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Background: In patients on mechanical ventilation, positive end-expiratory pressure (PEEP) can decrease cardiac output through a decrease in cardiac preload and/or an increase in right ventricular afterload. Increase in central blood volume by fluid administration or passive leg raising (PLR) may reverse these phenomena through an increase in cardiac preload and/or a reopening of closed lung microvessels. We hypothesized that a transient decrease in PEEP (PEEP-test) may be used as a test to detect volume responsiveness., Methods: Mechanically ventilated patients with PEEP ≥ 10 cmH 2 O ("high level") and without spontaneous breathing were prospectively included. Volume responsiveness was assessed by a positive PLR-test, defined as an increase in pulse-contour-derived cardiac index (CI) during PLR ≥ 10%. The PEEP-test consisted in reducing PEEP from the high level to 5 cmH 2 O for one minute. Pulse-contour-derived CI (PiCCO2) was monitored during PLR and the PEEP-test., Results: We enrolled 64 patients among whom 31 were volume responsive. The median increase in CI during PLR was 14% (11-16%). The median PEEP at baseline was 12 (10-15) cmH 2 O and the PEEP-test resulted in a median decrease in PEEP of 7 (5-10) cmH 2 O, without difference between volume responsive and unresponsive patients. Among volume responsive patients, the PEEP-test induced a significant increase in CI of 16% (12-20%) (from 2.4 ± 0.7 to 2.9 ± 0.9 L/min/m 2 , p < 0.0001) in comparison with volume unresponsive patients. In volume unresponsive patients, PLR and the PEEP-test increased CI by 2% (1-5%) and 6% (3-8%), respectively. Volume responsiveness was predicted by an increase in CI > 8.6% during the PEEP-test with a sensitivity of 96.8% (95% confidence interval (95%CI): 83.3-99.9%) and a specificity of 84.9% (95%CI 68.1-94.9%). The area under the receiver operating characteristic curve of the PEEP-test for detecting volume responsiveness was 0.94 (95%CI 0.85-0.98) (p < 0.0001 vs. 0.5). Spearman's correlation coefficient between the changes in CI induced by PLR and the PEEP-test was 0.76 (95%CI 0.63-0.85, p < 0.0001)., Conclusions: A CI increase > 8.6% during a PEEP-test, which consists in reducing PEEP to 5 cmH 2 O, reliably detects volume responsiveness in mechanically ventilated patients with a PEEP ≥ 10 cmH 2 O. Trial registration ClinicalTrial.gov (NCT 04,023,786). Registered July 18, 2019. Ethics Committee approval CPP Est III (N° 2018-A01599-46)., (© 2023. The Author(s).)

Purpose: In the absence of recent international recommendations supported by scientific societies like Anesthesiology or Intensive Care Medicine, healthcare professionals (HCP) knowledge on IV fluid is expected to vary. We undertook a cross-sectional survey, aiming to assess prescription patterns and test the knowledge of HCP for IV fluid use in the operating room (OR) and intensive care unit (ICU)., Methods: An online international cross-sectional survey was conducted between October 20, 2019, and November 27, 2021. The survey included multiple-choice questions on demographics, practice patterns and knowledge of IV fluids, and a hemodynamically unstable patient assessment., Results: 1045 HCP, from 97 countries responded to the survey. Nearly three-quarters reported the non-existence of internal hospital or ICU-based guidelines on IV fluids. The respondents' mean score on the knowledge assessment questions was 46.4 ± 14.4. The cumulative mean scores were significantly higher among those supervising trainees (p = 0.02), specialists (p < 0.001) and those working in high-income (p < 0.001) countries. Overall performance of respondents on the knowledge testing for IV fluid was unsatisfactory with only 6.5% respondents performed above average., Conclusion: There is a wide difference in the knowledge and prescription of IV fluids among the HCP surveyed. These findings reflect the urgent need for education on IV fluids., Competing Interests: Declaration of Competing Interest PN reports speaker honorarium from Tabuk Pharmaceuticals, PeerVoice and Edward Lifesciences. PWGE, AW, XM, NVR, and MLNGM are member of the Executive Committee of International Fluid Academy (IFA). NVR reports speaker's fees from Baxter Belgium and served advisory board on fluid therapy organized by Baxter (2017). MLNGM is member of the medical advisory Board of Pulsion Medical Systems (part of Getinge group), Potrero Medical and Serenno Medical, consults for Baxter, BD, BBraun, ConvaTec, Spiegelberg, and Holtech Medical, and received speaker's fees from PeerVoice. NVR and MLNGM are co-founders and chairs of IFA, which is integrated within the not-for-profit charitable organization iMERiT (International Medical Education and Research Initiative) under the Belgian law and promotes education on fluid management and hemodynamic monitoring that received sponsoring from the industry. All other authors declare no competing interest in relation to the contents of this manuscript., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Pulse pressure variation (PPV) is not reliable in predicting preload responsiveness in patients receiving mechanical with spontaneous breathing (SB) activity. We hypothesised that an increase in PPV after a tidal volume (V T ) challenge (TVC) or a decrease in PPV during passive leg raising (PLR) can predict preload responsiveness in such cases., Methods: This prospective observational study was performed in two ICUs and included patients receiving mechanical ventilation with SB, for whom the treating physician decided to test preload responsiveness. Transthoracic echocardiography was used to measure the velocity-time integral (VTI) of the left ventricular outflow tract. Patients exhibiting an increase in VTI ≥12% during PLR were defined as PLR+ patients (or preload responders). Then, a TVC was performed by increasing V T by 2 ml kg -1 predicted body weight (PBW) for 1 min. PPV was recorded at each step., Results: Fifty-four patients (Simplified Acute Physiology Score II: 60 (25) ventilated with a V T of 6.5 (0.8) ml kg -1 PBW, were included. Twenty-two patients were PLR+. The absolute decrease in PPV during PLR and the absolute increase in PPV during TVC discriminated between PLR+ and PLR- patients with area under the receiver operating characteristic (AUROC) curve of 0.78 and 0.73, respectively, and cut-off values of -1% and +2%, respectively. Those AUROC curve values were similar but were significantly different from that of baseline PPV (0.61)., Conclusion: In patients undergoing mechanical ventilation with SB activity, PPV does not predict preload responsiveness. However, the decrease in PPV during PLR and the increase in PPV during a TVC help discriminate preload responders from non-responders with moderate accuracy., Clinical Trial Registration: NCT04369027 (ClinicalTrials.gov)., Competing Interests: Declarations of interest OH is a member of the medical advisory board of AMOMED. J-LT and XM are members of the medical advisory board of Pulsion/Getinge., (Copyright © 2021 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.)

