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Defining the hemodynamic response to volume therapy is integral to managing critically ill patients with acute circulatory failure, especially in the absence of cardiac index (CI) measurement. This study aimed at investigating whether changes in central venous-to-arterial CO2 difference (Δ-ΔPCO2) and central venous oxygen saturation (ΔScvO2) induced by volume expansion (VE) are reliable parameters to define fluid responsiveness in sedated and mechanically ventilated septic patients. We prospectively studied 49 critically ill septic patients in whom VE was indicated because of circulatory failure and clinical indices. CI, ΔPCO2, ScvO2, and oxygen consumption (VO2) were measured before and after VE. Responders were defined as patients with a > 10% increase in CI (transpulmonary thermodilution) after VE. We calculated areas under the receiver operating characteristic curves (AUCs) for Δ-ΔPCO2, ΔScvO2, and changes in CI (ΔCI) after VE in the whole population and in the subgroup of patients with an increase in VO2 (ΔVO2) ≤ 10% after VE (oxygen-supply independency). Twenty-five patients were fluid responders. In the whole population, Δ-ΔPCO2 and ΔScvO2 were significantly correlated with ΔCI after VE (r = − 0.30, p = 0.03 and r = 0.42, p = 0.003, respectively). The AUCs for Δ-ΔPCO2 and ΔScvO2 to define fluid responsiveness (increase in CI > 10% after VE) were 0.76 (p p = 0.02), respectively. In patients with ΔVO2 ≤ 10% (n = 36) after VE, the correlation between ΔScvO2 and ΔCI was 0.62 (p 2 and ΔCI was − 0.47 (p = 0.004). The AUCs for Δ-ΔPCO2 and ΔScvO2 were 0.83 (p p = 0.006), respectively. In these patients, Δ-ΔPCO2 ≤ -37.5% after VE allowed the categorization between responders and non-responders with a positive predictive value of 100% and a negative predictive value of 60%. In sedated and mechanically ventilated septic patients with no signs of tissue hypoxia (oxygen-supply independency), Δ-ΔPCO2 is a reliable parameter to define fluid responsiveness.

Malcolm Lemyze,1,2 Quentin Bury,3 Aurélie Guiot,4 Marie Jonard,1,2 Usman Mohammad,2 Nicolas Van Grunderbeeck,5 Gaelle Gasan,1 Didier Thevenin,2 Jihad Mallat2 1Department of Respiratory and Critical Care Medicine, Schaffner Hospital, Lens, 2Intensive Care Unit, Arras Hospital, Arras, 3Respiratory Intermediate Care Unit, Béthune Beuvry Hospital, Béthune, 4Department of Cardiology, Bois Bernard Hospital, Bois Bernard, 5Respiratory Step Down Unit, Schaffner Hospital, Lens, France Background: We evaluated a new noninvasive ventilation (NIV) protocol that allows the pursuit of NIV in the case of persistent severe respiratory acidosis despite a first NIV challenge in COPD patients with acute hypercapnic respiratory failure (AHRF). Patients and methods: A prospective observational multicentric pilot study was conducted in three tertiary hospitals over a 12-month study period. A total of 155 consecutive COPD patients who were admitted for AHRF and treated by NIV were enrolled. Delayed response to NIV was defined as a significant clinical improvement in the first 48h following NIV initiation despite a persistent severe respiratory acidosis (pH&nbsp

BACKGROUNDCentral venous-to-arterial carbon dioxide partial pressure difference (ΔPCO2) can be used as a marker for the efficacy of venous blood in removing the total CO2 produced by the tissues. To date, this role of ΔPCO2 has been assessed only in patients after resuscitation from septic shock wit

To evaluate the extent to which sitting position and applied positive end-expiratory pressure improve respiratory mechanics of severely obese patients under mechanical ventilation.Prospective cohort study.A 15-bed ICU of a tertiary hospital.Fifteen consecutive critically ill patients with a body mass index (the weight in kilograms divided by the square of the height in meters) above 35 were compared to 15 controls with body mass index less than 30.Respiratory mechanics was first assessed in the supine position, at zero end-expiratory pressure, and then at positive end-expiratory pressure set at the level of auto-positive endexpiratory pressure. Second, all measures were repeated in the sitting position.Assessment of respiratory mechanics included plateau pressure, auto-positive end-expiratory pressure, and flow-limited volume during manual compression of the abdomen, expressed as percentage of tidal volume to evaluate expiratory flow limitation. In supine position at zero end-expiratory pressure, all critically ill obese patients demonstrated expiratory flow limitation (flow-limited volume, 59.4% [51.3-81.4%] vs 0% [0-0%] in controls; p0.0001) and greater auto-positive end-expiratory pressure (10 [5-12.5] vs 0.7 [0.4-1.25] cm H2O in controls; p0.0001). Applied positive end-expiratory pressure reverses expiratory flow limitation (flow-limited volume, 0% [0-21%] vs 59.4% [51-81.4%] at zero end-expiratory pressure; p0.001) in almost all the obese patients, without increasing plateau pressure (24 [19-25] vs 22 [18-24] cm H2O at zero end-expiratory pressure; p = 0.94). Sitting position not only reverses partially or completely expiratory flow limitation at zero end-expiratory pressure (flow-limited volume, 0% [0-58%] vs 59.4% [51-81.4%] in supine obese patients; p0.001) but also results in a significant drop in auto-positive end-expiratory pressure (1.2 [0.6-4] vs 10 [5-12.5] cm H2O in supine obese patients; p0.001) and plateau pressure (15.6 [14-17] vs 22 [18-24] cm H2O in supine obese patients; p0.001).In critically ill obese patients under mechanical ventilation, sitting position constantly and significantly relieved expiratory flow limitation and auto-positive end-expiratory pressure resulting in a dramatic drop in alveolar pressures. Combining sitting position and applied positive end-expiratory pressure provides the best strategy.

