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

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

doi:10.1186/s13613-017-0258-5

Jihad Mallat, Malcolm Lemyze + Show 10 more

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https://doi.org/10.1186/s13613-017-0258-5

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Abstract

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

Highlights

To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO2) in hemodynamically stable septic shock patients
The increase in ∆PCO2 that has been observed in low-flow states is mainly related to venous hypercapnia, rather than a decrease in arterial CO2 partial pressure (PaCO2), which can be explained by the tissue CO2 stagnation phenomenon
The main findings of our study were as follows: (1) acute increase in alveolar ventilation resulted in a significant increase in ∆PCO2 accompanied with a significant decrease in central venous oxygen saturation (ScvO2); (2) these changes were linked to a significant increase in oxygen consumption induced by acute hyperventilation

Summary

Introduction

To evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO2) in hemodynamically stable septic shock patients. Awareness that tissue hypoperfusion is a key factor in the pathogenesis of the multiple organ failures has focused the attention on surrogate indicators of tissue perfusion in the critically ill patient [1, 2]. Morel et al [21] found, in a small study that included mechanically ventilated postoperative patients, that acute decreases in PaCO2 resulted in significant increases in ∆PCO2 without any change in cardiac output. It is not clear so far what the impact of the rapid decrease in PaCO2 on ∆PCO2 is. The aim of this study was to investigate the impact of acute hyperventilation on ∆PCO2 in mechanically ventilated and hemodynamically stable septic shock patients

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