Objectives: To evaluate the preload dependence of femoral maximal change in pressure over time (dP/dtmax) during volume expansion in preload dependent and independent critically ill patients., Design: Retrospective database analysis., Setting: Two adult polyvalent ICUs., Patients: Twenty-five critically ill patients with acute circulatory failure., Interventions: Thirty-five fluid infusions of 500 mL normal saline., Measurements and Main Results: Changes in femoral dP/dtmax, systolic, diastolic, and pulse femoral arterial pressure were obtained from the pressure waveform analysis using the PiCCO2 system (Pulsion Medical Systems, Feldkirchen, Germany). Stroke volume index was obtained by transpulmonary thermodilution. Statistical analysis was performed comparing results before and after volume expansion and according to the presence or absence of preload dependence (increases in stroke volume index ≥ 15%). Femoral dP/dtmax increased by 46% after fluid infusion in preload-dependent cases (mean change = 510.6 mm Hg·s; p = 0.005) and remained stable in preload-independent ones (mean change = 49.2 mm Hg·s; p = 0.114). Fluid-induced changes in femoral dP/dtmax correlated with fluid-induced changes in stroke volume index in preload-dependent cases (r = 0.618; p = 0.032), but not in preload-independent ones. Femoral dP/dtmax strongly correlated with pulse and systolic arterial pressures and with total arterial stiffness, regardless of the preload dependence status (r > 0.9 and p < 0.001 in all cases)., Conclusions: Femoral dP/dtmax increased with volume expansion in case of preload dependence but not in case of preload independence and was strongly related to pulse pressure and total arterial stiffness regardless of preload dependence status. Therefore, femoral dP/dtmax is not a load-independent marker of left ventricular contractility and should be not used to track contractility in critically ill patients.

Purpose of Review: On the basis of recent literature, we summarized the new advances on the use of available dynamic indices of fluid responsiveness., Recent Findings: Reliability of passive leg raising to assess fluid responsiveness is well established provided that a real-time haemodynamic assessment is available. Recent studies have focused on totally noninvasive techniques to assess its haemodynamic effects with promising results. Presence of intra-abdominal hypertension is associated with false-negative cases of passive leg raising. Use of pulse pressure and stroke volume variations is limited and other heart-lung interaction tests have been developed. The tidal volume challenge may overcome the limitation of low tidal volume ventilation. Preliminary data suggest that changes in pulse pressure variation during this test well predict fluid responsiveness. Growing evidence confirms the good predictive performance of the end-expiratory occlusion test. All these dynamic tests allow selecting appropriate fluid responders and preventing excessive fluid administration. Performance of a mini-fluid challenge may help for the decision-making process of fluid management if other tests are not available., Summary: Several new dynamic variables and monitoring techniques to predict fluid responsiveness were investigated in the past years. Nevertheless, further research investigating their reliability and feasibility in larger cohorts is warranted. VIDEO ABSTRACT.

Background: The end-expiratory occlusion test predicts fluid responsiveness in ventilated intensive care patients; however, its utility in the operating room is questioned. We assessed end-expiratory occlusion test in laparotomic surgery for predicting volume expansion., Methods: Forty-six patients were included in this study: stage 1 (n = 26) with an end-expiratory occlusion test of 15 seconds, followed by volume expansion, which consisted of 250 mL of colloid over 5 minutes and stage 2 (n = 20) with an end-expiratory occlusion test of 25 seconds followed by volume expansion. The last 10 patients had transdiaphragmatic pressures probed. Patients with an increase in cardiac index >15% after volume expansion were responders. Pulse pressure variation, stroke volume (SV) index, and cardiac index were analyzed. Receiver operating characteristic curves were established for changes in SV and pulse pressure induced by end-expiratory occlusion test and pulse pressure variation using the responders status for volume expansion as outcome., Results: A total of 44 (38%) volume expansions were deemed responders. After end-expiratory occlusion test of 15 seconds, no hemodynamic variables were significantly increased. After end-expiratory occlusion test of 25 seconds, SV index increased in responders (37.1 ± 8.8 mL/m after end-expiratory occlusion test of 25 seconds versus 35.7 ± 8.6 before; P < .0001). End-expiratory occlusion test could not discriminate responders from nonresponders. Only pulse pressure variation had significantly different area under the curve from that expected by chance (0.7 [0.57-0.81]; P = .002 for end-expiratory occlusion test of 15 seconds; and 0.78 [0.64-0.89]; P = .0001 for end-expiratory occlusion test of 25 seconds). After laparotomy, gastric pressure decreased significantly (4 [2.75-5] vs 2 [2-4] cm H2O; P = .0417); no difference was noticed in the transdiaphragmatic gradient., Conclusions: End-expiratory occlusion test was not reliable to discriminate responders from nonresponders after volume expansion during laparotomic surgery.