Objective:To evaluate the impact of switching to total face mask in cases where face mask-delivered noninvasive mechanical ventilation has already failed in do-not-intubate patients in acute respiratory failure.Design and Setting:Prospective observational study in an ICU and a respiratory stepdown u

To examine the repeatability of Stewart's parameters and anion gap in a cohort of critically ill patients and to determine the smallest detectable changes in individual patients.A total of 161 patients were included prospectively. They underwent two subsequent blood samplings within 10 min of each other and samples were analyzed using the same central laboratory analyzer. Measured and calculated parameters from the two samples were compared. The repeatability was expressed as the smallest detectable difference (SDD), coefficient of variation (CV) and intraclass correlation coefficient (ICC).The mean differences ± SD (mEq/L) for the repeated measurements were 0.1 ± 0.76, 0.12 ± 0.68, -0.02 ± 1.02, and -0.08 ± 1.05 for the apparent strong ion difference (SID(app)), effective strong ion difference (SID(eff)), strong ion gap (SIG), and albumin-corrected anion gap (AG(corr)), respectively. The SDDs (mEq/L) for SID(app), SID(eff), SIG, and AG(corr), were ±1.49, ±1.33, ±2, and ±2.06, respectively. The CVs (%) for these variables were 1.4, 1.45, 13.3, and 4.15, respectively. The ICCs for all these variables were high, largely above 0.75.The repeatability of all these calculated variables was good. In repeated measurements, a change in value of these parameters exceeding 1.96√2 CV (%), the least significant change (LSC) or the SDD should be regarded as significant. Use of SDD is preferable to CV and LSC (%) because of its independence from the levels of variables and its expression in absolute units. Expressed as SDD, a SIG change value, e.g., of at least ±2 mEq/L should be significant.

Purpose The purpose was to investigate whether extravascular lung water (EVLW) indexed to actual body weight (EVLWa) is an independent predictor of mortality in patients with septic shock, to determine the relationship between EVLWa and other markers of lung injury, and to test if indexing EVLW with predicted body weight (EVLWp) strengthens its predictive power. Methods Extravascular lung water, pulmonary vascular permeability index, and other markers of lung injury were measured prospectively in 55 patients with septic shock for 3 days. Results At day 1, EVLWa, EVLWp, and pulmonary vascular permeability index were not significantly different between survivors and nonsurvivors. However, in parallel to the course of septic shock, these variables decreased only in the survivors and remained elevated in the nonsurvivors, reaching intergroup difference by day 3. In multiple logistic regression analysis, both EVLWa and EVLWp (at day 3) were predictors of mortality with an odds ratio of 2 (95% confidence interval, 1.12-3.7) and 1.7 (95% confidence interval, 1.1-2.5) per SD increase, respectively. The receiver operating characteristic curve analysis showed that EVLWp did not improve the discriminative power of EVLW to predict mortality. Extravascular lung water indexed to actual body weight correlated with lung injury score and with the ratio of arterial oxygen partial pressure to inspired oxygen fraction but not with static respiratory compliance. Indexing EVLW to predicted body weight did not ameliorate these correlations. Conclusions Extravascular lung water indexed or not to predicted body weight is an independent predictor of mortality in patients with septic shock. Repeated measurements of EVLW indexes over time, rather than a too-early measurement, seem to be more appropriate for predicting outcome.

