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Scritto da Critical Care
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 I read with great interest the article by Morel et al. [1], suggesting that acute changes in the arterial partial pressure of carbon dioxide (PaCO2) can affect the venous-arterial difference in carbon dioxide tension ([increment]CO2). Ten ventilated and hemodynamically stable patients were included after elective cardiac surgery. Hypocapnia was induced by increasing of respiratory rate. The authors found that a decrease of PaCO2 was associated with a significant increase in [increment]CO2. 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 therefore increased the gap. However, as all patients were monitored with a pulmonary artery catheter (PAC), the authors should have shown if there were any increase in systemic vascular resistance to support their hypothesize. Furthermore, there is a possible another explanation of the increase of [increment]CO2 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 PCO2 gap.On the other hand, it is unclear why the authors have used the central venous sample to calculate [increment]CO2 instead of the mixed venous sample (PAC), which is the gold standard. If a PAC is in place, even though the mixed and central PCO2 difference showed a good agreement [4], the clinical utility of an alternative method of measurement is diminished. Nevertheless, I agree that acute hyperventilation could be a potential limitation of clinical application of the [increment]CO2.
Fonte: Critical Care |