Objectives: To assess whether, in patients under mechanical ventilation, fluid responsiveness is predicted by the effects of short respiratory holds on cardiac index estimated by esophageal Doppler., Design: Prospective, monocentric study., Setting: Medical ICU., Patients: Twenty-eight adult patients with acute circulatory failure and a decision of the clinicians in charge to administer fluids., Interventions: Before and after infusing 500 mL of saline, we measured cardiac index estimated by esophageal Doppler before and during the last 5 seconds of successive 15-second end-inspiratory occlusion and end-expiratory occlusion, separated by 1 minute. Patients in whom volume expansion increased cardiac index measured by transpulmonary thermodilution greater than or equal to 15% were defined as "fluid responders." Cardiac index measured by the Pulse Contour Cardiac Output device (from pulse contour analysis or transpulmonary thermodilution) was used as the reference., Measurements and Main Results: End-expiratory occlusion increased cardiac index estimated by esophageal Doppler more in responders than in nonresponders (8% ± 2% vs 3% ± 1%, respectively; p < 0.0001) and end-inspiratory occlusion decreased cardiac index estimated by esophageal Doppler more in responders than in nonresponders (-8% ± 5% vs -4% ± 2%, respectively; p = 0.0002). Fluid responsiveness was predicted by the end-expiratory occlusion induced percent change in cardiac index estimated by esophageal Doppler with an area under the receiver operating characteristic curve of 1.00 (95% CI, 0.88-1.00) and a threshold value of 4% increase in cardiac index estimated by esophageal Doppler. It was predicted by the sum of absolute values of percent changes in cardiac index estimated by esophageal Doppler during both occlusions with a similar area under the receiver operating characteristic curve (0.99 [0.86-1.00]) and with a threshold of 9% change in cardiac index estimated by esophageal Doppler, which is compatible with the esophageal Doppler precision., Conclusions: If the absolute sum of the percent change in cardiac index estimated by esophageal Doppler induced by two successive end-inspiratory occlusion and end-expiratory occlusion maneuvers is greater than 9%, it is likely that a 500 mL fluid infusion will increase cardiac output. This diagnostic threshold is higher than if only end-expiratory occlusion induced percent changes in cardiac index estimated by esophageal Doppler are taken into account.

Background: The accuracy of respiratory variation of the inferior vena cava (rvIVC) in predicting fluid responsiveness, particularly in spontaneously breathing patients is unclear., Objectives: To consider the evidence to support the accuracy of rvIVC in identifying patients who are unlikely to benefit from fluid administration., Design: Systematic review and meta-analysis., Data Source: We searched MEDLINE, EMBASE, Cochrane Library, KoreaMed, LILCAS and WHO Clinical Trial Registry from inception to June 2017., Eligibility Criteria: Case-control or cohort studies that evaluated the accuracy of rvIVC in living adult humans were included. A study was included in the meta-analysis if data enabling construction of 2 × 2 tables were reported, calculated or could be obtained from authors and met the above cited criteria., Result: A total of 23 studies including 1574 patients were included in qualitative analysis. The meta-analysis involved 20 studies and 761 patients. Pooled sensitivity and specificity of rvIVC in 330 spontaneously breathing patients were 0.80 [95% confidence interval (CI) 0.68 to 0.89] and 0.79 (95% CI 0.60 to 0.90). Pooled sensitivity and specificity of rvIVC in 431 mechanically ventilated patients were 0.79 (95% CI 0.67 to 0.86) and 0.70 (95% CI 0.63 to 0.76)., Conclusion: Decreased inferior vena caval respiratory variation is moderately accurate in predicting fluid unresponsiveness both in spontaneous and mechanically ventilated patients. The findings of this review should be used in the appropriate clinical context and in conjunction with other clinical assessments of fluid status., Identifier: CRD 42017068028.

The prognosis of septic shock is tightly linked to the earliness of both appropriate antibiotic therapy and early hemodynamic resuscitation. This latter is essentially based on fluid and vasopressors administration. The step-by-step strategy, called "early goal-directed therapy" (EGDT) developed in 2001 and endorsed by the Surviving Sepsis Campaign (SSC) between 2004 and 2016 is no longer recommended. Indeed, recent multicenter randomized clinical trials showed no reduction in all-cause mortality, duration of organ support and in-hospital length of stay with EGDT in comparison with standard care. The most recent SCC guidelines have dropped the original EGDT by deleting the central venous pressure and the central venous oxygen saturation from the recommendations. Dynamic variables of fluid responsiveness are now recommended to be used after an initial fluid infusion of a fixed volume (30 mL/kg) during the first three hours of resuscitation. However, this approach is also questionable due to the lack of individualization at the early and crucial phase of resuscitation. In this review, we propose a more personalized approach for the early and later phases of fluid resuscitation during sepsis.

Purpose of Review: In the field of prediction of fluid responsiveness, the most recent studies have focused on validating new tests, on clarifying the limitations of older ones, and better defining their modalities., Recent Findings: The limitations of pulse pressure/stroke volume variations are numerous, but recent efforts have been made to overcome these limitations, like in case of low tidal volume ventilation. Following pulse pressure/stroke volume variations, new tests have emerged which assess preload responsiveness by challenging cardiac preload through heart-lung interactions, like during recruitment manoeuvres and end-expiratory/inspiratory occlusions. Given the risk of fluid overload that is inherent to the 'classical' fluid challenge, a 'mini' fluid challenge, made of 100 ml of fluid only, has been developed and investigated in recent studies. The reliability of the passive leg raising test is now well established and the newest publications have mainly aimed at defining several noninvasive estimates of cardiac output that can be monitored to assess its effects., Summary: Research in this field is still very active, such that several indices and tests of fluid responsiveness are now available. They may contribute to reduce excessive fluid balance by avoiding unnecessary fluid administration and, also, by ensuring safe fluid removal.

