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Introduction: The purpose of this study was to evaluate the clinical relevance of high values of central venous-to-arterial carbon dioxide difference (PCO2 gap) in high-risk surgical patients admitted to a postoperative ICU. We hypothesized that PCO2 gap could serve as a useful tool to identify patients still requiring hemodynamic optimization at ICU admission., Methods: One hundred and fifteen patients were included in this prospective single-center observational study during a 1-year period. High-risk surgical inclusion criteria were adapted from Schoemaker and colleagues. Demographic and biological data, PCO2 gap, central venous oxygen saturation, lactate level and postoperative complications were recorded for all patients at ICU admission, and 6 hours and 12 hours after admission., Results: A total of 78 (68%) patients developed postoperative complications, of whom 54 (47%) developed organ failure. From admission to 12 hours after admission, there was a significant difference in mean PCO2 gap (8.7 ± 2.8 mmHg versus 5.1 ± 2.6 mmHg; P = 0.001) and median lactate values (1.54 (1.1-3.2) mmol/l versus 1.06 (0.8-1.8) mmol/l; P = 0.003) between patients who developed postoperative complications and those who did not. These differences were maximal at admission to the ICU. At ICU admission, the area under the receiver operating characteristic curve for occurrence of postoperative complications was 0.86 for the PCO2 gap compared to Sequential Organ Failure Assessment score (0.82), Simplified Acute Physiology Score II score (0.67), and lactate level (0.67). The threshold value for PCO2 gap was 5.8 mmHg. Multivariate analysis showed that only a high PCO2 gap and a high Sequential Organ Failure Assessment score were independently associated with the occurrence of postoperative complications. A high PCO2 gap (≥6 mmHg) was associated with more organ failure, an increase in duration of mechanical ventilation and length of hospital stay., Conclusion: A high PCO2 gap at admission in the postoperative ICU was significantly associated with increased postoperative complications in high-risk surgical patients. If the increase in PCO2 gap is secondary to tissue hypoperfusion then the PCO2 gap might be a useful tool complementary to central venous oxygen saturation as a therapeutic target.

Dynamic variables of fluid responsiveness are useful guides for fluid management in patients under controlled positive pressure ventilation. In the previous issue of Critical Care, Jacques and colleagues show that these variables remain reliable predictors of fluid responsiveness in a porcine model of intra-abdominal hypertension, but threshold values are higher than during normal intra-abdominal pressure. Their threshold values, however, cannot be applied to clinical practice. This study suggests that intra-abdominal pressure must be measured in critically ill patients, and 'supranormal' values of dynamic variables should be analyzed with caution. The 'fluid responsive part' of an increased dynamic variable in such patients may be estimated by measuring its change during a fluid challenge.

Introduction: Dynamic predictors of fluid responsiveness have made automated management of fluid resuscitation more practical. We present initial simulation data for a novel closed-loop fluid-management algorithm (LIR, Learning Intravenous Resuscitator)., Methods: The performance of the closed-loop algorithm was tested in three phases by using a patient simulator including a pulse-pressure variation output. In the first phase, LIR was tested in three different hemorrhage scenarios and compared with no management. In the second phase, we compared LIR with 20 practicing anesthesiologists for the management of a simulated hemorrhage scenario. In the third phase, LIR was tested under conditions of noise and artifact in the dynamic predictor., Results: In the first phase, we observed a significant difference between the unmanaged and the LIR groups in moderate to large hemorrhages in heart rate (76 ± 8 versus 141 ± 29 beats/min), mean arterial pressure (91 ± 6 versus 59 ± 26 mm Hg), and cardiac output (CO; (6.4 ± 0.9 versus 3.2 ± 1.8 L/min) (P < 0.005 for all comparisons). In the second phase, LIR intervened significantly earlier than the practitioners (16.0 ± 1.3 minutes versus 21.5 ± 5.6 minutes; P < 0.05) and gave more total fluid (2,675 ± 244 ml versus 1,968 ± 644 ml; P < 0.05). The mean CO was higher in the LIR group than in the practitioner group (5.9 ± 0.2 versus 5.2 ± 0.6 L/min; P < 0.05). Finally, in the third phase, despite the addition of noise to the pulse-pressure variation value, no significant difference was found across conditions in mean, final, or minimum CO., Conclusion: These data demonstrate that LIR is an effective volumetric resuscitator in simulated hemorrhage scenarios and improved physician management of the simulated hemorrhages.

