Tissue oxygen saturation is predictive of lactate clearance in patients with circulatory shock.

BACKGROUND: Tissue oxygen saturation (StO2) decrease could appear earlier than lactate alteration. However, the correlation between StO2 and lactate clearance was unknown. METHODS: This was a prospective observational study. All consecutive patients with circulatory shock and lactate over 3 mmol/L were included. Based on the rule of nines, a BSA (body surface area) weighted StO2 was calculated from four sites of StO2 (masseter, deltoid, thenar and knee). The formulation was as follows: masseter StO2 × 9% + (deltoid StO2 + thenar StO2) × (18% + 27%)/ 2 + knee StO2 × 46%. Vital signs, blood lactate, arterial and central venous blood gas were measured simultaneously within 48 h of ICU admission. The predictive value of BSA-weighted StO2 on 6-hour lactate clearance > 10% since StO2 initially monitored was assessed. RESULTS: A total of 34 patients were included, of whom 19 (55.9%) had a lactate clearance higher than 10%. The mean SOFA score was lower in cLac ≥ 10% group compared with cLac < 10% group (11 ± 3 vs. 15 ± 4, p = 0.007). Other baseline characteristics were comparable between groups. Compared to non-clearance group, StO2 in deltoid, thenar and knee were significantly higher in clearance group. The area under the receiver operating curves (AUROC) of BSA-weighted StO2 for prediction of lactate clearance (0.92, 95% CI [Confidence Interval] 0.82-1.00) was significantly higher than StO2 of masseter (0.65, 95% CI 0.45-0.84; p < 0.01), deltoid (0.77, 95% CI 0.60-0.94; p = 0.04), thenar (0.72, 95% CI 0.55-0.90; p = 0.01), and similar to knee (0.87, 0.73-1.00; p = 0.40), mean StO2 (0.85, 0.73-0.98; p = 0.09). Additionally, BSA-weighted StO2 model had continuous net reclassification improvement (NRI) over the knee StO2 and mean StO2 model (continuous NRI 48.1% and 90.2%, respectively). The AUROC of BSA-weighted StO2 was 0.91(95% CI 0.75-1.0) adjusted by mean arterial pressure and norepinephrine dose. CONCLUSIONS: Our results suggested that BSA-weighted StO2 was a strong predictor of 6-hour lactate clearance in patients with shock.

Accuracy of Mean Value of Central Venous Pressure from Monitor Digital Display: Influence of Amplitude of Central Venous Pressure during Respiration.

Background A simple measurement of central venous pressure (CVP)-mean by the digital monitor display has become increasingly popular. However, the agreement between CVP-mean and CVP-end (a standard method of CVP measurement by analyzing the waveform at end-expiration) is not well determined. This study was designed to identify the relationship between CVP-mean and CVP-end in critically ill patients and to introduce a new parameter of CVP amplitude (ΔCVP= CVPmax - CVPmin) during the respiratory period to identify the agreement/disagreement between CVP-mean and CVP-end.Methods In total, 291 patients were included in the study. CVP-mean and CVP-end were obtained simultaneously from each patient. CVP measurement difference (|CVP-mean - CVP-end|) was defined as the difference between CVP-mean and CVP-end. The ΔCVP was calculated as the difference between the peak (CVPmax) and the nadir value (CVPmin) during the respiratory cycle, which was automatically recorded on the monitor screen. Subjects with |CVP-mean - CVP-end|≥ 2 mmHg were divided into the inconsistent group, while subjects with |CVP-mean - CVP-end| < 2 mmHg were divided into the consistent group.Results ΔCVP was significantly higher in the inconsistent group [7.17(2.77) vs.5.24(2.18), P<0.001] than that in the consistent group. There was a significantly positive relationship between ΔCVP and |CVP-mean - CVP-end| (r=0.283, P <0.0001). Bland-Altman plot showed the bias was -0.61 mmHg with a wide 95% limit of agreement (-3.34, 2.10) of CVP-end and CVP-mean. The area under the receiver operating characteristic curves (AUC) of ΔCVP for predicting |CVP-mean - CVP-end| ≥ 2 mmHg was 0.709. With a high diagnostic specificity, using ΔCVP<3 to detect |CVP-mean - CVP-end| lower than 2mmHg (consistent measurement) resulted in a sensitivity of 22.37% and a specificity of 93.06%. Using ΔCVP>8 to detect |CVP-mean - CVP-end| >8 mmHg (inconsistent measurement) resulted in a sensitivity of 31.94% and a specificity of 91.32%.Conclusions CVP-end and CVP-mean have statistical discrepancies in specific clinical scenarios. ΔCVP during the respiratory period is related to the variation of the two CVP methods. A high ΔCVP indicates a poor agreement between these two methods, whereas a low ΔCVP indicates a good agreement between these two methods.

