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Respiratory Acidosis Treatment & Management

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

Approach Considerations

Treatment of respiratory acidosis is primarily directed at the underlying disorder or pathophysiologic process. Caution should be exercised in the correction of chronic hypercapnia: too-rapid correction of the hypercapnia can result in metabolic alkalemia. Alkalization of the cerebrospinal fluid (CSF) can result in seizures.

The criteria for admission to the intensive care unit (ICU) vary from institution to institution but may include patient confusion, lethargy, respiratory muscle fatigue, and a low pH (< 7.25). All patients who require tracheal intubation and mechanical ventilation must be admitted to the ICU. Most acute care facilities require that all patients being treated acutely with noninvasive positive-pressure ventilation (NIPPV) be admitted to the ICU.

Consider consultation with pulmonologists and neurologists for assistance with the evaluation and treatment of respiratory acidosis. Results from the history, physical examination, and available laboratory studies should guide the selection of the subspecialty consultants.


Pharmacologic Therapy

Pharmacologic therapies are generally used as treatment of the underlying disease process.


Bronchodilators such as beta agonists (eg, albuterol and salmeterol), anticholinergic agents (eg, ipratropium bromide and tiotropium), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive airway disease and severe bronchospasm. Theophylline may improve diaphragm muscle contractility and may stimulate the respiratory center.

Respiratory stimulants

Respiratory stimulants have been used but have limited efficacy in respiratory acidosis caused by disease.

Medroxyprogesterone increases central respiratory drive and may be effective in treating obesity-hypoventilation syndrome (OHS). Medroxyprogesterone has also been shown to stimulate ventilation is some patients with COPD and alveolar hypoventilation. This medication does not improve apnea frequency or sleepiness symptoms in patients with sleep apnea.

There is an increased risk of thromboembolism with progestational agents. Many experts do not recommend the use of medroxyprogesterone as a means to increase alveolar ventilation.

Acetazolamide is a diuretic that increases bicarbonate excretion and induces a metabolic acidosis, which subsequently stimulates ventilation. However, acetazolamide must be used with caution in this setting. Inducing a metabolic acidosis in a patient with a respiratory acidosis could result in a severely low pH. If the patient's respiratory system cannot compensate for the metabolic acidosis it induces, the patient may suffer hyperkalemia and potentially a life-threatening cardiac arrhythmia.

Theophylline increases diaphragm muscle strength and stimulates the central ventilatory drive. In addition, theophylline is a bronchodilator.

Drug antagonists

Drug therapy aimed at reversing the effects of certain sedative drugs may be helpful in the event of an accidental or intentional overdosage. Naloxone may be used to reverse the effects of narcotics. Flumazenil may be used to reverse the effects of benzodiazepines. However, care must be taken in reversing the effects of benzodiazepines because patients may have seizures if benzodiazepine reversal is accomplished too vigorously.


Infusion of sodium bicarbonate is rarely indicated. This measure may be considered after cardiopulmonary arrest with an extremely low pH (< 7.0-7.1). In most other situations, sodium bicarbonate has no role in the treatment of respiratory acidosis.


Oxygen Therapy

Because many patients with hypercapnia are also hypoxemic, oxygen therapy may be indicated. Oxygen therapy is employed to prevent the sequelae of long-standing hypoxemia. Patients with COPD who meet the criteria for oxygen therapy have been shown to have decreased mortality when treated with continuous oxygen therapy. Oxygen therapy has also been shown to reduce pulmonary hypertension in some patients.

Oxygen therapy should be used with caution because it may worsen hypercapnia in some situations. For example, patients with COPD may experience exacerbation of hypercapnia during oxygen therapy. This observation is thought by many to be primarily a consequence of ventilation-perfusion mismatching, in opposition to the commonly accepted concept of a reduction in hypoxic ventilatory drive. The exact pathophysiology, however, remains controversial.

Hypercapnia is best avoided by titrating oxygen delivery to maintain oxygen saturation in the low 90% range and partial arterial pressure of oxygen (PaO2) in the range of 60-65 mm Hg.


Ventilatory Support

Therapeutic measures that may be lifesaving in severe hypercapnia and respiratory acidosis include endotracheal intubation with mechanical ventilation and noninvasive positive pressure ventilation (NIPPV) techniques such as nasal continuous positive-pressure ventilation (NCPAP) and nasal bilevel ventilation. The latter techniques of NIPPV are preferred treatment for OHS and neuromuscular disorders, because they help improve PaO2 and decrease the partial pressure of arterial carbon dioxide (PaCO2).

Noninvasive external negative-pressure ventilation devices are also available for the treatment of selected patients with chronic respiratory failure.

Rapid correction of the hypercapnia by the application of external noninvasive positive-pressure ventilation or invasive mechanical ventilation can result in alkalemia. Accordingly, these techniques should be used with caution.

A study comparing noninvasive techniques with invasive ventilation in myasthenic crisis found that patients who underwent noninvasive ventilation had better outcomes than patients who underwent invasive ventilation.[10]

A 4-year retrospective study reported that NIPPV was highly beneficial in the treatment of COPD with hypercapnia (type II) respiratory failure.[11] NIPPV led to a decreased length of stay and a reduced cost of hospitalization.

Investigational therapy

Extracorporeal carbon dioxide removal (ECCO2 R) is a newer technique for removing carbon dioxide via venovenous bypass without affecting oxygenation. ECCO2 R is being evaluated in the treatment of respiratory acidosis as a complication of the low tidal volume lung-protective ventilation with permissive hypercapnia. However, this technique has been associated with serious complications and requires more investigation.[12]

Contributor Information and Disclosures

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.


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.


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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