Background To evaluate the ability of the central venous-to-arterial CO2 content and tension differences to arteriovenous oxygen content difference ratios (∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2, respectively), blood lactate concentration, and central venous oxygen saturation (ScvO2) to detect the presence of global anaerobic metabolism through the increase in oxygen consumption (VO2) after an acute increase in oxygen supply (DO2) induced by volume expansion (VO2/DO2 dependence). Methods We prospectively studied 98 critically ill mechanically ventilated patients in whom a fluid challenge was decided due to acute circulatory failure related to septic shock. Before and after volume expansion (500 mL of colloid solution), we measured cardiac index, VO2, DO2, ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios, lactate, and ScvO2. Fluid-responders were defined as a ≥15 % increase in cardiac index. Areas under the receiver operating characteristic curves (AUC) were determined for these variables. Results Fifty-one patients were fluid-responders (52 %). DO2 increased significantly (31 ± 12 %) in these patients. An increase in VO2 ≥ 15 % (“VO2-responders”) concurrently occurred in 57 % of the 51 fluid-responders (45 ± 16 %). Compared with VO2-non-responders, VO2-responders were characterized by higher lactate levels and higher ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios. At baseline, lactate predicted a fluid-induced increase in VO2 ≥ 15 % with AUC of 0.745. Baseline ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios predicted an increase of VO2 ≥ 15 % with AUCs of 0.965 and 0.962, respectively. Baseline ScvO2 was not able to predict an increase of VO2 ≥ 15 % (AUC = 0.624). Conclusions ∆ContCO2/∆ContO2 and ∆PCO2/∆ContO2 ratios are more reliable markers of global anaerobic metabolism than lactate. ScvO2 failed to predict the presence of global tissue hypoxia. Electronic supplementary material The online version of this article (doi:10.1186/s13613-016-0110-3) contains supplementary material, which is available to authorized users.

Supplemental Digital Content is available in the text, The objective of this study was to examine the repeatability of blood gas (BG) parameters and their derived variables such as the central venous-to-arterial carbon dioxide tension difference (▵Pco2) and the ratio of ▵Pco2 over the central arteriovenous oxygen content difference (▵Pco2/C(a-cv)O2) and to determine the smallest detectable changes in individual patients. A total of 192 patients with arterial and central venous catheters were included prospectively. Two subsequent arterial and central venous blood samples were collected immediately one after the other and analyzed using the same point-of-care BG analyzer. The samples were analyzed for arterial and venous BG parameters, ▵Pco2, and ▵Pco2/C(a-cv)O2 ratio. Repeatability was expressed as the smallest detectable difference (SDD) and the least significant change (LSC). A change in value of these parameters exceeding the SDD or the LSC should be regarded as real. The SDDs for arterial carbon dioxide tension, arterial oxygen saturation, central venous oxygen saturation (ScvO2), and ▵Pco2 were small: ±2.06 mm Hg, ±1.23%, 2.92%, and ±1.98 mm Hg, respectively, whereas the SDDs for arterial oxygen tension (Pao2) and ▵Pco2/C(a-cv)O2 were high: ±9.09 mm Hg and ±0.57 mm Hg/mL, respectively. The LSCs (%) for these variables were 5.06, 1.27, 4.44, 32.4, 9.51, and 38.5, respectively. The repeatability of all these variables was good except for Pao2 and ▵Pco2/C(a-cv)O2 ratio for which we observed an important inherent variability. Expressed as SDD, a ScvO2 change value of at least ±3% should be considered as true. The clinician must be aware that an apparent change in these variables in an individual patient might represent only an inherent variation.

To investigate the effects of fenofibrate, an activator of peroxysome proliferator activated receptor (PPAR) alpha, on vascular endothelium and on hemostasis in a rabbit endotoxic shock model.Prospective laboratory study in a university laboratory.36 male New Zealand rabbits weighing 2.5-3 kg.We determined in vitro vascular reactivity, endothelium CD31-platelet/endothelial cell adhesion molecule (PECAM) 1 immunohistochemistry, plasma coagulation factors, and monocyte tissue factor expression 5 days after onset of endotoxic shock (0.5 mg/kg intravenous bolus, Escherichia coli lipopolysaccharide) with or without treatment by fenofibrate (mixed in the chow at a concentration of 0.5%) for 15 days before lipopolysaccharide injection and 5 days afterward.Metabolic acidosis and coagulation activation confirmed presence of shock. Fenofibrate decreased monocyte tissue factor expression. It improved endothelial-dependent relaxation at 5 days (Emax=68.2+/-3.3%, vs. 44.2+/-2.5% in the non-treated group). Endotoxin-induced deendothelialization was significantly decreased by fenofibrate at 5 days (8.5+/-1.3% vs. 19.2+/-3.1% in the nontreated group) .These data indicate for the first time that fenofibrate, an activator of PPAR-alpha, inhibits monocyte tissue factor expression and protects against endothelial dysfunction and histological injury in endotoxin-induced shock.