Cross-sectional study for the clinical application of extracorporeal membrane oxygenation in Mainland China, 2018.

BACKGROUND: To investigate the epidemiology and in-hospital mortality of veno-venous (VV) and veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) in Mainland China throughout 2018. METHODS: Patients supported by ECMO from 1700 tertiary hospitals in 31 provinces from January 1 to December 31, 2018, were selected from the National Clinical Improvement System database. RESULTS: The 1700 included hospitals had 2073 cases of ECMO in 2018, including 714 VV and 1359 VA ECMOs. The average patient age was 50 years (IQR 31-63), and 1346 were male. The average hospital stay was 17 days (IQR 7-30), and the average costs per case was $36,334 (IQR 22,547-56,714). The three provinces with the highest number of ECMO cases were Guangdong, Beijing, and Zhejiang; the southeast coastal areas and regions with higher GDP levels had more cases. Overall in-hospital mortality was 29.6%. Mortality was higher among patients who were male, over 70 years old, living in underdeveloped areas, and who were treated during the summer. Mortality in provinces with more ECMO cases was relatively low. The co-existence of congenital malformations, blood system abnormalities, or nervous system abnormalities increased in-hospital mortality. CONCLUSIONS: Mortality and medical expenses of ECMO among patients in China were relatively low, but large regional and seasonal differences were present. Risk factors for higher in-hospital mortality were older age, male sex, in underdeveloped areas, and treatment during the summer. Additionally, congenital malformations and blood system and nervous system abnormalities were associated with in-hospital mortality.

The effect of variable arterial transducer level on the accuracy of pulse contour waveform-derived measurements in critically ill patients.

We know that a 10 cm departure from the reference level of pressure transducer position is equal to a 7.5 mmHg change of invasive hemodynamic pressure monitoring in a fluid-filled system. However, the relationship between the site level of a variable arterial pressure transducer and the pulse contour-derived parameters has yet to be established in critically ill patients. Moreover, the related quantitative analysis has never been investigated. Forty-two critically ill patients requiring PiCCO-Plus cardiac output monitoring were prospectively studied. The phlebostatic axis was defined as the zero reference level; the arterial pressure transducer was then vertically adjusted to different positions (+5, +10, +15, +20, -20, -15, -10, -5 cm) of departure from the zero reference site. The pulse contour waveform-derived parameters were recorded at each position. Elevation of the pressure transducer caused significantly positive changes in the continuous cardiac index (+CCI), stroke volume index (+SVI), and stroke volume variation (+SVV), and negative changes in the rate of left ventricular pressure rise during systole (-dP/dtmax), the systemic vascular resistance index (-SVRI), and vice versa. At the 5 cm position, the SVRI changes reached statistical significance with error. At the 10 cm position, the changes in CCI and dP/dtmax reached statistical significance with error, while the change in SVV reached statistical significance at 15 cm. The change rate of CCI was more than 5 % at the 15 cm position and approximately 10 % at the 20 cm position. On average, for every centimeter change of the transducer, there was a corresponding 0.014 L/min/m(2) CCI change and 0.36 % change rate, a 1.41 mmHg/s dP/dtmax change and 0.13 % change rate, and a 25 dyne/s/cm(5) SVRI change and 1.2 % change rate. The variation of arterial transducer position can result in inaccurate measurement of pulse contour waveform-derived parameters, especially when the transducer's vertical distance is more than 10 cm from the phlebostatic axis. These findings have clinical implications for continuous hemodynamic monitoring.

The peripheral perfusion index and transcutaneous oxygen challenge test are predictive of mortality in septic patients after resuscitation.