Objectives: First, we aimed at assessing whether fluid responsiveness is predicted by the effects of an end-expiratory occlusion on the velocity-time integral of the left ventricular outflow tract. Second, we investigated whether adding the effects of an end-inspiratory occlusion and of an end-expiratory occlusion on velocity-time integral can predict fluid responsiveness with similar reliability than end-expiratory occlusion alone but with a higher threshold, which might be more compatible with the precision of echocardiography., Design: Diagnostic study., Setting: Medical ICU., Patients: Thirty mechanically ventilated patients in whom fluid administration was planned., Interventions: A 15-second end-expiratory occlusion and end-inspiratory occlusion, separated by 1 minute, followed by a 500-mL saline administration., Measurements and Main Results: Pulse contour analysis-derived cardiac index and velocity-time integral were measured during the last 5 seconds of 15-second end-inspiratory occlusion and end-expiratory occlusion and after fluid administration. End-expiratory occlusion increased velocity-time integral more in responders than in nonresponders to fluid administration (11% ± 5% vs 3% ± 1%, respectively; p < 0.0001), and end-inspiratory occlusion decreased velocity-time integral more in responders than in nonresponders (12% ± 5% vs 5% ± 2%, respectively; p = 0.0002). When adding the absolute values of changes in velocity-time integral observed during both occlusions, velocity-time integral changed by 23% ± 9% in responders and by 8% ± 3% in nonresponders. Fluid responsiveness was predicted by the end-expiratory occlusion-induced change in velocity-time integral with an area under the receiver operating characteristic curve of 0.938 (0.785-0.989) and a threshold value of 5%. Fluid responsiveness was predicted by the sum of absolute values of changes in velocity-time integral during both occlusions with a similar reliability (area under the receiver operating characteristic curve = 0.973 [0.838-1.000]) but with a threshold of 13%. Both sensitivity and specificity were 93% (68-100%)., Conclusions: If consecutive end-inspiratory occlusion and end-expiratory occlusion change velocity-time integral is greater than or equal to 13% in total, fluid responsiveness is accurately predicted. This threshold is more compatible with the precision of echocardiography than that obtained by end-expiratory occlusion alone.

Objectives: Stroke volume variation and pulse pressure variation do not reliably predict fluid responsiveness during low tidal volume ventilation. We hypothesized that with transient increase in tidal volume from 6 to 8 mL/kg predicted body weight, that is, "tidal volume challenge," the changes in pulse pressure variation and stroke volume variation will predict fluid responsiveness., Design: Prospective, single-arm study., Setting: Medical-surgical ICU in a university hospital., Patients: Adult patients with acute circulatory failure, having continuous cardiac output monitoring, and receiving controlled low tidal volume ventilation., Interventions: The pulse pressure variation, stroke volume variation, and cardiac index were recorded at tidal volume 6 mL/kg predicted body weight and 1 minute after the "tidal volume challenge." The tidal volume was reduced back to 6 mL/kg predicted body weight, and a fluid bolus was given to identify fluid responders (increase in cardiac index > 15%). The end-expiratory occlusion test was performed at tidal volumes 6 and 8 mL/kg predicted body weight and after reducing tidal volume back to 6 mL/kg predicted body weight., Results: Thirty measurements were obtained in 20 patients. The absolute change in pulse pressure variation and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight predicted fluid responsiveness with areas under the receiver operating characteristic curves (with 95% CIs) being 0.99 (0.98-1.00) and 0.97 (0.92-1.00), respectively. The best cutoff values of the absolute change in pulse pressure variation and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight were 3.5% and 2.5%, respectively. The pulse pressure variation, stroke volume variation, central venous pressure, and end-expiratory occlusion test obtained during tidal volume 6 mL/kg predicted body weight did not predict fluid responsiveness., Conclusions: The changes in pulse pressure variation or stroke volume variation obtained by transiently increasing tidal volume (tidal volume challenge) are superior to pulse pressure variation and stroke volume variation in predicting fluid responsiveness during low tidal volume ventilation.

Purpose: We performed a systematic review and meta-analysis of studies investigating the passive leg raising (PLR)-induced changes in cardiac output (CO) and in arterial pulse pressure (PP) as predictors of fluid responsiveness in adults., Methods: MEDLINE, EMBASE and Cochrane Database were screened for relevant original and review articles. The meta-analysis determined the pooled area under the ROC curve, the sensitivity, specificity and threshold for the PLR test when assessed with CO and PP., Results: Twenty-one studies (991 adult patients, 995 fluid challenges) were included. CO was measured by echocardiography in six studies, calibrated pulse contour analysis in six studies, bioreactance in four studies, oesophageal Doppler in three studies, transpulmonary thermodilution or pulmonary artery catheter in one study and suprasternal Doppler in one study. The pooled correlation between the PLR-induced and the fluid-induced changes in CO was 0.76 (0.73-0.80). For the PLR-induced changes in CO, the pooled sensitivity was 0.85 (0.81-0.88) and the pooled specificity was 0.91 (0.88-0.93). The area under the ROC curve was 0.95 ± 0.01. The best threshold was a PLR-induced increase in CO ≥10 ± 2 %. For the PLR-induced changes in PP (8 studies, 432 fluid challenges), the pooled sensitivity was 0.56 (0.49-0.53), the pooled specificity was 0.83 (0.77-0.88) and the pooled area under the ROC curve was 0.77 ± 0.05. Sensitivity and subgroup analysis were consistent with the primary analysis., Conclusions: PLR-induced changes in CO very reliably predict the response of CO to volume expansion in adults with acute circulatory failure. When PLR effects are assessed by changes in PP, the specificity of the PLR test remains acceptable but its sensitivity is poor.

