Acute hyperventilation increases the central venous-to-arterial PCO2 difference in stable septic shock patients

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To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO 2 ) in hemodynamically stable septic shock patients. Eighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI), ∆PCO 2 , oxygen consumption (VO 2 ), central venous oxygen saturation (ScvO 2 ), and blood gas parameters, before and 30 min after an increase in alveolar ventilation (increased respiratory rate by 10 breaths/min). Arterial pH increased significantly (from 7.35 ± 0.07 to 7.42 ± 0.09, p < 0.001) and arterial carbon dioxide tension decreased significantly (from 44.5 [41–48] to 34 [30–38] mmHg, p < 0.001) when respiratory rate was increased. A statistically significant increase in VO 2 (from 93 [76–105] to 112 [95–134] mL/min/m 2 , p = 0.002) was observed in parallel with the increase in alveolar ventilation. While CI remained unchanged, acute hyperventilation led to a significant increase in ∆PCO 2 (from 4.7 ± 1.0 to 7.0 ± 2.6 mmHg, p < 0.001) and a significant decrease in ScvO 2 (from 73 ± 6 to 67 ± 8%, p < 0.001). A good correlation was found between changes in arterial pH and changes in VO 2 ( r = 0.67, p = 0.002). Interestingly, we found a strong association between the increase in VO 2 and the increase in ∆PCO 2 ( r = 0.70, p = 0.001). Acute hyperventilation provoked a significant increase in ∆PCO 2 , which was the result of a significant increase in VO 2 induced by hyperventilation. The clinician should be aware of the effects of acute elevation of alveolar ventilation on ∆PCO 2 .

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