Mechanisms, causes, and effects of hypercapnia
- David J Feller-Kopman, MD
David J Feller-Kopman, MD
- Associate Professor of Medicine
- Johns Hopkins Hospital
- Richard M Schwartzstein, MD
Richard M Schwartzstein, MD
- Professor of Medicine
- Harvard Medical School
Hypercapnia, defined as an elevation in the arterial carbon dioxide tension, is commonly encountered during the evaluation of patients with dyspnea and/or altered sensorium. Understanding the mechanisms, causes, and effects of hypercapnia is critical to its management.
The relevant physiology of ventilatory control, mechanisms, causes, and effects of hypercapnia are presented in this topic review. The evaluation and treatment of patients with acute hypercapnia are presented separately. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure".)
FORMULA FOR ARTERIAL CARBON DIOXIDE TENSION
The partial pressure of carbon dioxide in arterial blood (PaCO2) is directly proportional to the rate of carbon dioxide (CO2) production (VCO2) by oxidative metabolism and indirectly proportional to the rate of CO2 elimination by the lung (alveolar ventilation; VA). Alveolar ventilation is the component of the expired minute volume that reaches perfused alveoli, and is in turn determined by minute ventilation (VE) and the ratio of dead space (VD) to tidal volume (VT) or VD/VT.
The following calculation is used to determine the PaCO2:
PaCO2 = (k) x VCO2/[VE(1 - VD/VT)]
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- FORMULA FOR ARTERIAL CARBON DIOXIDE TENSION
- MECHANISMS AND ETIOLOGIES OF HYPERCAPNIA
- Decreased minute ventilation/global hypoventilation
- - Mechanism
- - Etiologies
- Increased dead space
- - Mechanism
- - Etiologies
- Increased production of carbon dioxide
- Chronic obstructive pulmonary disease
- - Hypercapnia at baseline/during exacerbations
- - Oxygen-induced hypercapnia
- EFFECTS OF HYPERCAPNIA
- Cerebral effects
- Cardiorespiratory effects
- Physiologic effects
- Metabolic effects
- SUMMARY AND RECOMMENDATIONS