INTRODUCTION: The peripheral perfusion index (PI) is a noninvasive numerical value of peripheral perfusion, and the transcutaneous oxygen challenge test (OCT) is defined as the degree of transcutaneous partial pressure of oxygen (PtcO2) response to 1.0 FiO2. The value of noninvasive monitoring peripheral perfusion to predict outcome remains to be established in septic patients after resuscitation. Moreover, the prognostic value of PI has not been investigated in septic patients. METHODS: Forty-six septic patients, who were receiving PiCCO-Plus cardiac output monitoring, were included in the study group. Twenty stable postoperative patients were studied as a control group. All the patients inspired 1.0 of FiO2 for 10 minutes during the OCT. Global hemodynamic variables, traditional metabolic variables, PI and OCT related-variables were measured simultaneously at 24 hours after PiCCO catheter insertion. We obtained the 10 min-OCT ((PtcO2 after 10 minutes on inspired 1.0 oxygen)--(baseline PtcO2)), and the oxygen challenge index ((10 min-OCT)/(PaO2 on inspired 1.0 oxygen--baseline PaO2)) during the OCT. RESULTS: The PI was significantly correlated with baseline PtcO2, 10 min-OCT and oxygen challenge index (OCI) in all the patients. The control group had a higher baseline PtcO2, 10 min-OCT and PI than the septic shock group. In the sepsis group, the macro hemodynamic parameters and ScvO2 showed no differences between survivors and nonsurvivors. The nonsurvivors had a significantly lower PI, 10 min-OCT and OCI, and higher arterial lactate level. The PI, 10 min-OCT and OCI predicted the ICU mortality with an accuracy that was similar to arterial lactate level. A PI<0.2 and a 10 min-OCT<66 mmHg were related to poor outcome after resuscitation. CONCLUSIONS: The PI and OCT are predictive of mortality for septic patients after resuscitation. Further investigations are required to determine whether the correction of an impaired level of peripheral perfusion may improve the outcome of septic shock patients.

[Value of peripheral perfusion index in the assessment of reactive hyperemia in septic patients].

OBJECTIVE: To explore the changes of peripheral perfusion index (PI) during forearm vascular occlusion test (VOT) and examine its evaluative value of reactive hyperemia in septic patients. METHODS: Twenty-one patients with septic shock, 21 postoperative ones without infection and 18 health volunteers were prospectively recruited to undergo vascular occlusion test. An arrest of forearm blood flow was applied for 3 min with a sphygmomanometer inflated to a pressure approximately 30 mm Hg greater than systolic pressure around forearm. PI was measured and recorded continuously by conventional pulse oximetry during VOT. RESULTS: (1)In all subjects, the PI values decreased to zero during ischemic period. There were no changes in heart rate or blood pressure between baseline and reperfusion. The maximum PI (PI-max) after a release of pneumatic cuff was significantly higher than baseline PI; (2)The change rates of PI-max and PI were significantly lower and the time to PI-max was longer in septic group after reperfusion; (3) A negative relationship existed between PI change rate and sequential organ failure assessment (SOFA) score in septic group. CONCLUSIONS: PI may be used to assess vascular reactive hyperemia in critically ill patients. And the capacity of peripheral vascular reactive hyperemia decreases in septic patients.

[Variations of left ventricular-arterial coupling in septic shock].

OBJECTIVE: To explore the variations of left ventricular-arterial coupling and elucidate its mechanisms in septic shock. METHODS: Septic shock rabbits were established by an intravenous injection of endotoxin. A total of 12 rabbits were divided randomly into sham operation group (S, n = 6) and endotoxin injection group (E, n = 6). Ultrasonic echocardiography and hemodynamic monitoring were conducted at 0h (30-min post-operation), 2h (1-hour after endotoxin or saline injection) and 4h (3-hour after endotoxin or saline injection) and the relative hemodynamic indices were recorded. RESULTS: (1) In E group, end-systolic elastance (Ees) at 2h was lower than that at 0h (75.72 ± 5.16 vs 90.77 ± 7.17 mm Hg/ml) and Ees at 4h was lower than that at 2h (58.45 ± 3.63 vs 75.72 ± 5.16 mm Hg/ml, P < 0.05); (2) In E group, left ventricular diastolic volume (LVDV) at 2h and 4h were both lower than that at 0h (3.26 ± 0.21 vs 3.58 ± 0.25 ml, 3.27 ± 0.19 vs 3.58 ± 0.25 ml). And left ventricular end diastolic compliance (Ced) at 4h were lower than that at 0h and 2h (0.61 ± 0.05 vs 0.74 ± 0.07 ml/mm Hg, 0.61 ± 0.05 vs 0.75 ± 0.08 ml/mm Hg, P < 0.05); (3) In E group, Ea at 2h and 4h was lower than that at 0h (41.35 ± 2.87 vs 50.46 ± 3.22 mm Hg/ml, 40.13 ± 2.68 vs 50.46 ± 3.22 mm Hg/ml, P < 0.05); (4) In E group, Ea/Ees at 4h was higher than that at 0h and 4h (0.70 ± 0.07 vs 0.57 ± 0.06, 0.70 ± 0.07 vs 0.56 ± 0.05, P < 0.05). And Ea/Ees at 2h had no significant difference with that at 0h (0.56 ± 0.05 vs 0.57 ± 0.06, P < 0.05). CONCLUSION: During compensatory stage of septic shock, left ventricular-arterial coupling shows no significant variation. However, during decompensatory stage of septic shock, there is significant left ventricular-arterial decoupling. The main reason for decoupling lies in that the decrease of left myocardial contractility is more significant than that of left ventricular afterload. And ventricular diastolic dysfunction may also participate.

