Effect of acute hyperventilation on the venous-arterial PCO2 difference
Intensive Care Unit, Centre Hospitalier du Dr. Schaffner, Service de Réanimation polyvalente, 99 route de la bassée, 62307 Lens cedex, France
Critical Care 2012, 16:408 doi:10.1186/cc11139
See related letter by Morel et al., http://ccforum.com/content/15/6/456Published: 30 January 2012
First paragraph (this article has no abstract)
I read with great interest the letter by Morel and colleagues  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.