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. 2017 Dec;7(1):31.
doi: 10.1186/s13613-017-0258-5. Epub 2017 Mar 20.

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

Jihad Mallat  1   2 , Usman Mohammad  3 , Malcolm Lemyze  4   3 , Mehdi Meddour  4 , Marie Jonard  4   3 , Florent Pepy  4 , Gaelle Gasan  4 , Stephanie Barrailler  4 , Johanna Temime  4 , Nicolas Vangrunderbeeck  4 , Laurent Tronchon  4 , Didier Thevenin  4   3
Affiliations

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

Jihad Mallat et al. Ann Intensive Care. 2017 Dec.

Abstract

Background: To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆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), ∆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).

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/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).

Conclusions: 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.

Keywords: Acute hyperventilation; Central venous oxygen saturation; Central venous-to-arterial CO2 tension gap; Oxygen consumption; Septic shock.

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Figures

Fig. 1
Fig. 1
Relationship between changes in VO2 and changes in pH induced by the increase in alveolar ventilation
Fig. 2
Fig. 2
Relationship between changes in VO2 and the changes in ∆PCO2 (a) and ScvO2 (b) between after and before the increase in alveolar ventilation
See this image and copyright information in PMC

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