Introduction: The aim of this study was to assess how mean systemic pressure (Psm) and resistance to venous return (Rvr) behave during passive leg raising (PLR) in cases of fluid responsiveness and fluid unresponsiveness., Method: In 30 patients with an acute circulatory failure, in order to estimate the venous return curve, we constructed the regression line between pairs of cardiac index (CI) and central venous pressure (CVP). Values were measured during end-inspiratory and end-expiratory ventilatory occlusions performed at two levels of positive end-expiratory pressure. The x-axis intercept was used to estimate Psm and the inverse of the slope to quantify Rvr. These measurements were obtained at baseline, during PLR and after fluid infusion. Patients in whom fluid infusion increased CI by more than 15 % were defined as "fluid-responders"., Results: In fluid-responders (n = 15), CVP and Psm significantly increased (from 7 ± 3 to 9 ± 4 mmHg and from 25 ± 13 to 31 ± 13 mmHg, respectively) during PLR. The Psm-CVP gradient significantly increased by 20 ± 30 % while Rvr did not change significantly during PLR. In fluid-nonresponders, CVP and Psm increased significantly but the Psm-CVP gradient did not change significantly during PLR. PLR did not change the intra-abdominal pressure in the whole population (14 ± 6 mmHg before vs. 13 ± 5 mmHg during PLR, p = 0.26) and in patients with intra-abdominal hypertension at baseline (17 ± 4 mmHg before vs. 16 ± 4 mmHg during PLR, p = 0.14). In the latter group, PLR increased Psm from 22 ± 11 to 27 ± 10 mmHg (p <0.01) and did not change Rvr (5.1 ± 2.6 to 5.2 ± 3 mmHg/min/m(2)/mL, p = 0.71). In fluid-responders, Psm, CVP and the Psm-CVP gradient significantly increased during fluid infusion while the Rvr did not change. In fluid-nonresponders, CVP and Psm increased significantly during fluid infusion while the Psm-CVP gradient and Rvr did not change., Conclusion: PLR significantly increased Psm without modifying Rvr. This was also the case in patients with intra-abdominal hypertension. In case of fluid responsiveness, PLR increased venous return by increasing Psm to a larger extent than CVP. In patients with fluid unresponsiveness, PLR increased Psm but did not change the Psm-CVP gradient. Fluid infusion induced similar effects on Psm and Rvr.

Fluid therapy is still the mainstay of acute care in patients with shock or cardiovascular compromise. However, our understanding of the critically ill pathophysiology has evolved significantly in recent years. The revelation of the glycocalyx layer and subsequent research has redefined the basics of fluids behavior in the circulation. Using less invasive hemodynamic monitoring tools enables us to assess the cardiovascular function in a dynamic perspective. This allows pinpointing even distinct changes induced by treatment, by postural changes, or by interorgan interactions in real time and enables individualized patient management. Regarding fluids as drugs of any other kind led to the need for precise indication, way of administration, and also assessment of side effects. We possess now the evidence that patient centered outcomes may be altered when incorrect time, dose, or type of fluids are administered. In this review, three major features of fluid therapy are discussed: the prediction of fluid responsiveness, potential harms induced by overzealous fluid administration, and finally the problem of protocol-led treatments and their timing.

Objectives: During circulatory failure, the ultimate goal of treatments that increase cardiac output is to reduce tissue hypoxia. This can only occur if oxygen consumption depends on oxygen delivery. We compared the ability of central venous oxygen saturation and markers of anaerobic metabolism to predict whether a fluid-induced increase in oxygen delivery results in an increase in oxygen consumption., Design: Prospective study., Setting: ICU., Patients: Fifty-one patients with an acute circulatory failure (78% of septic origin)., Measurements: Before and after a volume expansion (500 mL of saline), we measured cardiac index, o2- and Co2-derived variables and lactate., Main Results: Volume expansion increased cardiac index ≥ 15% in 49% of patients ("volume-responders"). Oxygen delivery significantly increased in these 25 patients (+32% ± 16%, p < 0.0001). An increase in oxygen consumption ≥ 15% concomitantly occurred in 56% of these 25 volume-responders (+38% ± 28%). Compared with the volume-responders in whom oxygen consumption did not increase, the volume-responders in whom oxygen consumption increased ≥ 15% were characterized by a higher lactate (2.3 ± 1.1 mmol/L vs. 5.5 ± 4.0 mmol/L, respectively) and a higher ratio of the veno-arterial carbon dioxide tension difference (P(v - a)Co2) over the arteriovenous oxygen content difference (C(a - v)o2). A fluid-induced increase in oxygen consumption greater than or equal to 15% was not predicted by baseline central venous oxygen saturation but by high baseline lactate and (P(v - a)Co2/C(a - v)o2 ratio (areas under the receiving operating characteristics curves: 0.68 ± 0.11, 0.94 ± 0.05, and 0.91 ± 0.06). In volume-nonresponders, volume expansion did not significantly change cardiac index, but the oxygen delivery decreased due to a hemodilution-induced decrease in hematocrit., Conclusions: In volume-responders, unlike markers of anaerobic metabolism, central venous oxygen saturation did not allow the prediction of whether a fluid-induced increase in oxygen delivery would result in an increase in oxygen consumption. This suggests that along with indicators of volume-responsiveness, the indicators of anaerobic metabolism should be considered instead of central venous oxygen saturation for starting hemodynamic resuscitation.

