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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. (See "Mechanisms, causes, and effects of hypercapnia", section on 'Mechanisms and etiologies of hypercapnia'.)


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. (See "Mechanisms, causes, and effects of hypercapnia", section on 'Mechanisms and etiologies of hypercapnia'.)


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.


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Literature review current through: Sep 2016. | This topic last updated: May 17, 2016.
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