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Increased venous to arterial carbon dioxide difference (Pv-aCO2) have been attributed to low cardiac output states. However, mechanisms conducting to Pv-aCO2 increases during normal or even high cardiac output conditions as in septic shock are not fully understood. We hypothesized that Pv-aCO2 could reflect the adequacy of microvascular perfusion during resuscitated septic shock
To test the hypothesis that Pv-aCO2 could reflect the microvascular blood flow during the early phases of resuscitation in septic shock
We included 80 patients with a first episode of septic shock admitted to a mixed ICU in a University Hospital over a 12-month period. Time 0 (T0) was set at ICU admission when a pulmonary artery catheter was inserted. Arterial and venous gases analyses were performed at T0 and 6 hours after (T6). We defined Pv-aCO2 as the difference between the mixed venous and arterial CO2 partial pressures. A Sidestream Dark-Field (SDF) imaging device (Microvision Medical, Amsterdam, the Netherlands) was used to evaluate the sublingual microcirculation both at T0 and T6. At each assessment, 5 sequences of 20 seconds each were recorded and stored under a random number. An investigator blinded to the sequence order and patient's clinical course, analyzed the sequences semi-quantitatively. The vessels were separated into large and small using a cut-off value of 20 µm in diameter. We evaluated the relation between the percentage of small vessels perfused and the Pv-aCO2 using linear and non-linear regressions and Spearman Rho test. A p< 0.05 was considered as significant.
We found significant but very weak relationships between general hemodynamics or oxygen derived parameters with Pv-CO2.Pv-aCO2 was inversely related to the percentage of small vessels perfused both at T0 and T6 (T0: R2:0.515, p< 0.001; T6: R2:0.453, p< 0.001).
Microvascular blood flow is a key determinant of Pv-aCO2 during normodynamic septic shock. Pv-aCO2 could track microvascular alterations during early phases of septic shock.