Erschienen in:
01.02.2012 | Letter
Effect of acute hyperventilation on the venous-arterial PCO2 difference
verfasst von:
Jihad Mallat
Erschienen in:
Critical Care
|
Ausgabe 1/2012
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Excerpt
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 (PaCO
2) can affect the venous-arterial difference in carbon dioxide tension (ΔCO
2). 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 PaCO
2 was associated with a significant increase in ΔCO
2. This was explained by the fact that acute hypocapnia resulted in systemic vasoconstriction, thus decreasing the elimination of the total CO
2 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 ΔCO
2 increase induced by the decrease in PaCO
2. Indeed, acute respiratory alkalosis has been shown to increase systemic oxygen consumption and CO
2 production [
2,
3]. Thus, for a given venous blood flow, the increase of tissue CO
2 production should increase the partial pressure of carbon dioxide (PCO
2) gap. …