Introduction: The aim of this study was to investigate the effects of activated protein C (aPC) on vascular function, endothelial injury, and haemostasis in a rabbit endotoxin-induced shock model., Method: This study included 22 male New Zealand rabbits weighing 2.5 to 3 kg each. In vitro vascular reactivity, endothelium CD31-PECAM1 immunohistochemistry, plasma coagulation factors and monocyte tissue factor (TF) expression were performed 5 days (D5) after onset of endotoxic shock (initiated by 0.5 mg/kg intravenous bolus of Escherichia coli lipopolysaccharide (LPS)) with or without treatment with aPC injected as an intravenous 2 mg/kg bolus 1 hour after LPS (LPS+aPC group and LPS group, respectively)., Results: LPS decreased the sensitivity to phenylephrine (PE) in aortic rings without endothelium (E-) when compared to E- rings from the control group (p < 0.05). This was abolished by NG-nitro-L-arginine methyl ester and not observed in E- rings from aPC-treated rabbits. Although aPC failed to decrease monocyte TF expression in endotoxinic animals at D5, aPC treatment restored the endothelium-dependent sensitivity in response to PE (2.0 +/- 0.2 muM in rings with endothelium (E+) versus 1.0 +/- 0.2 microM in E- rings (p < 0.05) in the LPS+aPC group versus 2.4 +/- 0.3 microM in E+ rings versus 2.2 +/- 0.2 microM in E- rings (p value not significant), in the LPS group). Endotoxin-induced de-endothelialisation was reduced by aPC at D5 (28.5 +/- 2.3% in the LPS+aPC group versus 40.4 +/- 2.4% in the LPS group, p < 0.05)., Conclusion: These data indicate that aPC increased the sensitivity to a vasoconstrictor agent (PE) associated with restoration of endothelial modulation, and protected against endothelial histological injury in endotoxin-induced shock. It failed to inhibit TF expression at D5 after LPS injection.

Introduction: Aging is associated with a decline in cardiac contractility and altered immune function. The aim of this study was to determine whether aging alters endotoxin-induced myocardial dysfunction., Methods: Senescent (24 month) and young adult (3 month) male Wistar rats were treated with intravenous lipopolysaccharide (LPS) (0.5 mg/kg (senescent and young rats) or 5 mg/kg (young rats only)), or saline (senescent and young control groups). Twelve hours after injection, cardiac contractility (isolated perfused hearts), myofilament Ca2+ sensitivity (skinned fibers), left ventricular nitric oxide end-oxidation products (NOx and NO2) and markers of oxidative stress (thiobarbituric acid reactive species (TBARS) and antioxidant enzymes) were investigated., Results: LPS (0.5 mg/kg) administration resulted in decreased contractility in senescent rats (left ventricular developed pressure (LVDP), 25 +/- 4 vs 53 +/- 4 mmHg/g heart weight in control; P < 0.05) of amplitude similar to that in young rats with LPS 5 mg/kg (LVDP, 48 +/- 7 vs 100 +/- 7 mmHg/g heart weight in control; P < 0.05). In contrast to young LPS rats (0.5 and 5 mg/kg LPS), myofilament Ca2+ sensitivity was unaltered in senescent LPS hearts. Myocardial NOx and NO2 were increased in a similar fashion by LPS in young (both LPS doses) and senescent rats. TBARS and antioxidant enzyme activities were unaltered by sepsis whatever the age of animals., Conclusion: Low dose of LPS induced a severe myocardial dysfunction in senescent rats. Ca2+ myofilament responsiveness, which is typically reduced in myocardium of young adult septic rats, however, was unaltered in senescent rats. If these results are confirmed in in vivo conditions, they may provide a cellular explanation for the divergent reports on ventricular diastolic function in septic shock. In addition, Ca2+-sensitizing agents may not be as effective in aged subjects as in younger subjects.