pCO2 is defined as the carbon dioxide partial pressure (or tension) in a gas phase in equilibrium with the blood. High and low values of pCO2 in arterial blood indicate blood hypercapnia and hypocapnia, respectively. Depending on the sample, the systematic symbol may be pCO2(a) for arterial blood or pCO2() for mixed venous blood. The analyzer symbol may be pCO2.
What does pCO2 tell you
Carbon dioxide readily diffuses across cell membranes, and the tension of pCO2 in normal inspired air is negligible. Therefore, pCO2 is a direct reflection of the adequacy of alveolar ventilation in relation to the metabolic carbon dioxide production (metabolic rate).
pCO2(a) reference range (adult):
male: 35-48 mmHg (4.67-6.40 kPa)
female: 32-45 mmHg (4.27-6.00 kPa)
A. Low pCO2 -Alveolar hyperventilation (hypocapnia):
Common causes of alveolar hyperventilation:
- Excessive mechanical ventilation
- Psychogenic hyperventilation
- Compensatory to metabolic acidosis
- Secondary to central nervous system affection
- Secondary to hypoxia
B. High pCO2 -Alveolar hypoventilation (hypercapnia):
Common causes of alveolar hypoventilation:
- Acute or chronic pulmonary disease
- Upper airway obstruction (e.g., sleep apnea syndrome)
- Diminished ventilatory drive due to central nervous system depression - either primary or secondary to sedation or analgesics - or compensatory to metabolic alkalosis
- Insufficient, or intentionally low (“permissive hypercapnia”), mechanical ventilation
pCO2 reflects the adequacy of pulmonary ventilation. Therefore, it is possible to distinguish between respiratory problems that are primarily of ventilatory origin or problems of oxygenation. The severity of ventilatory failure, as well as the chronicity, can be judged by the accompanying changes in acid-base status (see pH).
It is often part of the therapeutic strategy to accept or aim for values that are lower or higher than the reference range. In these situations, it is important to be aware of the effects of changes in pCO2(a).
Hypercapnia or hypocapnia are important causes of change in the arterial oxygen content. Decreasing pCO2(a) causes pulmonary vasodilatation and vasoconstriction in several parts of the systemic circulation, including the cerebral vasculature. The low alveolar pCO2 increases alveolar pO2, and the alkalosis causes a left shift of the ODC; both effects facilitate oxygen uptake in the lungs. However, the systemic circulatory effects, as well as the impairment of oxygen release to the tissues caused by the left shift of the ODC, may counteract these effects. The net result of decreasing pCO2 may therefore be an impairment of oxygen supply to the tissues.
Though the systemic vasoconstriction is compensated within minutes or hours, it may cause organ hypoperfusion and result in ischemia, especially in the central nervous system (CNS).
Increasing pCO2(a) may cause hypoxemia because the alveolar oxygen tension falls according to the alveolar gas equation. In addition, the right shift of the ODC, induced by acute respiratory acidosis, reduces arterial ctO2. On the other hand, increasing pCO2 may result in an increased cardiac output and facilitated oxygen release to the tissues.
In conclusion, the overall effects of changes in arterial pCO2 are quite complex and not yet completely elucidated. Therefore, the arterial pCO2 must always be evaluated in the clinical context
Be aware of the risk of preanalytical errors (storage) on pCO2 values.
For more information, go to Preanalytical considerations.