pCO₂(a)
Carbon dioxide tension

Definition
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).

Reference ranges
pCO₂(a) reference range (adult):
male: 35-48 mmHg (4.67-6.40 kPa)
female: 32-45 mmHg (4.27-6.00 kPa)
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Clinical interpretation

A. Low pCO₂  Alveolar hyperventilation (hypocapnia):

Common causes of alveolar hyperventilation:

Primary:

• Excessive mechanical ventilation
• Psychogenic hyperventilation

Secondary:

• 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

Considerations
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.