Respiratory Acidosis Treatment & Management

  • Author: Ryland P Byrd Jr, MD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Oct 3, 2011
 

Surgical Intervention

In severe kyphoscoliosis, spine fusion is sometimes indicated for thoracic spine angles greater than 40°.

Patients with obesity hypoventilation syndrome might benefit from weight reduction surgery. Bariatric surgical techniques, including vertical banded gastroplasty, adjustable gastric banding, and roux-en-Y gastric bypass, can be offered to these patients. Roux-en-Y gastric bypass is gaining more acceptance, because it is performed laparoscopically and because it has better short- and long-term outcomes than other bariatric techniques.

According to the US National Institutes of Health (NIH) consensus statement guidelines, surgery should be recommended to patients with a body mass index (BMI) greater than 35 kg/m2 and an obesity-related comorbid condition (including obesity hypoventilation syndrome) or patients with a BMI greater than 40 kg/m2.

Diaphragmatic pacing can be performed for the treatment for primary alveolar hypoventilation. One study reported that diaphragmatic pacing is an effective treatment of congenital central alveolar hypoventilation syndrome (Ondine curse).[10] This procedure is performed through bilateral axillary thoracotomy. It is still considered experimental.

Phrenic nerves have also been paced. Unfortunately, this technique over time often results in injury to the phrenic nerve, resulting in a dysfunctional phrenic nerve.

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Complications

Patients with chronic respiratory acidosis, by definition, have a component of alveolar hypoventilation. The patients have increased partial arterial pressure of carbon dioxide (PaCO2) and bicarbonate levels. They also have obligatory decreases in partial arterial pressure of oxygen (PaO2).

Complications are often related to the chronic hypoxemia, which can result in increased erythropoiesis, leading to secondary polycythemia.

Chronic hypoxia is a well-known cause of pulmonary vasoconstriction. This physiologic response can, in the long term, lead to pulmonary hypertension, right ventricular failure, and cor pulmonale.

The hypopneas and apneas during sleep lead to impaired sleep quality and cerebral vasodilation, causing morning headaches, daytime fatigue, and somnolence.

High levels of PaCO2 can lead to confusion, often referred to as carbon dioxide narcosis. As a late complication of cerebral vasodilation, patients may have papilledema.[11]

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Long-Term Monitoring

The morbidity, mortality, and prognosis for patients with of respiratory acidosis depends on the underlying cause of the respiratory acidosis, associated conditions, the patient's compensatory mechanisms, and effectiveness of medical care.

Oxygen therapy

Oxygen therapy should be continued in the outpatient setting in patients who meet the specific criteria for long-term oxygen therapy, including: (1) a partial arterial pressure of oxygen (PaO2) of less than 55 mm Hg or (2) a PaO2 of less than 59 mm Hg with evidence of polycythemia, cor pulmonale, or other complicating conditions.

Patients should be reevaluated 1-3 months after initiating oxygen therapy to reassess their ongoing need for continuing long-term oxygen therapy.

Noninvasive ventilation

Noninvasive ventilation can be continued in the outpatient setting. Nasal bilevel positive-pressure ventilation can be used long-term to treat patients with neuromuscular disorders, chronic obstructive pulmonary disease (COPD) with hypercapnia, primary alveolar hypoventilation, and obesity hypoventilation syndrome.

Noninvasive ventilation augments the benefits of pulmonary rehabilitation in COPD patients with chronic hypercapnic respiratory failure, because it improves several measures of health-related quality of life, functional status, and gas exchange.[12]

Patient counseling

Smoking cessation is an important aspect in the long-term treatment, particularly in patients with COPD.

Weight loss is very helpful, especially in patients with obesity hypoventilation syndrome. It improves daytime symptoms and the PCO2. In patients with obstructive sleep apnea, weight loss decreases the number of apneas and hypopneas.

For patient education information, see Lung Disease & Respiratory Health Center, as well as Chronic Obstructive Pulmonary Disease (COPD).

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Approach Considerations

The treatment of respiratory acidosis is primarily directed at correcting the underlying disorder/pathophysiologic process. Caution should be exercised when correcting chronic hypercapnia. Rapid correction of the hypercapnia can result in metabolic alkalemia. Alkalinization 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. All patients who require tracheal intubation and mechanical ventilation require ICU admission. Most acute care facilities require that all patients being treated acutely with noninvasive positive-pressure ventilation (NIPPV) also 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.

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Pharmacologic Therapy

Bronchodilating agents, respiratory stimulants, drug antagonists, and/or bicarbonate infusion may play roles in managing asthmatic and chronic obstructive pulmonary disease (COPD) patients with respiratory acidosis. See also Medications.

Bronchodilating agents

Bronchodilators such as beta-agonists (eg, albuterol, salmeterol), anticholinergic agents (eg, ipratropium bromide, tiotropium), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive lung 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 the central respiratory drive and is effective in treating obesity-hypoventilation syndrome. Acetazolamide is a diuretic that increases bicarbonate excretion and induces a metabolic acidosis. The metabolic acidosis subsequently stimulates ventilation. This drug, however, must be used with caution in this setting. Inducing an additional metabolic acidosis in a patient with a respiratory acidosis could result in a severely low pH. Theophylline increases diaphragm muscle strength and stimulates the central ventilatory drive.

