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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.

Objective: To compare cardiac index (CI) between Proaqt/PulsioFlex ® and oesophageal Doppler (OD) and the ability of the PulsioFlex ® to track CI changes induced by fluid challenge and secondly to assess the impact of the time interval between two auto-calibrations of PulsioFlex ® on the accuracy of the measured CI., Methods: In a single hospital, 49 intermediate-risk oncologic abdominal surgery patients were included in an observational study. We measured the cardiac Index (CI) provided by OD and by the Proaqt/PulsioFlex ® before and after internal calibration, which were performed randomly at specific intervals after the initial one (30, 60, 90 and 120min). The ability to track fluid responsiveness was evaluated by measuring stroke volume variation, pulse pressure variation (PPV) and CI before and after a 250ml fluid challenge and assessed by a receiver operating characteristic curve analysis., Results: The percentages of error before calibration were 51, 58, 82, 81% for 30, 60, 90 and 120min, they were 39, 57, 65, and 54% after calibration. Trending ability is assumed by a 93% concordance rate after applying a 15% exclusion zone. The trend interchangeability rate was 13.75%. The area under the curve for fluid responsiveness measured by PPV and SVV PulsioFlex were respectively 0.67 [0.57-0.77], P<0.01 and 0.75 [0.47-0.66], which was not clinically relevant., Conclusions: The Proaqt/Pulsioflex ® system is not equivalent to OD for haemodynamic monitoring during non-vascular abdominal surgery in intermediate-risk patients. More studies are required to define the effect of the auto-calibration on the system., (Copyright © 2018 Société française d'anesthésie et de réanimation (Sfar). Published by Elsevier Masson SAS. All rights reserved.)

Background: A passive leg raising (PLR) test is positive if the cardiac index (CI) increased by > 10%, but it requires a direct measurement of CI. On the oxygen saturation plethysmographic signal, the perfusion index (PI) is the ratio between the pulsatile and the non-pulsatile portions. We hypothesised that the changes in PI could predict a positive PLR test and thus preload responsiveness in a totally non-invasive way., Methods: In patients with acute circulatory failure, we measured PI (Radical-7) and CI (PiCCO2) before and during a PLR test and, if decided, before and after volume expansion (500-mL saline)., Results: Three patients were excluded because the plethysmography signal was absent and 3 other ones because it was unstable. Eventually, 72 patients were analysed. In 34 patients with a positive PLR test (increase in CI ≥ 10%), CI and PI increased during PLR by 21 ± 10% and 54 ± 53%, respectively. In the 38 patients with a negative PLR test, PI did not significantly change during PLR. In 26 patients in whom volume expansion was performed, CI and PI increased by 28 ± 14% and 53 ± 63%, respectively. The correlation between the PI and CI changes for all interventions was significant (r = 0.64, p < 0.001). During the PLR test, if PI increased by > 9%, a positive response of CI (≥ 10%) was diagnosed with a sensitivity of 91 (76-98%) and a specificity of 79 (63-90%) (area under the receiver operating characteristics curve 0.89 (0.80-0.95), p < 0.0001)., Conclusion: An increase in PI during PLR by 9% accurately detects a positive response of the PLR test., Trial Registration: ID RCB 2016-A00959-42. Registered 27 June 2016.

Monitoring cardiac output is of special interest for detecting early hemodynamic impairment and for guiding its treatment. Among the techniques that are available to monitor cardiac output, pressure waveform analysis estimates cardiac output from the shape of the arterial pressure curve. It is based on the general principle that the amplitude of the systolic part of the arterial curve is proportional to cardiac output and arterial compliance. Such an estimation of cardiac output has the advantage of being continuous and in real time. With "calibrated" devices, the initial estimation of cardiac output by pressure waveform analysis is calibrated by measurements of cardiac output made by transpulmonary thermal or lithium dilution. Later, at each time transpulmonary dilution is performed, the estimation by pressure waveform analysis, which may drift over time, is calibrated again. By contrast, uncalibrated devices do not use any independent measurement of cardiac output. Unlike calibrated devices, they can be plugged to any arterial catheter. Nevertheless, uncalibrated devices are not reliable in cases of significant short-term changes in arterial resistance, as for instance in patients undergoing liver surgery or those with vasodilatory shock receiving vasopressors. Perioperative hemodynamic monitoring is recommended for high-risk surgical patients since it reduces the number of complications in these patients. The pressure waveform analysis monitoring, especially with uncalibrated devices, is suitable for this purpose. In the intensive care setting, hemodynamic monitoring is recommended for patients with acute circulatory failure, who do not respond to initial therapy. Since these patients often experience large changes in arterial resistance, either spontaneously or due to vasoactive drugs, calibrated devices are more suitable in this context. Not only are they more reliable than uncalibrated devices but also they provide a comprehensive hemodynamic assessment through measurements of a variety of transpulmonary thermodilution-related variables. In this review, we summarize the characteristics of the monitoring devices using the pressure waveform analysis and discuss the appropriate use of different devices in the perioperative and intensive care unit settings.

