Acute hyperventilation increases the central venous-to-arterial PCO_2 difference in stable septic shock patients

Background

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

Methods

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)

Results

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)

Conclusions

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.