Authors ’ response

I read with great interest the letter by Morel and colleagues [1] in the previous issue of Critical Care. Th e letter suggested that acute changes in the arterial partial pressure of carbon dioxide (PaCO2) can aff ect the venous-arterial diff erence 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. Th e authors found that a decrease of PaCO2 was associated with a signifi cant increase in ΔCO2. Th is was explained by the fact that acute hypocapnia resulted in systemic vaso con striction, 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 expla na tion 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]. Th us, for a given venous blood fl ow, 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 diff erence showed good agreement [4]. Nevertheless, I agree that acute hyperventilation could be a potential limitation of the clinical application of the ΔCO2. © 2010 BioMed Central Ltd Eff ect of acute hyperventilation on the venous-arterial PCO2 diff erenc