Ursodeoxycholic Acid (UDCA) Reduces Hepatocyte Apoptosis by Inhibiting Farnesoid X Receptor (FXR) in Hemorrhagic Shock (HS).

BACKGROUND: Hemorrhagic shock (HS) is the most common cause of potentially preventable death after traumatic injury. Acute liver injury is an important manifestation of HS. Apoptosis plays an important role in liver injury. Farnesoid X receptor (FXR) can alleviate liver injury. This study aimed to examine the effects of ursodeoxycholic acid (UDCA) on hepatocyte apoptosis in HS and its relationship with the FXR pathway. METHODS: Mice were randomly divided into 4 groups: sham group, HS group, HS + UDCA group, and FXR (-) + HS + UDCA group. There were 6 mice in each group. As to the model of HS, MAP of 40 ± 5 mmHg was maintained for 1 hour. As to UDCA intervention, UDCA (300mg/kg) was given nasally. Real-time RT-PCR and Western blotting were used to detect changes in the expression level of Caspase-3, Bax, LC3Ⅰ, LC3Ⅱ, Bcl-2, and Beclin-1 in the liver. TUNEL assay was used to detect changes in hepatocyte apoptosis. RESULTS: The expression level of Caspase-3 and Bax in the liver decreased significantly after treatment with UDCA under HS conditions. The expression level of LC3Ⅰ, LC3Ⅱ, Bcl-2, and Beclin-1 in the liver increased significantly after treatment with UDCA under HS conditions. TUNEL positive percentage of liver decreased significantly after treatment with UDCA under HS conditions. In the case of FXR (-), the influence of UDCA was inhibited. CONCLUSION: These results indicated that UDCA could reduce hepatocyte apoptosis during HS through the FXR pathway.

[The value of bedside lung ultrasound in emergency-plus protocol for the assessment of lung consolidation and atelectasis in critical patients].

OBJECTIVE: To investigate the effect of the bedside lung ultrasound in emergency(BLUE)-plus lung ultrasound protocol on lung consolidation and atelectasis of critical patients. METHODS: All patients who need to receive mechanical ventilation for more than 48 hours in ICU from June 2010 to December 2011 in Peking Union Medical College Hospital were included in the study. BLUE-plus and BLUE lung ultrasound, bedside X-ray, lung CT examination were performed on all patients at the same time. The condition of lung consolidation and atelectasis discovered by BLUE-plus lung ultrasound protocol was recorded and compared with bedside X-ray or lung CT. The difference in assessment of lung consolidation and atelectasis between BLUE-plus lung ultrasound protocol and BLUE protocol was compared. RESULTS: A total of 78 patients were finally enrolled in the study. The lung CT found 70 cases (89.74%) had different degrees of lung consolidation and atelectasis. The sensitivity, specificity and diagnostic accuracy of lung consolidation and atelectasis by the bedside chest X-ray were 31.29%, 75.00% and 38.46%, respectively. BLUE-plus lung ultrasound protocol found 68 cases with lung consolidation and atelectasis, and its sensitivity, specificity, and diagnostic accuracy were 95.71%, 87.50% and 94.87%, respectively, which were significantly higher than those of lung CT. BLUE protocol found 48 cases of lung consolidation and atelectasis, and its sensitivity, specificity, and diagnostic accuracy were 65.71%, 75.00% and 66.67%, respectively. The position of lung consolidation and atelectasis which hadn't been found by BLUE protocol was mainly proved to be located in the basement of lung by lung CT. CONCLUSIONS: The incidence of lung consolidation and atelectasis in critical patients who received mechanical ventilation is high. The BLUE-plus lung ultrasound protocol has a relatively higher sensitivity, specificity and diagnostic accuracy for consolidation and atelectasis, which can find majority of consolidation and atelectasis. As BLUE-plus lung ultrasound is a bedside noninvasive method allowing immediate assessment of most lung consolidation and atelectasis, it will be likely the alternative of the CT and play a key role in assessment of lung consolidation and atelectasis.

