respiratory acidosis require admission to the intensive care unit (ICU) for close monitoring and possible advanced airway management with mechanical respiratory support.

Failure to aggressively manage acute respiratory acidosis with assisted ventilation can lead to an otherwise avoidable respiratory or cardiovascular arrest. Use of sedative medications in a nonintubated patient can worsen mild respiratory acidosis, leading to unrecognized carbon dioxide narcosis.

If hypoxemia accompanies hypercapnia, oxygen should be administered. Diagnosis and directed therapy must accompany oxygen administration. In chronic hypercapnia, supplemental oxygen therapy can worsen hypercapnia by reducing the respiratory drive and increasing dead-space ventilation through loss of hypoxic pulmonary vasoconstriction.

Some institutions have successfully used extracorporeal membrane oxygenation (ECMO) to reduce high-Pa CO2 states (eg, in treatment of patients with severe asthma).

Correct electrolyte abnormalities associated with muscle weakness, such as hypophosphatemia, hypokalemia, hypomagnesemia, and hypocalcemia. Maximize nutrition, but avoid overfeeding and high carbohydrate content, because these can increase carbon dioxide production. If a metabolic alkalosis develops during diuretic therapy, correct it by replacing chloride and, if needed, careful replacement of potassium.


Assisted Ventilation

Noninvasive positive-pressure ventilation

Noninvasive positive-pressure ventilation (NPPV) can be delivered continuously or intermittently to increase alveolar ventilation and decrease work of breathing. It is effective in the treatment of chronic respiratory failure in patients with restrictive lung disease (eg, neuromuscular disease or kyphoscoliosis).

In patients with chronic obstructive pulmonary disease (COPD), early application of NPPV in hypercapnic respiratory failure can decrease the need for invasive mechanical ventilation and decrease length of stay in the hospital.

Advantages of NPPV include a decreased incidence of nosocomial infections (eg, sinusitis or pneumonia), increased comfort in comparison with tracheal intubation, and the ability to maintain verbal communication. Disadvantages include facial skin necrosis, conjunctivitis, and aspiration.

Mechanical ventilation

Mechanical ventilation increases minute ventilation and decreases dead space. It is the mainstay of treatment for acute hypercapnia. The decision to start mechanical ventilation when an underlying disease is associated with chronic respiratory acidosis should be well thought out and well informed. Because of limited baseline pulmonary reserve, weaning from ventilatory support and extubation is usually difficult.

Various clinical factors determine the proper timing and method of mechanical ventilation, including the etiology of the ventilatory failure and patient factors (eg, exhaustion, prognosis, and prospect of improvement with concurrent therapy).

In acute hypercapnia, mechanical ventilation usually can quickly and safely correct Pa CO2 to a normal value. In chronic hypercapnia, the goal of mechanical ventilation is near-normal pH with the patient’s baseline Pa CO2. If the Pa CO2 must be normalized, this should be done over 2-3 days to prevent a sudden increase in cerebrospinal fluid (CSF) pH, which can cause seizures.

Intratracheal pulmonary ventilation

Sometimes, mechanical ventilation is ineffective in reducing hypercapnia because of increased dead space. In such cases, intratracheal pulmonary ventilation can help in treating intractable hypercapnia.[4] This procedure involves passing a catheter down the endotracheal tube to produce a reverse flow up the tube. The dead-space gas is flushed out, and rebreathing of carbon dioxide decreases.

Permissive hypercapnia

In acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), a strategy of low tidal volume (4-6 mL/kg) allows the Pa CO2 to rise to 60-70 mm Hg so as to avoid stretch-induced lung injury.[5] In a multicenter randomized trial, mechanical ventilation with a low tidal volume decreased mortality and increased the number of days without ventilator use.[6]

A respiratory acidosis (pH >7.25) is acceptable as long as adequate oxygenation and cardiovascular stability are maintained. Permissive hypercapnia is contraindicated in patients with traumatic brain injury, pulmonary hypertension, or renal disease, because an elevated Pa CO2 may worsen the underlying disease.


Pharmacologic Therapy

Treatment of a concurrent metabolic acidosis or buffering the acidemia with a respiratory acidosis can be considered. Tromethamine (THAM) has been used to prevent and correct systemic or respiratory acidosis. NaHCO3 administration should be used carefully if the patient cannot increase minute ventilation because it increases the amount of carbon dioxide to be excreted. Therefore, NaHCO3 should be administered slowly if it is used.