Fluid therapy represents, most of the time, the first-line treatment of circulatory failure in critically ill patients. However, after initial resuscitation, fluid administration can be deleterious in patients with sepsis and/or acute respiratory distress syndrome. In this context, several tests have been developed to predict fluid responsiveness and fluid unresponsiveness to identify patients who can be eligible for fluid therapy (fluid respondents) and those who cannot benefit from volume expansion (fluid non-respondents) and in whom fluid loading can even be deleterious. For this purpose, 'static' markers of cardiac preload have been used for many years. However, a large number of studies clearly showed that neither pressure nor volume markers of cardiac preload could predict fluid responsiveness. This is the reason why a 'dynamic approach' has been developed to assess preload responsiveness. The respiratory variation of arterial pulse pressure and of other surrogates of stroke volume has been used first for this purpose and has received a large amount of evidence. However, such indices suffer from several limitations. In such instances, alternative methods such as passive leg raising, end-expiratory occlusion test or 'mini' fluid challenge have been developed., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: In patients receiving an infusion of norepinephrine, the relationship between the amplitude of the oximeter plethysmographic waveform and stroke volume may be variable and quality of the waveform might be reduced, compared with patients not receiving norepinephrine. We assessed the reliability of the pleth variability index (PVI), an automatic measurement of the respiratory variation of the plethysmographic waveform, for predicting fluid responsiveness in patients receiving norepinephrine infusions., Methods: We measured the response of cardiac index (transpulmonary thermodilution) to i.v. fluid administration in 42 critically ill patients receiving norepinephrine. Patients with arrhythmias, spontaneous breathing, tidal volume <8 ml kg(-1), and respiratory system compliance <30 ml cm H(2)O(-1) were excluded. Before fluid administration, we recorded the arterial pulse pressure variation (PPV) and pulse contour analysis-derived stroke volume variation (SVV, PiCCO2) and PVI (Masimo Radical-7)., Results: In seven patients, the plethysmographic signal could not be obtained. Among the 35 remaining patients [mean SAPS II score=77 (sd=17)], i.v. fluid increased cardiac index ≥15% in 15 'responders'. A baseline PVI ≥16% predicted fluid responsiveness with a sensitivity of 47 (inter-quartile range=21-73)% and a specificity of 90 (68-99)%. The area under the receiver operating characteristic curve was significantly lower for PVI [0.68 (0.09)] than for PPV and SVV [0.93 (0.06) and 0.89 (0.07), respectively]. Considering all pairs of measurements, PVI was correlated with PPV (r(2)=0.27). The fluid-induced changes in PVI and PPV were not significantly correlated., Conclusions: PVI was less reliable than PPV and SVV for predicting fluid responsiveness in critically ill patients receiving norepinephrine. In addition, PVI could not be measured in a significant proportion of patients. This suggests that PVI is not useful in patients receiving norepinephrine.

Introduction: The Nexfin device estimates arterial pressure by the volume clamp method through a finger pneumatic cuff. It also allows to estimate cardiac index (CInoninv) by pulse contour analysis of the non-invasive arterial pressure curve. We evaluated the ability of the device to track changes in cardiac index induced by a fluid challenge., Methods: We included 45 patients for whom a volume expansion (500 mL of saline infused over 30 min) was planned. The volume expansion-induced changes in cardiac index measured by transpulmonary thermodilution (CIinv, PiCCO device) and in CInoninv were recorded., Results: In seven patients, the Nexfin could not record the arterial curve due to finger hypoperfusion. Considering both the values obtained before and after volume expansion (n = 76 pairs of measurements), the bias (lower and upper limits of agreement) between CIinv and CInoninv was 0.2 (-1.8 to 2.2) L/min/m2. The mean change in CInoninv was 10 ± 11%. The percentage error of CInoninv was 57%. The correlation between the changes in CIinv and CInoninv observed during volume expansion was significant (P = 0.0002) with an r2 = 0.31., Conclusions: The estimation of CI by the Nexfin device in critically ill patients is not reliable, neither for estimating absolute values of CI nor for tracking its changes during volume expansion.

Background: We evaluated the ability of an infrared photoplethysmography arterial waveform (continuous non-invasive arterial pressure, CNAP) to estimate arterial pulse pressure variation (PPV). We compared the ability of non-invasive PPV to predict fluid responsiveness with invasive PPV, respiratory variation of pulse contour-derived stroke volume, and changes in cardiac index induced by passive leg raising (PLR) and end-expiratory occlusion (EEO) tests., Methods: We measured the responses of cardiac index (PiCCO) to 500 ml of saline in 47 critically ill patients with haemodynamic failure. Before fluid administration, we recorded non-invasive and invasive PPVs, stroke volume variation, and changes in cardiac index induced by PLR and by 15 s EEO. Logistic regressions were performed to investigate the advantage of combining invasive PPV, stroke volume variation, PLR, and EEO when predicting fluid responsiveness., Results: In eight patients, CNAP could not record arterial pressure. In the 39 remaining patients, fluid increased cardiac index by ≥15% in 17 'responders'. Considering the 195 pairs of measurements, the bias (sd) between invasive and non-invasive PPVs was -0.6 (2.3)%. The areas under the receiver operating characteristic (ROC) curves for predicting fluid responsiveness were 0.89 (95% confidence interval, 0.78-1.01) for non-invasive PPV compared with 0.89 (0.77-1.01), 0.84 (0.70-0.96), 0.95 (0.88-1.03), and 0.97 (0.91-1.03) for invasive pulse pressure, stroke volume variations, PLR, and EEO tests (no significant difference). Combining multiple tests did not significantly improve the area under the ROC curves., Conclusions: Non-invasive assessment of PPV seems valuable in predicting fluid responsiveness.