Changes of farnesoid X receptor and Takeda G-protein coupled receptor 5 following biliary tract external drainage in hemorrhagic shock.

Since biliary tract external drainage (BTED) is increasingly used to treat patients with shock, it is necessary to clarify pathophysiological changes following BTED in hemorrhagic shock (HS). The present study aimed to investigate the effect of BTED on farnesoid X receptor (FXR) and Takeda G-protein coupled receptor 5 (TGR-5) expression in HS. A total of 24 Sprague-Dawley rats were randomly allocated to sham, BTED, HS and HS + BTED groups. Rat models of HS were induced by drawing blood from the femoral artery until a mean arterial pressure of 40±5 mmHg was achieved and maintained for 60 min. Rat models of BTED were induced by inserting a catheter into the bile duct. The distal end of the bile duct was ligated, and the catheter was passed through the rat flank to allow external collection of bile. Reverse transcription-quantitative PCR, western blotting and immunohistochemistry were performed to detect changes in expression levels of FXR and TGR-5 in the jejunum, ileum and liver. Expression levels of FXR and TGR-5 increased significantly in jejunum and liver following HS (P<0.05). BTED significantly decreased expression levels of FXR in the liver (P<0.05) and TGR-5 in the jejunum, ileum and liver (P<0.05). In conclusion, expression levels of FXR and TGR-5 increased in HS but BTED decreased expression levels of FXR and TGR-5 in HS.

G1 cell cycle arrest signaling in hepatic injury after intraperitoneal sepsis in rats.

OBJECTIVE AND DESIGN: Hepatocytes emerge from a quiescent state into a proliferative state to recover from septic injury. We hypothesize that hepatocyte cell cycle regulation after sepsis potentially contributes to the recovery of liver function. METHODS: An animal model of sepsis was induced by cecal ligation and puncture (CLP) in rats. At serial time points after CLP, hepatocyte expression of p21, P53, cyclin D1, cyclin E, CDK2, CDK4 and PCNA was determined by immunoblot analysis, and the DNA content of isolated hepatocytes was analyzed using flow cytometry. RESULTS: Sepsis-induced liver injury of rats was associated with G1 cell cycle arrest. Recovery of liver function was related to cell cycle progression 48 h after CLP. The upregulation of p53 and p21 correlated with G1 cell arrest 48 h after CLP. The upregulation of cyclin D1/CDK4 and cyclin E/CDK2 also correlated with the G1/S transition 48 h after CLP, resulting in PCNA expression. CONCLUSIONS: The data suggests that G1 cell cycle arrest and p53, p21, CDKs, cyclins and PCNA expression may be involved in the injury/recovery of liver function after intraperitoneal sepsis.

[Impact of extended focus assessed transthoracic echocardiography protocol in septic shock patients].

OBJECTIVE: To investigate the impact of extended focus assessed transthoracic echocardiography (eFATE) in septic shock patients. METHODS: A total of 83 septic shock patients were recruited. And they were divided into the eFATE and routine groups. In the routine group, the patients were assessed by routine methods. And in the eFATE group, the following parameters of central venous pressure (CVP), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI) and ScvO(2) (central venous oxygen saturation) were measured routinely. The PiCCO (pulse indicator continuous cardiac output) method was employed when needed. All parameters and the others [acute physiology and chronic health evaluation II (APACHEII) & lactate] were recorded every 6 h. At 6, 24, 72 h and 1 w, the fluid intake volumes were recorded. All values were analyzed by statistic methods. And the mortality rates of intensive care unit and Day 28 were recorded. RESULTS: In the eFATE group, the 24 h targeting rate was markedly higher than the routine group. Yet there was no effect on the 6 h targeting rate. In the eFATE group, the fluid intake volumes at 6, 24 h and 1 w were markedly lowered than those of the control group. And the myocardial inhibition occurred earlier versus the control group. There was no difference in mortality rate between two groups. CONCLUSION: eFATE plays an important role in the correct assessment of septic shock patients. But its prognostic impact remains to be further defined.