PurposeAcute respiratory failure (ARF) is a common life-threatening complication in morbidly obese patients with obesity hypoventilation syndrome (OHS). We aimed to identify the determinants of noninvasive ventilation (NIV) success or failure for this indication.MethodsWe prospectively included 76 consecutive patients with BMI>40 kg/m2 diagnosed with OHS and treated by NIV for ARF in a 15-bed ICU of a tertiary hospital.ResultsNIV failed to reverse ARF in only 13 patients. Factors associated with NIV failure included pneumonia (n = 12/13, 92% vs n = 9/63, 14%; pConclusionsMultiple organ failure and pneumonia were the main factors associated with NIV failure and death in morbidly obese patients in hypoxemic ARF. On the opposite, NIV was constantly successful and could be safely pushed further in case of severe hypercapnic acute respiratory decompensation of OHS.

INTRODUCTION: To investigate whether the difference between sodium and chloride ([Na(+)] - [Cl(-)]) and anion gap corrected for albumin and lactate (AG(corr)) could be used as apparent strong ion difference (SID(app)) and strong ion gap (SIG) surrogates (respectively) in critically ill patients. METHODS: A total of 341 patients were prospectively observed; 161 were allocated to the modeling group, and 180 to the validation group. Simple regression analysis was used to construct a mathematical model between SID(app) and [Na(+)] - [Cl(-)] and between SIG and AG(corr) in the modeling group. Area under the receiver operating characteristic (ROC) curve was also measured. The mathematical models were tested in the validation group. RESULTS: in the modeling group, SID(app) and SIG were well predicted by [Na(+)] - [Cl(-)] and AG(corr) (R(2) = 0.973 and 0.96, respectively). Accuracy values of [Na(+)] - [Cl(-)] for the identification of SID(app) acidosis (47.5 mEq/L) were 0.992 (95% confidence interval [CI], 0.963-1) and 0.998 (95%CI, 0.972-1), respectively. The accuracy of AG(corr) in revealing SIG acidosis (>8 mEq/L) was 0.974 (95%CI: 0.936-0.993). These results were validated by showing excellent correlations and good agreements between predicted and measured SID(app) and between predicted and measured SIG in the validation group (R(2) = 0.977; bias = 0±1.5 mEq/L and R(2) = 0.96; bias = -0.2±1.8 mEq/L, respectively). CONCLUSIONS: SID(app) and SIG can be substituted by [Na(+)] - [Cl(-)] and by AG(corr) respectively in the diagnosis and management of acid-base disorders in critically ill patients.

Bone marrow stem cells are able to differentiate into nervous and endothelial cells. In our study, we found that administration of a bone marrow-stimulating factor (granulocyte colony-stimulating factor; G-CSF 50 microg/kg) decrease the brain infarct volume and enhance survival rate in a model of cerebral ischemia. Taken together, these data suggest a beneficial effect of a pharmacological endogenous bone marrow mobilization in the course of cerebral ischemia and open a new direction for cellular therapy strategy in stroke.

The measurement of cardiac output and its adequacy to tissue needs are essential for hemodynamic evaluation. In a recent review it was stated that the venous-to-arterial carbon dioxide difference (dPCO2) could be considered a marker of adequacy of venous blood flow to remove the total CO2 produced by the peripheral tissues. Several studies have already shown that dPCO2 and the cardiac index (CI) are inversely correlated in critically ill patients. However, the dPCO2 can be influenced not only by CI, but also by other factors governing CO2 production and CO2 elimination. The aim of this work was to study the behaviour of dPCO2, measured from central venous blood, and its evolution during the early stage of septic shock.

Background Even in developed countries, severe specific pregnancy complications may occur in the immediate postpartum period and require admission to the ICU. The characteristics and risk factors of acute renal failure (ARF) induced by these complications and their treatments are not well known. Methods We performed a retrospective multicenter study in three intensive care departments linked to level III maternity wards in the north of France. All patients admitted to ICU for postpartum complications over a 5-year period (2008 to 2012) were included. Clinical and biological data, delivery characteristics, type of complications, and treatments were compared by univariate and multivariate analyses according to the occurrence and severity of ARF. Results One hundred eighty-two patients admitted to ICU for postpartum complications were included in the study. Sixty-eight patients (37%) developed an ARF: 49 with a low or medium severity and 19 with a severe ARF requiring renal replacement therapy. Hemolysis, elevated liver enzyme, and low platelet count (HELLP) syndrome on its own (p = 0.047) or combined with postpartum haemorrhage (p = 0.003), previous treatment by hyperoncotic albumin infusion (p = 0.001) and blockade of fibrinolysis by tranexamic acid (p = 0.03), was associated with secondary ARF. By multivariate analysis, the only independent factors were the association of HELLP syndrome with postpartum haemorrhage and the use of hyperoncotic albumin infusion. Conclusions HELLP syndrome associated with postpartum haemorrhage induces a high risk of ARF in the complicated postpartum setting. A particular attention should be given to treatments that could worsen the kidney function in that situation.

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