Objectives: We tested whether the poor ability of pulse pressure variation to predict fluid responsiveness in cases of acute respiratory distress syndrome was related to low lung compliance. We also tested whether the changes in cardiac index induced by passive leg-raising and by an end-expiratory occlusion test were better than pulse pressure variation at predicting fluid responsiveness in acute respiratory distress syndrome patients., Design: Prospective study., Setting: Medical intensive care unit., Patients: We included 54 patients with circulatory shock (63 ± 13 yrs; Simplified Acute Physiology Score II, 63 ± 24). Twenty-seven patients had acute respiratory distress syndrome (compliance of the respiratory system, 22 ± 3 mL/cm H2O). In nonacute respiratory distress syndrome patients, the compliance of the respiratory system was 45 ± 9 mL/cm H2O., Measurements and Main Results: We measured the response of cardiac index (transpulmonary thermodilution) to fluid administration (500 mL saline). Before fluid administration, we recorded pulse pressure variation and the changes in pulse contour analysis-derived cardiac index induced by passive leg-raising and end-expiratory occlusion. Fluid increased cardiac index ≥ 15% (44% ± 39%) in 30 "responders." Pulse pressure variation was significantly correlated with compliance of the respiratory system (r = .58), but not with tidal volume. The higher the compliance of the respiratory system, the better the prediction of fluid responsiveness by pulse pressure variation. A compliance of the respiratory system of 30 mL/cm H2O was the best cut-off for discriminating patients regarding the ability of pulse pressure variation to predict fluid responsiveness. If compliance of the respiratory system was >30 mL/cm H2O, then the area under the receiver-operating characteristics curve for predicting fluid responsiveness was not different for pulse pressure variation and the passive leg-raising and end-expiratory occlusion tests (0.98 ± 0.03, 0.91 ± 0.06, and 0.97 ± 0.03, respectively). By contrast, if compliance of the respiratory system was ≤ 30 mL/cm H2O, then the area under the receiver-operating characteristics curve was significantly lower for pulse pressure variation than for the passive leg-raising and end-expiratory occlusion tests (0.69 ± 0.10, 0.94 ± 0.05, and 0.93 ± 0.05, respectively)., Conclusions: The ability of pulse pressure variation to predict fluid responsiveness was inversely related to compliance of the respiratory system. If compliance of the respiratory system was ≤ 30 mL/cm H2O, then pulse pressure variation became less accurate for predicting fluid responsiveness. However, the passive leg-raising and end-expiratory occlusion tests remained valuable in such cases.

Purpose: To document the relationship between stroke volume (SV) and pulse pressure (PP) recorded at the femoral and aortic sites during volume expansion (VE) in patients in shock. We hypothesized that non-invasively estimated aortic PP would exhibit the same ability as PP recorded invasively at the femoral level to track SV changes., Methods: Included in this prospective study were 56 ICU patients needing VE. Femoral PP (indwelling catheter), aortic PP (tonometry) and cardiac output (thermodilution) were recorded before and after VE. Responders were defined as patients who showed an increase in SV of ≥15% after VE., Results: Of the 56 included patients in shock, 39 (age 57 ± 14 years, SAPS II 46 ± 18) completed the study. At both sites, PP increased after VE in responders (n=17, mean SV increase 30 ± 15%) but not in non-responders. In the overall population, there was a positive relationship between VE-induced changes in SV and in PP at the femoral (r=0.60, p<0.001) and aortic (r=0.52, p<0.001) sites. Increases in femoral PP of ≥9% indicated SV increases of ≥15% with 82% sensitivity and 95% specificity. Increases in aortic PP of ≥4.5% indicated SV increases of ≥15% with 76% sensitivity and 82% specificity. Areas under the ROC curves indicated that aortic PP was not different from femoral PP for tracking changes in SV., Conclusion: The ability of non-invasively estimated aortic PP to track fluid response was the same as that of invasively recorded femoral PP. This may have implications for non-invasive haemodynamic monitoring., (© Copyright jointly held by Springer and ESICM 2011)

Objective: During mechanical ventilation, inspiration cyclically decreases the left cardiac preload. Thus, an end-expiratory occlusion may prevent the cyclic impediment in left cardiac preload and may act like a fluid challenge. We tested whether this could serve as a functional test for fluid responsiveness in patients with circulatory failure., Design: Prospective study., Setting: Medical intensive care unit., Patients: Thirty-four mechanically ventilated patients with shock in whom volume expansion was planned., Intervention: A 15-second end-expiratory occlusion followed by a 500 mL saline infusion., Measurements: Arterial pressure and pulse contour-derived cardiac index (PiCCOplus) at baseline, during passive leg raising (PLR), during the 5-last seconds of the end-expiratory occlusion, and after volume expansion., Main Results: Volume expansion increased cardiac index by >15% (2.4 +/- 1.0 to 3.3 +/- 1.2 L/min/m, p < 0.05) in 23 patients ("responders"). Before volume expansion, the end-expiratory occlusion significantly increased arterial pulse pressure by 15% +/- 15% and cardiac index by 12% +/- 11% in responders whereas arterial pulse pressure and cardiac index did not change significantly in nonresponders. Fluid responsiveness was predicted by an increase in pulse pressure >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively. The response of pulse pressure and cardiac index to the end-expiratory occlusion predicted fluid responsiveness with an accuracy that was similar to the response of cardiac index to PLR and that was significantly better than the response of pulse pressure to PLR (receiver operating characteristic curves area 0.957 [95% confidence interval [CI:] 0.825-0.994], 0.972 [95% CI: 0.849-0.995], 0.937 [95% CI: 0.797-0.990], and 0.675 [95% CI: 0.497-0.829], respectively)., Conclusions: The hemodynamic response to an end-expiratory occlusion can predict volume responsiveness in mechanically ventilated patients.

Policies of fluid administration/restriction in critically ill patients have evolved over recent years. Abundant fluid resuscitation is encouraged during the early stage of severe sepsis. But a conservative fluid strategy is recommended in later stages, in particular when lungs are injured. Both strategies are risky if uncontrolled. Tests detecting volume unresponsiveness at any moment of fluid resuscitation or detecting volume unresponsiveness at any moment of fluid restriction would help to better assess the benefit/risk ratio of continuing such strategies. Measuring the short-term hemodynamic changes during passive leg raising can be reliably used for that purpose in both situations, even when patients are breathing spontaneously.

Objective: To assess whether the passive leg raising test can help in predicting fluid responsiveness., Design: Nonsystematic review of the literature., Results: Passive leg raising has been used as an endogenous fluid challenge and tested for predicting the hemodynamic response to fluid in patients with acute circulatory failure. This is now easy to perform at the bedside using methods that allow a real time measurement of systolic blood flow. A passive leg raising induced increase in descending aortic blood flow of at least 10% or in echocardiographic subaortic flow of at least 12% has been shown to predict fluid responsiveness. Importantly, this prediction remains very valuable in patients with cardiac arrhythmias or spontaneous breathing activity., Conclusions: Passive leg raising allows reliable prediction of fluid responsiveness even in patients with spontaneous breathing activity or arrhythmias. This test may come to be used increasingly at the bedside since it is easy to perform and effective, provided that its effects are assessed by a real-time measurement of cardiac output.

