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

To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO₂) in hemodynamically stable septic shock patients.

Eighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI), ∆PCO₂, oxygen consumption (VO₂), central venous oxygen saturation (ScvO₂), 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 VO₂ (from 93 [76-105] to 112 [95-134] mL/min/m², 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 ∆PCO₂ (from 4.7 ± 1.0 to 7.0 ± 2.6 mmHg, p < 0.001) and a significant decrease in ScvO₂ (from 73 ± 6 to 67 ± 8%, p < 0.001). A good correlation was found between changes in arterial pH and changes in VO₂ (r = 0.67, p = 0.002). Interestingly, we found a strong association between the increase in VO₂ and the increase in ∆PCO₂ (r = 0.70, p = 0.001).

Acute hyperventilation provoked a significant increase in ∆PCO₂, which was the result of a significant increase in VO₂ induced by hyperventilation. The clinician should be aware of the effects of acute elevation of alveolar ventilation on ∆PCO₂.