Disease-specific interventions may be needed, such as the following:

  • Antibiotics for pneumonia
  • Naloxone for narcotic-associated hypoventilation
  • Bronchodilators (eg, albuterol) and steroids for asthma

Complications of Treatment

Respiratory acidosis may precede acute respiratory failure and possible cardiovascular failure. Convulsions may result if Pa CO2 levels are restored too quickly in patients with chronic hypercapnia. Posthypercapnic alkalosis can occur in patients with chronic hypercapnia if Pa CO2 is rapidly reduced with mechanical ventilation.

The kidneys have a relatively slow mechanism to correct the HCO3 excess. The metabolic alkalosis can be treated by replacing chloride, potassium, or by increasing renal HCO3 excretion with acetazolamide. Care must be taken not to correct a compensating metabolic alkalosis without addressing the underlying respiratory acidosis.

Tracheal intubation may lead to upper-airway edema and difficult extubation, especially in chronically ill patients with limited baseline pulmonary reserve. If tracheal intubation is required in a spontaneously breathing person with high minute ventilation, care must be taken to maintain that level of minute ventilation to avoid a sudden increase in Pa CO2 that could contribute to hemodynamic instability, CNS injury, or cardiopulmonary arrest.



As noted (see Pathophysiology), the respiratory quotient (RQ) is defined as the ratio of carbon dioxide produced to the amount of oxygen consumed while making energy. The RQ varies according to the fuel source substrate: It is 1.0 for carbohydrate, 0.8 for protein, and 0.7 for fat.

Thus, for a given amount of substrate burned, carbohydrate produces the greatest amount of carbon dioxide, and fat produces the least. Patients on a high-carbohydrate diet must be able to accommodate or must be provided with higher minute ventilation in order to balance the increased carbon dioxide load, or else they run the risk of developing a respiratory acidosis.

Data have suggested that a specialized enteral formula can be a useful adjunctive therapy in the management of ARDS because it reduces lung inflammation and improves oxygenation. The prototype is a low-carbohydrate, calorically dense formula containing eicosapentaenoic acid (EPA) from fish oil, gamma-linolenic acid (GLA) from borage oil, and elevated levels of antioxidants. One commercially available formula is Oxepa (Abbott Laboratories, Abbott Park, IL).

The function of selected micronutrients, including those that serve antioxidant roles, is important in the course of ARDS and should be considered in the care of patients. Relevant antioxidants include vitamins E and C and the carotenoids.

If obesity is contributing to obstructive sleep apnea, a weight-reduction and exercise program should be part of the management plan.


Long-Term Monitoring

For chronic respiratory acidosis, frequent follow-up with pulmonary function testing is necessary to provide a reference baseline and to monitor for changes during acute illness.

NPPV is an effective home therapy for chronic respiratory failure caused by obstructive sleep apnea, obesity-hypoventilation syndrome, or neuromuscular disease. Therapy can be continuous, intermittent with certain activities, or nocturnal. Home nursing can provide additional care.

Contributor Information and Disclosures

Mithilesh K Lal, MBBS, MD, MRCP, FRCPCH MRCP, MRCPCH, FRCPCH, Consultant Neonatologist, James Cook University Hospital, UK

Mithilesh K Lal, MBBS, MD, MRCP, FRCPCH is a member of the following medical societies: British Medical Association, Royal College of Physicians, Royal College of Paediatrics and Child Health, British Association of Perinatal Medicine, American Pediatric Society, Society for Pediatric Research, Neonatal Society, Nepal Medical Association

Disclosure: Nothing to disclose.


Ronald Litman, DO Professor of Anesthesiology and Pediatrics, University of Pennsylvania School of Medicine

Ronald Litman, DO is a member of the following medical societies: American Academy of Pediatrics, American Society of Anesthesiologists, Society for Pediatric Anesthesia

Disclosure: Nothing to disclose.

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.

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.


G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, University of Miami, Leonard M Miller School of Medicine; Chief, Division of Pediatric Critical Care Medicine, Medical Manager, Urban Search & Rescue, South Florida TF-2, Medical Director, Holtz Children's Hospital Palliative Care Team, Medical Director, Tilli Kids – Pediatric Initiative of Hospice Care of SE Florida, Director, Pediatric Critical Care Transport, Holtz Children's Hospital/Jackson Memorial Hospital

G Patricia Cantwell, MD, FCCM 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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