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). 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. 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). ∆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.

Objective: To evaluate the extent to which sitting position and applied positive end-expiratory pressure improve respiratory mechanics of severely obese patients under mechanical ventilation. Design: Prospective cohort study. Settings: A 15-bed ICU of a tertiary hospital. Participants: 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. Interventions: 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. Measurements and Main Results: 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; p < 0.0001) and greater auto-positive end-expiratory pressure (10 [5–12.5] vs 0.7 [0.4–1.25] cm H₂O in controls; p < 0.0001). 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; p < 0.001) 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; p < 0.001) 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; p < 0.001) and plateau pressure (15.6 [14–17] vs 22 [18–24] cm H₂O in supine obese patients; p < 0.001). Conclusions: 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.

Acute 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. We 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. NIV failed to reverse ARF in only 13 patients. Factors associated with NIV failure included pneumonia (n = 12/13, 92% vs n = 9/63, 14%; p<0.0001), high SOFA (10 vs 5; p<0.0001) and SAPS2 score (63 vs 39; p<0.0001) at admission. These patients often experienced poor outcome despite early resort to endotracheal intubation (in-hospital mortality, 92.3% vs 17.5%; p<0.001). The only factor significantly associated with successful response to NIV was idiopathic decompensation of OHS (n = 30, 48% vs n = 0, 0%; p = 0.001). In the NIV success group (n = 63), 33 patients (53%) experienced a delayed response to NIV (with persistent hypercapnic acidosis during the first 6 hours). Multiple 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.

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 unit over a 12-month study period. Intervention: Switching to total face mask, which covers the entire face, when noninvasive mechanical ventilation using facial mask (oronasal mask) failed to reverse acute respiratory failure. Patients: Seventy-four patients with a do-not-intubate order and treated by noninvasive mechanical ventilation for acute respiratory failure. Main Results: Failure of face mask-delivered noninvasive mechanical ventilation was associated with a three-fold increase in in-hospital mortality (36% vs. 10.5%; p = 0.009). Nevertheless, 23 out of 36 patients (64%) in whom face mask-delivered noninvasive mechanical ventilation failed to reverse acute respiratory failure and, therefore, switched to total face mask survived hospital discharge. Reasons for switching from facial mask to total face mask included refractory hypercapnic acute respiratory failure (n = 24, 66.7%), painful skin breakdown or facial mask intolerance (n = 11, 30%), and refractory hypoxemia (n = 1, 2.7%). In the 24 patients switched from facial mask to total face mask because of refractory hypercapnia, encephalopathy score (3 [3–4] vs. 2 [2–3]; p < 0.0001), PaCO₂ (87 ± 25 mm Hg vs. 70 ± 17 mm Hg; p < 0.0001), and pH (7.24 ± 0.1 vs. 7.32 ± 0.09; p < 0.0001) significantly improved after 2 hrs of total face mask-delivered noninvasive ventilation. Patients switched early to total face mask (in the first 12 hrs) developed less pressure sores (n = 5, 24% vs. n = 13, 87%; p = 0.0002), despite greater length of noninvasive mechanical ventilation within the first 48 hrs (44 hrs vs. 34 hrs; p = 0.05) and less protective dressings (n = 2, 9.5% vs. n = 8, 53.3%; p = 0.007). The optimal cutoff value for face mask-delivered noninvasive mechanical ventilation duration in predicting facial pressure sores was 11 hrs (area under the receiver operating characteristic curve, 0.86 ± 0.04; 95% confidence interval 0.76–0.93; p < 0.0001; sensitivity, 84%; specificity, 71%). Conclusion: In patients in hypercapnic acute respiratory failure, for whom escalation to intubation is deemed inappropriate, switching to total face mask can be proposed as a last resort therapy when face mask-delivered noninvasive mechanical ventilation has already failed to reverse acute respiratory failure. This strategy is particularly adapted to provide prolonged periods of continuous noninvasive mechanical ventilation while preventing facial pressure sores.