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.

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.

Although use of the classic pulmonary artery catheter has declined, several techniques have emerged to estimate cardiac output. Arterial pressure waveform analysis computes cardiac output from the arterial pressure curve. The method of estimating cardiac output for these devices depends on whether they need to be calibrated by an independent measure of cardiac output. Some newer devices have been developed to estimate cardiac output from an arterial curve obtained noninvasively with photoplethysmography, allowing a noninvasive beat-by-beat estimation of cardiac output. This article describes the different devices that perform pressure waveform analysis., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Rationale: The effects of prone positioning during acute respiratory distress syndrome on all the components of cardiac function have not been investigated under protective ventilation and maximal alveolar recruitment., Objectives: To investigate the hemodynamic effects of prone positioning., Methods: We included 18 patients with acute respiratory distress syndrome ventilated with protective ventilation and an end-expiratory positive pressure titrated to a plateau pressure of 28-30 cm H2O. Before and within 20 minutes of starting prone positioning, hemodynamic, respiratory, intraabdominal pressure, and echocardiographic data were collected. Before prone positioning, preload reserve was assessed by a passive leg raising test., Measurements and Main Results: In all patients, prone positioning increased the ratio of arterial oxygen partial pressure over inspired oxygen fraction, the intraabdominal pressure, and the right and left cardiac preload. The pulmonary vascular resistance decreased along with the ratio of the right/left ventricular end-diastolic areas suggesting a decrease of the right ventricular afterload. In the nine patients with preload reserve, prone positioning significantly increased cardiac index (3.0 [2.3-3.5] to 3.6 [3.2-4.4] L/min/m(2)). In the remaining patients, cardiac index did not change despite a significant decrease in the pulmonary vascular resistance., Conclusions: In patients with acute respiratory distress syndrome under protective ventilation and maximal alveolar recruitment, prone positioning increased the cardiac index only in patients with preload reserve, emphasizing the important role of preload in the hemodynamic effects of prone positioning.

Objective: The hemodynamic impact of positive end-expiratory pressure in acute respiratory distress syndrome and the underlying mechanisms have not been extensively investigated during low stretch ventilation. Our aim was to evaluate the hemodynamic effect of increasing positive end-expiratory pressure when tidal volume and the plateau pressure are limited and to explore the underlying mechanisms., Design: Prospective study., Setting: Medical intensive care unit., Patients: Twenty-one acute respiratory distress syndrome patients ventilated with a tidal volume of 6.0 +/- 0.5 mL/kg of predicted body weight., Intervention: Positive end-expiratory pressure was significantly increased from 5 +/- 1 cm H2O to 13 +/- 4 cm H2O for reaching a plateau pressure of 30 +/- 1 cm H2O. At high positive end-expiratory pressure, passive leg raising was performed for increasing the central blood volume., Measurements: We performed echocardiography and pulmonary artery catheterization during positive end-expiratory pressure increase and during passive leg raising at high positive end-expiratory pressure., Main Results: With positive end-expiratory pressure elevation, the cardiac index decreased by 13% +/- 9%. The right ventricular end-diastolic area, right atrial pressure, and pulmonary vascular resistance increased by 13% +/- 20%, 34% +/- 24% and 32% +/- 31%, respectively (p < .01; p = .04; and p < .01 vs. baseline, respectively). The transpulmonary pressure difference (mean pulmonary artery pressure--pulmonary artery occlusion pressure) increased (p < .05). Both at low and high positive end-expiratory pressure, an acute cor pulmonale was observed in the same three (14%) patients. At high positive end-expiratory pressure, the passive leg raising significantly increased the right and left ventricular end-diastolic areas and right atrial pressure. Passive leg raising also decreased the transpulmonary pressure difference (p < .05), increased the cardiac index by 14% +/- 10%, and decreased the pulmonary vascular resistance by 21% +/- 20% (both p < .01 vs. baseline)., Conclusions: In acute respiratory distress syndrome patients, a positive end-expiratory pressure increase with limited tidal volume and plateau pressure reduced cardiac output by increasing the right ventricular afterload. Passive leg raising restored cardiac output by reducing the transpulmonary pressure difference and the pulmonary vascular resistance. This suggests that some pulmonary microvessels were collapsed by positive end-expiratory pressure elevation and were recruited by increasing the central blood volume.

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.