Purpose of Review: In the ICU only half of the patients are volume responsive - that is, they respond to fluid administration by increasing their cardiac output. We aim to summarize the methods available for predicting volume responsiveness, focusing on recent findings in patients with spontaneous breathing activity., Recent Findings: New information mainly comes from studies that have attempted to find accurate predictors of volume responsiveness in cases of spontaneous breathing activity when heart-lung interaction indices cannot be reliably used. Passive leg raising has emerged as a reliable test for this purpose. The hemodynamic response to this maneuver, which induces a transient increase in cardiac preload, has been shown to provide a robust prediction of volume responsiveness. Assessment of the effects of passive leg raising requires real-time measurement of cardiac output/stroke volume or their surrogates., Summary: Predicting the hemodynamic response to fluid administration in patients with acute circulatory failure is of major importance and numerous methods are now available. While the respiratory variations of stroke volume (or its surrogates) can be used in patients fully adapted to their ventilator, the passive leg-raising test has become a reliable predictive method in patients with spontaneous breathing activity.

Objective: In hemodynamically unstable patients with spontaneous breathing activity, predicting volume responsiveness is a difficult challenge since the respiratory variation in arterial pressure cannot be used. Our objective was to test whether volume responsiveness can be predicted by the response of stroke volume measured with transthoracic echocardiography to passive leg raising in patients with spontaneous breathing activity. We also examined whether common echocardiographic indices of cardiac filling status are valuable to predict volume responsiveness in this category of patients., Design and Setting: Prospective study in the medical intensive care unit of a university hospital., Patients: 24 patients with spontaneously breathing activity considered for volume expansion., Measurements: We measured the response of the echocardiographic stroke volume to passive leg raising and to saline infusion (500 ml over 15 min). The left ventricular end-diastolic area and the ratio of mitral inflow E wave velocity to early diastolic mitral annulus velocity (E/Ea) were also measured before and after saline infusion., Results: A passive leg raising induced increase in stroke volume of 12.5% or more predicted an increase in stroke volume of 15% or more after volume expansion with a sensitivity of 77% and a specificity of 100%. Neither left ventricular end-diastolic area nor E/Ea predicted volume responsiveness., Conclusions: In our critically ill patients with spontaneous breathing activity the response of echocardiographic stroke volume to passive leg raising was a good predictor of volume responsiveness. On the other hand, the common echocardiographic markers of cardiac filling status were not valuable for this purpose.

Objective: Passive leg raising (PLR) represents a "self-volume challenge" that could predict fluid response and might be useful when the respiratory variation of stroke volume cannot be used for that purpose. We hypothesized that the hemodynamic response to PLR predicts fluid responsiveness in mechanically ventilated patients., Design: Prospective study., Setting: Medical intensive care unit of a university hospital., Patients: We investigated 71 mechanically ventilated patients considered for volume expansion. Thirty-one patients had spontaneous breathing activity and/or arrhythmias., Interventions: We assessed hemodynamic status at baseline, after PLR, and after volume expansion (500 mL NaCl 0.9% infusion over 10 mins)., Measurements and Main Results: We recorded aortic blood flow using esophageal Doppler and arterial pulse pressure. We calculated the respiratory variation of pulse pressure in patients without arrhythmias. In 37 patients (responders), aortic blood flow increased by > or =15% after fluid infusion. A PLR increase of aortic blood flow > or =10% predicted fluid responsiveness with a sensitivity of 97% and a specificity of 94%. A PLR increase of pulse pressure > or =12% predicted volume responsiveness with significantly lower sensitivity (60%) and specificity (85%). In 30 patients without arrhythmias or spontaneous breathing, a respiratory variation in pulse pressure > or =12% was of similar predictive value as was PLR increases in aortic blood flow (sensitivity of 88% and specificity of 93%). In patients with spontaneous breathing activity, the specificity of respiratory variations in pulse pressure was poor (46%)., Conclusions: The changes in aortic blood flow induced by PLR predict preload responsiveness in ventilated patients, whereas with arrhythmias and spontaneous breathing activity, respiratory variations of arterial pulse pressure poorly predict preload responsiveness.

Objective: To test whether fluid responsiveness can be predicted by the respiratory variation in aortic blood flow and/or the flow time corrected for heart rate monitored with esophageal Doppler., Design and Setting: Prospective study in a 24-bed medical intensive care unit of a university hospital., Patients: 38 mechanically ventilated patients with sinus rhythm and without spontaneous breathing activity in whom volume expansion was planned., Interventions: The aortic blood flow was measured using an esophageal Doppler monitoring device before and after fluid infusion (500 ml NaCl 0.9% over 10 min). The variation in aortic blood flow over a respiratory cycle between its minimal and maximal values was calculated. The flow time was also measured., Measurements and Results: Aortic blood flow increased by at least 15% after volume expansion in 20 patients (defined as responders). Before fluid infusion the respiratory variation in aortic flow was higher in responders than in nonresponders (28+/-12% vs. 12+/-5%). It significantly decreased after volume expansion (18+/-11%) in responders only. A respiratory variation in aortic flow before volume expansion of at least 18% predicted fluid responsiveness with a sensitivity of 90% and a specificity of 94%. Flow time increased with fluid infusion in responders and nonresponders. A flow time corrected for heart rate below 277 ms predicted fluid responsiveness with a sensitivity of 55% and a specificity of 94%. The area under the ROC curve generated for variation in aortic blood flow ABF was greater than that generated for flow time., Conclusions: The respiratory variation in aortic blood flow reliably predicts fluid responsiveness in patients with sinus rhythm and without breathing activity.