The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure
- David J Feller-Kopman, MD
David J Feller-Kopman, MD
- Professor of Medicine
- Johns Hopkins Hospital
- Richard M Schwartzstein, MD
Richard M Schwartzstein, MD
- Professor of Medicine
- Harvard Medical School
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.
MECHANISM AND ETIOLOGY
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.
WHEN TO SUSPECT ACUTE 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. 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.
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- MECHANISM AND ETIOLOGY
- WHEN TO SUSPECT ACUTE HYPERCAPNIA
- Clinical features of hypercapnia
- Clinical features of the underlying cause
- Other features
- INITIAL EVALUATION AND DIAGNOSTIC APPROACH
- Assess airway, breathing, circulation
- Arterial blood gas analysis
- - Distinguishing acute and chronic hypercapnia
- - Determining the alveolar arterial gradient
- Bedside clinical assessment
- - History and examination
- - Laboratory assessment
- - Imaging assessment
- - Physiologic assessment
- INITIAL BEDSIDE THERAPIES
- Reversal and avoidance of sedatives
- Bag-valve mask or noninvasive ventilation
- Titration of oxygen
- - Administration of oxygen
- - Risk of hypercapnia
- Empiric therapies for underlying etiology
- Criteria for intensive care unit admission
- DIFFERENTIAL DIAGNOSIS
- DEFINITIVE MAINTENANCE THERAPY
- Reverse the cause
- Reverse hypercapnia
- THERAPIES OF UNPROVEN BENEFIT
- SUMMARY AND RECOMMENDATIONS