• Annals of intensive care · Dec 2017

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

    • Jihad Mallat, Usman Mohammad, Malcolm Lemyze, Mehdi Meddour, Marie Jonard, Florent Pepy, Gaelle Gasan, Stephanie Barrailler, Johanna Temime, Nicolas Vangrunderbeeck, Laurent Tronchon, and Didier Thevenin.
    • Department of Anesthesiology and Critical Care Medicine, Service de Réanimation polyvalente, Centre Hospitalier du Dr. Schaffner, 99 route de La Bassée, 62307, Lens Cedex, France. mallatjihad@gmail.com.
    • Ann Intensive Care. 2017 Dec 1; 7 (1): 31.

    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.

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