Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure

David J Feller-Kopman, MD
Richard M Schwartzstein, MD
Section Editor
James K Stoller, MD, MS
Deputy Editor
Geraldine Finlay, MD


Acute hypercapnic respiratory failure can be encountered in the emergency department and inpatient floor, as well as in postoperative and intensive care units. Acute hypercapnia is often not suspected, leading to delayed diagnosis. If left untreated, acute hypercapnic respiratory failure may become life-threatening resulting in respiratory arrest, seizures, coma, and death.

The approach to adult patients with suspected hypercapnia, as well as the diagnosis and treatment of acute hypercapnic respiratory failure are discussed in this topic. For the most part, this topic discusses the approach in patients who are spontaneously breathing, although many of the same principles can be applied to patients who are receiving invasive or noninvasive ventilatory support. The mechanisms, etiologies, and end-organ effects associated with hypercapnia are discussed more extensively separately.


Hypercapnia is defined as an elevation in the arterial carbon dioxide tension (PaCO2). The carbon dioxide level in arterial blood is directly proportional to the rate of carbon dioxide (VCO2) production and inversely proportional to the rate of CO2 elimination by the lung (alveolar ventilation). Alveolar ventilation (VA) is, in turn, determined by minute ventilation (VE) and the ratio of dead space (VD) to tidal volume (VT) (VA = VE x [1 - VD/VT]). Increased dead space and reduced minute ventilation are common causes of hypercapnia. In contrast, unless a patient has limited pulmonary reserve, increased CO2 production rarely results in clinically important hypercapnia. Etiologies associated with hypercapnia are listed in the table (table 1). Detailed discussion of the mechanisms and etiologies of hypercapnia is provided separately.


Hypercapnia should always be suspected in those who are at risk for hypoventilation (eg, sedatives) or increased physiologic dead space and limited pulmonary reserve (eg, chronic obstructive pulmonary disease [COPD] exacerbation) who present with shortness of breath, a change in mental status, new hypoxemia, and/or hypersomnolence.

The presenting features of acute hypercapnia are variable with no signs or symptoms that are sensitive or specific for the diagnosis. Patients can present with the manifestations of hypercapnia itself as well as with the manifestations associated with the underlying disorder, both of which are discussed in detail in the sections below. It is important to remember that tachypnea does not always equate to increased alveolar ventilation; patients with increased dead space and mechanical abnormalities of the respiratory system may have elevated respiratory rate and accessory muscle use, yet still be hypercapnic.

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Oct 2017. | This topic last updated: Jul 20, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Davidson AC, Banham S, Elliott M, et al. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016; 71 Suppl 2:ii1.
  2. O'Driscoll BR, Howard LS, Earis J, et al. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax 2017; 72:ii1.
  3. Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2016. http://www.goldcopd.org (Accessed on March 17, 2016).
  4. Celli BR, MacNee W, ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J 2004; 23:932.
  5. Rudolf M, Banks RA, Semple SJ. Hypercapnia during oxygen therapy in acute exacerbations of chronic respiratory failure. Hypothesis revisited. Lancet 1977; 2:483.
  6. Durrington HJ, Flubacher M, Ramsay CF, et al. Initial oxygen management in patients with an exacerbation of chronic obstructive pulmonary disease. QJM 2005; 98:499.
  7. Joosten SA, Koh MS, Bu X, et al. The effects of oxygen therapy in patients presenting to an emergency department with exacerbation of chronic obstructive pulmonary disease. Med J Aust 2007; 186:235.
  8. Bone RC, Pierce AK, Johnson RL Jr. Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: a reappraisal. Am J Med 1978; 65:896.
  9. Campbell EJ. The J. Burns Amberson Lecture. The management of acute respiratory failure in chronic bronchitis and emphysema. Am Rev Respir Dis 1967; 96:626.
  10. Gay PC, Edmonds LC. Severe hypercapnia after low-flow oxygen therapy in patients with neuromuscular disease and diaphragmatic dysfunction. Mayo Clin Proc 1995; 70:327.
  11. Adler D, Pépin JL, Dupuis-Lozeron E, et al. Comorbidities and Subgroups of Patients Surviving Severe Acute Hypercapnic Respiratory Failure in the Intensive Care Unit. Am J Respir Crit Care Med 2017; 196:200.
  12. Kaushik M, Wojewodzka-Zelezniakowicz M, Cruz DN, et al. Extracorporeal carbon dioxide removal: the future of lung support lies in the history. Blood Purif 2012; 34:94.