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

Background: To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (Delta PCO2) in hemodynamically stable septic shock patients. Methods: Eighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI),Delta PCO2, oxygen consumption (VO2), 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 VO2 (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 Delta PCO2 (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 VO2 (r = 0.67, p = 0.002). Interestingly, we found a strong association between the increase in VO2 and the increase in Delta PCO2 (r = 0.70, p = 0.001). Conclusions: Acute hyperventilation provoked a significant increase in Delta 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 Delta PCO2.