[Correlation of transcutaneous oxygen challenge test and central venous oxygen saturation in septic shock patients].

OBJECTIVE: To investigate the correlation of transcutaneous oxygen challenge test (OCT) [the degree of PtcO2 response to increased fractional inspired oxygen concentration (FiO2) of 1.0 is identified as transcutaneous OCT] and central venous oxygen saturation (ScvO2) in septic shock patients after resuscitation. METHODS: A total of 49 septic shock patients were prospectively studied. They underwent PtcO2 monitoring and OCT (a temporary increase of FiO2 for 10 min). Baseline central venous blood gases, baseline arterial blood gases and post-OCT arterial blood gases were examined. The parameters of PtcO2 index (baseline PtcO2/PaO2), tissue oxygen index (baseline PtcO2/FiO2), 10 min OCT value [(PtcO2 after 10 min on FiO2 of 1.0) minus (baseline PtcO2)], oxygen challenge index [(10 min OCT value)/(PaO2 on FiO2 1.0 minus baseline PaO2)] were calculated during OCT. The patients were divided into 2 groups according to ScvO2 values: normal ScvO2 group (ScvO2 ≥ 70%) versus low ScvO2 group (ScvO2 < 70%). The parametric differences of transcutaneous OCT were compared between two groups. RESULTS: (1) There was a significant correlation between baseline PtcO2 (r = 0.382, P = 0.007), tissue oxygen index (r = 0.355, P = 0.012), 10 min OCT value (r = 0.427, P = 0.002), oxygen challenge index (r = 0.5, P < 0.001) and ScvO2, but not with arterial blood lactate concentration; (2) there were 27 patients in the low ScvO2 group and 22 patients in the normal ScvO2 group. ScvO2 was significantly lower in the low ScvO2 group than in the normal ScvO2 group (61 ± 8 vs 77 ± 6, P < 0.05). No differences in age, severity score, vital signs, arterial blood lactate concentration, vasoactive drugs, PtcO2, PtcO2 index and tissue oxygen index were observed between these groups. Compared with those in the normal ScvO2 group, the patients in the low ScvO2 group had a lower 10 min OCT value and oxygen challenge index (P < 0.05); (3) the area under the receiver operating characteristic curve (ROC) for detecting the lower ScvO2 values was 0.621, 0.560, 0.589, 0.721 and 0.763 respectively according to baseline PtcO2, PtcO2 index, tissue oxygen index, 10 min OCT value and oxygen challenge index. The cutoff of 10 min OCT value was ≤ 57 mm Hg (1 mm Hg = 0.133 kPa) for detecting ScvO2 values under 70%, resulting in a sensitivity of 51.9% and a specificity of 95.5%. CONCLUSION: OCT may improve the diagnostic accuracy of PtcO2 in assessing the low ScvO2 values in septic shock patients after resuscitation.

[Stroke volume variation in the evaluation of fluid responsiveness in refractory septic shock].

OBJECTIVE: To evaluate fluid responsiveness by stroke volume variation(SVV) in mechanically ventilated patients with refractory septic shock. METHODS: Forty-two refractory septic shock patients were enrolled in the study. According to the responsiveness of fluid loading, the patients were divided into responsive group and non-responsive group. The SVV values of two groups were retrospectively analyzed. The receiver operating characteristic curve was drafted to determine the cut-off value of SVV for predicting fluid responsiveness. RESULTS: Among the 42 refractory septic shock patients, 24 were found responsive to fluid loading, 18 were not; before the fluid loading, central venous pressure, heart rate, mean arterial pressure and global end-diastolic volume index in the both groups showed no significant differences whereas the SVV in the responsive group was much higher than that in the nonresponsive group (P=0.006). Using SVV≥12% as the threshold to predict fluid responsiveness, the sensitivity was 77%, specificity was 85%. CONCLUSION: SVV can accurately predict fluid responsiveness in refractory septic shock patients.

