Effect of acute hyperventilation on the venous-arterial PCO₂ difference

I read with great interest the letter by Morel and colleagues [1] in the previous issue of Critical Care. The letter suggested that acute changes in the arterial partial pressure of carbon dioxide (PaCO₂) can affect the venous-arterial difference in carbon dioxide tension (ΔCO₂). In a study by the authors, 10 ventilated and hemodynamically stable patients were included after elective cardiac surgery. Hypocapnia was induced by increasing the respiratory rate. The authors found that a decrease of PaCO₂ was associated with a significant increase in ΔCO₂. This was explained by the fact that acute hypocapnia resulted in systemic vasoconstriction, thus decreasing the elimination of the total CO₂ produced by the peripheral tissues and increasing the gap. However, as all patients were monitored with a pulmonary artery catheter (PAC), the authors should have shown whether there was any increase in systemic vascular resistance to support their hypothesis. Furthermore, there is another possible explanation of the ΔCO₂ increase induced by the decrease in PaCO₂. Indeed, acute respiratory alkalosis has been shown to increase systemic oxygen consumption and CO₂ production [2, 3]. Thus, for a given venous blood flow, the increase of tissue CO₂ production should increase the partial pressure of carbon dioxide (PCO₂) gap.

On the other hand, it is unclear why the authors have used the central venous sample to calculate ΔCO₂ instead of using the mixed venous sample (PAC), which is the gold standard. If a PAC is in place, the clinical utility of an alternative method of measurement is diminished even though the mixed and central PCO₂ difference showed good agreement [4]. Nevertheless, I agree that acute hyperventilation could be a potential limitation of the clinical application of the ΔCO₂.

Authors' response

Jerome Morel and Laurent Gergele

We thank Mallat for his comments. Indeed, we hypothesized that hypocapnia resulted in microcirculatory vasoconstriction, thus decreasing the elimination of CO₂ produced by the peripheral tissues and increasing the venous-arterial CO₂ gradient [1]. Only specific microcirculatory monitoring can answer this question. Measurement of systemic vascular resistance could not help as microcirculation and systemic circulation are relatively dissociated, particularly when systemic hemodynamics are within normal ranges (as was the case in our study) [5].

As mentioned, it has been shown that central venous CO₂ and mixed venous CO₂ were in good agreement for the calculation of venous-arterial CO₂ gradient, as was the case in our study (data not shown). We chose to present central venous data because nowadays patients are more frequently monitored with a central venous catheter than a PAC. However, Mallat raised an interesting hypothesis concerning the effects of acute respiratory alkalosis on systemic oxygen consumption and CO₂ production, which could be an explanation of our results [2].