First paragraph (this article has no abstract)

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.