Can venous-to-arterial carbon dioxide differences reflect microcirculatory alterations in patients with septic shock?

Ospina-Tascón, Gustavo Adolfo; Umaña, Mauricio; Bermúdez, William; Bautista-Rincón, Diego F.; Valencia, Juan D.; Madriñán, Humberto J.; Hernández, Glenn; Bruhn, Alejandro; Arango-Dávila, César Augusto; Backer, Daniel De

doi:10.1007/s00134-015-4133-2

Cited by 142 publications

(82 citation statements)

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“…When ScvO2 is abnormal, PvaCO2 mostly reflects a low cardiac output. However, when ScvO2 is above 70%, then PvaCO2 may reflect microcirculatory perfusion [45]. In patients with septic shock, PvaCO2 values >6 mmHg were associated with poor outcomes in patients who had normalized their ScvO2 [46].…”

Section: Resuscitation Triggers and Targetsmentioning

confidence: 99%

Sepsis: frontiers in diagnosis, resuscitation and antibiotic therapy

et al. 2016

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Sepsis is a major growing global burden and a major challenge to intensive care clinicians, researchers, guideline committee members and policy makers, because of its high and increasing incidence and great pathophysiological, molecular, genetic and clinical complexity. In spite of recent progress short term mortality remains high and there is growing evidence of long term morbidity and increased long term mortality in survivors of sepsis both in developed and developing countries. Further improvement in the care of patients with sepsis will impact upon global health.In this narrative review, invited experts describe the expected challenges and progress to be made in the near future. We focus on resuscitation (fluids, vasopressors, inotropes, blood transfusion and hemodynamic targets) and infection control (antibiotics and infection biomarkers) as these areas are key, if initial management and subsequent outcomes are to be improved in patients with sepsis.

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Section: Resuscitation Triggers and Targetsmentioning

confidence: 99%

Sepsis: frontiers in diagnosis, resuscitation and antibiotic therapy

et al. 2016

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“…In this context, venous-to-arterial carbon dioxide tension difference (∆PCO 2 ) has been proposed as a marker of tissue hypoperfusion in patients with septic shock [3–9]. In fact, the increase in ∆PCO 2 that has been observed in low-flow states is mainly related to venous hypercapnia, rather than a decrease in arterial CO 2 partial pressure (PaCO 2 ), which can be explained by the tissue CO 2 stagnation phenomenon.…”

Section: Introductionmentioning

confidence: 99%

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

Mallat

Mohammad

Lemyze

et al. 2017

Ann. Intensive Care

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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.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-017-0258-5) contains supplementary material, which is available to authorized users.

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“…The presence of systemic hypoperfusion, as demonstrated by hyperlactatemia and/or increased venousarterial PCO 2 gradients, raises the odds of finding severe sublingual microcirculatory alterations [4,5]. Profound macrohemodynamic and microcirculatory derangements coexist in unpredictable patterns in patients with progressive septic shock.…”

Section: Can Microcirculatory Abnormalities Be Tracked By Systemic Pementioning

confidence: 99%

“…Since the landmark paper by De Backer et al [1], numerous studies have addressed microcirculatory dysfunction in septic shock, established its pathophysiological relevance, and demonstrated the prognostic impact of persistent abnormalities [2][3][4][5]. Sublingual microcirculation, which is easy to access with video-microscopic techniques, is the most frequently explored territory in humans.…”

Section: Introductionmentioning

confidence: 99%