Drug antagonists

Drug therapy aimed at reversing the effects of certain sedative drugs may be helpful in the event of an overdosage. Naloxone (Narcan) may be used to reverse the effects of narcotics. Flumazenil (Romazicon) may be used to reverse the effects of benzodiazepines. However, care must be used when reversing the effects of benzodiazepines, as patients may have seizures if benzodiazepine reversal is accomplished too vigorously.

Bicarbonate infusion

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.

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Oxygen Therapy

Oxygen therapy may be indicated because many patients with hypercapnia are also hypoxemic. Oxygen therapy is indicated to prevent the sequelae of long-standing hypoxemia. Patients with chronic obstructive pulmonary disease (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.

Precautions

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

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

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Ventilatory Support

Therapeutics that may be life saving in severe hypercapnea 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 are preferred treatment for obesity hypoventilation syndrome and neuromuscular disorders, because they help improve the partial arterial pressure of oxygen (PaO2) and decrease the partial arterial pressure of 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 external noninvasive positive-pressure ventilation or invasive mechanical ventilation can result in alkalemia. These techniques should be used with caution.

NIPPV studies

A study comparing noninvasive techniques with invasive ventilation in myasthenic crisis found that patients had better outcomes with noninvasive ventilation compared with patients who had invasive ventilation.[7]

A 4-year retrospective study reported that NIPPV is highly beneficial in the treatment of chronic obstructive pulmonary disease (COPD) with hypercapnia (type II) respiratory failure.[8] NIPPV led to decreased length of stay and cost of hospitalization.[8]

Investigational therapy

Extracorporeal carbon dioxide removal (ECCO2 R) is a newer technique to remove 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 hypercapnea. However, this technique has been associated with serious complications and requires more investigation.[9]

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

Thomas M Roy, MD  Chief, Division of Pulmonary Diseases and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Pulmonary Medicine, East Tennessee State University, James H Quillen College of Medicine

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, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Jackie A Hayes, MD, FCCP, and Wael El Minaoui, MBBS,to the development and writing of the source article.

References
  1. Murray J, Nadel J. Hypoventilation syndromes. In: Textbook of Respiratory Medicine. Vol 2. 4th ed. Philadelphia, Pa: WB Saunders; 2005:2075-80.

  2. Adnet F, Plaisance P, Borron SW, Levy A, Payen D. Prolonged severe hypercapnia complicating near fatal asthma in a 35-year-old woman. Intensive Care Med. Dec 1998;24(12):1335-8. [Medline].

  3. Cham GW, Tan WP, Earnest A, Soh CH. Clinical predictors of acute respiratory acidosis during exacerbation of asthma and chronic obstructive pulmonary disease. Eur J Emerg Med. Sep 2002;9(3):225-32. [Medline].

  4. Theerthakarai R, El-Halees W, Javadpoor S, Khan MA. Severe pectus excavatum associated with cor pulmonale and chronic respiratory acidosis in a young woman. Chest. Jun 2001;119(6):1957-61. [Medline].

  5. Ehrsam RE, Heigenhauser GJ, Jones NL. Effect of respiratory acidosis on metabolism in exercise. J Appl Physiol. Jul 1982;53(1):63-9. [Medline].

  6. Kazmaier S, Weyland A, Buhre W, et al. Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease. Anesthesiology. Oct 1998;89(4):831-7. [Medline].

  7. Wu JY, Kuo PH, Fan PC, Wu HD, Shih FY, Yang PC. The Role of Non-invasive Ventilation and Factors Predicting Extubation Outcome in Myasthenic Crisis. Neurocrit Care. 2009;10(1):35-42. [Medline].

  8. Zhang WB, Wang XY, Tian XY, Zhang H, Wang ZP, Gao YY. [Clinical value of noninvasive positive-pressure ventilation in chronic obstruction pulmonary disease combined with type II respiratory failure: a 4-year retrospective study]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. Oct 2008;20(10):601-3. [Medline].

  9. Terragni PP, Birocco A, Faggiano C, Ranieri VM. Extracorporeal CO(2) Removal. Contrib Nephrol [serial online]. 2010 April 20;165:185-196. [Medline]. Available at http://-.

  10. Ali A, Flageole H. Diaphragmatic pacing for the treatment of congenital central alveolar hypoventilation syndrome. J Pediatr Surg. May 2008;43(5):792-6. [Medline].

  11. Pollock JM, Deibler AR, Whitlow CT, et al. Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity. AJNR Am J Neuroradiol. Oct 14 2008;[Medline].

  12. Duiverman ML, Wempe JB, Bladder G, et al. Nocturnal non-invasive ventilation in addition to rehabilitation in hypercapnic patients with COPD. Thorax. Dec 2008;63(12):1052-7. [Medline].

  13. Kellum JA. Determinants of plasma acid-base balance. Crit Care Clin. Apr 2005;21(2):329-46. [Medline].

  14. Wiseman AC, Linas S. Disorders of potassium and acid-base balance. Am J Kidney Dis. May 2005;45(5):941-9. [Medline].

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