Progress of mechanical power in the intensive care unit.

Mechanical power of ventilation, currently defined as the energy delivered from the ventilator to the respiratory system over a period of time, has been recognized as a promising indicator to evaluate ventilator-induced lung injury and predict the prognosis of ventilated critically ill patients. Mechanical power can be accurately measured by the geometric method, while simplified equations allow an easy estimation of mechanical power at the bedside. There may exist a safety threshold of mechanical power above which lung injury is inevitable, and the assessment of mechanical power might be helpful to determine whether the extracorporeal respiratory support is needed in patients with acute respiratory distress syndrome. It should be noted that relatively low mechanical power does not exclude the possibility of lung injury. Lung size and inhomogeneity should also be taken into consideration. Problems regarding the safety limits of mechanical power and contribution of each component to lung injury have not been determined yet. Whether mechanical power-directed lung-protective ventilation strategy could improve clinical outcomes also needs further investigation. Therefore, this review discusses the algorithms, clinical relevance, optimization, and future directions of mechanical power in critically ill patients.

Ursodeoxycholic Acid (UDCA) Promotes Lactate Metabolism in Mouse Hepatocytes through Cholic Acid (CA) - Farnesoid X Receptor (FXR) Pathway.

BACKGROUND: Persistent hyperlactatemia is associated with greater mortality in shock. Liver is the main site of lactate metabolism. METHOD: In the first part, freshly isolated hepatocytes were incubated in 10% fetal bovine serum William's E medium supplemented with 10 mM lactate. Cells were then exposed to 100 µM ursodeoxycholic acid (UDCA), with no addition (control) for 2, 4, 6, 8 h. In the second part, hepatocytes were treated with Silencer select siRNA targeting FXR or scramble siRNA. The siRNA treatment was repeated twenty four hours later, and the cells were used in the experiments twenty-four hours after the second treatment. Then hepatocytes were incubated in 10% fetal bovine serum William's E medium supplemented with 10 mM lactate. Cells were then exposed to 100 µM UDCA for 2, 4, 6, 8 h. Lactate concentration was determined by ABL80 automatic blood gas analyzer. RESULTS: UDCA increased ability of hepatocytes to remove lactate. After the knockdown of FXR, effects caused by UDCA were weakened. CONCLUSION: These results demonstrate that UDCA promotes lactate metabolism in mouse hepatocytes through CA-FXR pathway.

Effect of mean arterial pressure change by norepinephrine on peripheral perfusion index in septic shock patients after early resuscitation.

BACKGROUND: The peripheral perfusion index (PI), as a real-time bedside indicator of peripheral tissue perfusion, may be useful for determining mean arterial pressure (MAP) after early resuscitation of septic shock patients. The aim of this study was to explore the response of PI to norepinephrine (NE)-induced changes in MAP. METHODS: Twenty septic shock patients with pulse-induced contour cardiac output catheter, who had usual MAP under NE infusion after early resuscitation, were enrolled in this prospective, open-label study. Three MAP levels (usual MAP -10 mmHg, usual MAP, and usual MAP +10 mmHg) were obtained by NE titration, and the corresponding global hemodynamic parameters and PI were recorded. The general linear model with repeated measures was used for analysis of variance of related parameters at three MAP levels. RESULTS: With increasing NE infusion, significant changes were found in MAP (F = 502.46, P < 0.001) and central venous pressure (F = 27.45, P < 0.001) during NE titration. However, there was not a significant and consistent change in continuous cardiac output (CO) (F = 0.41, P = 0.720) and PI (F = 0.73, P = 0.482) at different MAP levels. Of the 20 patients enrolled, seven reached the maximum PI value at usual MAP -10 mmHg, three reached the maximum PI value at usual MAP, and ten reached the maximum PI value at usual MAP +10 mmHg. The change in PI was not significantly correlated with the change in CO (r = 0.260, P = 0.269) from usual MAP -10 mmHg to usual MAP. There was also no significant correlation between the change in PI and change in CO (r = 0.084, P = 0.726) from usual MAP to usual MAP +10 mmHg. CONCLUSIONS: Differing MAP levels by NE infusion induced diverse PI responses in septic shock patients, and these PI responses may be independent of the change in CO. PI may have potential applications for MAP optimization based on changes in peripheral tissue perfusion.