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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).)

Background: Prone position is frequently used in patients with acute respiratory distress syndrome (ARDS), especially during the Coronavirus disease 2019 pandemic. Our study investigated the ability of pulse pressure variation (PPV) and its changes during a tidal volume challenge (TVC) to assess preload responsiveness in ARDS patients under prone position., Methods: This was a prospective study conducted in a 25-bed intensive care unit at a university hospital. We included patients with ARDS under prone position, ventilated with 6 mL/kg tidal volume and monitored by a transpulmonary thermodilution device. We measured PPV and its changes during a TVC (ΔPPV TVC 6-8 ) after increasing the tidal volume from 6 to 8 mL/kg for one minute. Changes in cardiac index (CI) during a Trendelenburg maneuver (ΔCI TREND ) and during end-expiratory occlusion (EEO) at 8 mL/kg tidal volume (ΔCI EEO 8 ) were recorded. Preload responsiveness was defined by both ΔCI TREND  ≥ 8% and ΔCI EEO 8  ≥ 5%. Preload unresponsiveness was defined by both ΔCI TREND  < 8% and ΔCI EEO 8  < 5%., Results: Eighty-four sets of measurements were analyzed in 58 patients. Before prone positioning, the ratio of partial pressure of arterial oxygen to fraction of inspired oxygen was 104 ± 27 mmHg. At the inclusion time, patients were under prone position for 11 (2-14) hours. Norepinephrine was administered in 83% of cases with a dose of 0.25 (0.15-0.42) µg/kg/min. The positive end-expiratory pressure was 14 (11-16) cmH 2 O. The driving pressure was 12 (10-17) cmH 2 O, and the respiratory system compliance was 32 (22-40) mL/cmH 2 O. Preload responsiveness was detected in 42 cases. An absolute change in PPV ≥ 3.5% during a TVC assessed preload responsiveness with an area under the receiver operating characteristics (AUROC) curve of 0.94 ± 0.03 (sensitivity: 98%, specificity: 86%) better than that of baseline PPV (0.85 ± 0.05; p = 0.047). In the 56 cases where baseline PPV was inconclusive (≥ 4% and < 11%), ΔPPV TVC 6-8  ≥ 3.5% still enabled to reliably assess preload responsiveness (AUROC: 0.91 ± 0.05, sensitivity: 97%, specificity: 81%; p < 0.01 vs. baseline PPV)., Conclusion: In patients with ARDS under low tidal volume ventilation during prone position, the changes in PPV during a TVC can reliably assess preload responsiveness without the need for cardiac output measurements., Trial Registration: ClinicalTrials.gov (NCT04457739). Registered 30 June 2020 -Retrospectively registered, https://clinicaltrials.gov/ct2/show/record/NCT04457739., (© 2022. The Author(s).)

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.)

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.

Fluid administration leads to a significant increase in cardiac output in only half of ICU patients. This has led to the concept of assessing fluid responsiveness before infusing fluid. Pulse pressure variation (PPV), which quantifies the changes in arterial pulse pressure during mechanical ventilation, is one of the dynamic variables that can predict fluid responsiveness. The underlying hypothesis is that large respiratory changes in left ventricular stroke volume, and thus pulse pressure, occur in cases of biventricular preload responsiveness. Several studies showed that PPV accurately predicts fluid responsiveness when patients are under controlled mechanical ventilation. Nevertheless, in many conditions encountered in the ICU, the interpretation of PPV is unreliable (spontaneous breathing, cardiac arrhythmias) or doubtful (low Vt). To overcome some of these limitations, researchers have proposed using simple tests such as the Vt challenge to evaluate the dynamic response of PPV. The applicability of PPV is higher in the operating room setting, where fluid strategies made on the basis of PPV improve postoperative outcomes. In medical critically ill patients, although no randomized controlled trial has compared PPV-based fluid management with standard care, the Surviving Sepsis Campaign guidelines recommend using fluid responsiveness indices, including PPV, whenever applicable. In conclusion, PPV is useful for managing fluid therapy under specific conditions where it is reliable. The kinetics of PPV during diagnostic or therapeutic tests is also helpful for fluid management.

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.

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.

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2017. Other selected articles can be found online at http://ccforum.com/series/annualupdate2017 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901 .

Background: Weaning-induced pulmonary oedema (WiPO) is a well-recognised cause of failure of weaning from mechanical ventilation, but its incidence and risk factors have not been reliably described. We wanted to determine the incidence and risk factors in a population of critically ill patients. In addition, we wanted to describe the effects of diuretics when they are administered in this context., Methods: We monitored 283 consecutive spontaneous breathing trials (SBT; T-piece trial) performed in 81 patients. In cases with cardiac output monitoring (n = 85, 29 patients), a passive leg raising (PLR) test was performed before SBT. Three experts established the diagnosis of WiPO based on various patient characteristics., Results: SBT failed in 128 cases (45 % of all SBT). WiPO occurred in 59 % of these failing cases. Compared to patients without WiPO (n = 52), patients with at least one WiPO (n = 29) had a higher prevalence of chronic obstructive pulmonary disease (COPD) (38 % vs. 12 %, respectively; p < 0.01), previous "structural" cardiopathy (dilated and/or hypertrophic and/or hypokinetic cardiopathy and/or significant valvular disease, 9 % vs. 25 %, respectively; p < 0.01), obesity (45 % vs. 17 %, respectively; p < 0.01), and low left ventricular ejection fraction (55 % vs. 21 %, respectively; p = 0.01). At logistic regression, COPD (odds ratio (OR) 8.7, 95 % confidence interval (CI) 2.0-37.3), previous structural cardiopathy (OR 4.5, 95 % CI 1.4-14.1), and obesity (OR 3.6, 95 % CI 1.2-12.6) were independent risk factors for experiencing at least one episode of WiPO. In 16 cases with WiPO and a negative PLR at baseline, treatment including diuretics was started. In 9 of these cases, the PLR remained negative before the following SBT. A new episode of WiPO occurred in 7 of these instances, while the two other were extubated. In 7 other cases, the PLR became positive before the following SBT. WiPO did not occur anymore in 6 of these 7 patients who were extubated, while the remaining one was not., Conclusions: In our population of critically ill patients, WiPO was responsible for 59 % of weaning failures. COPD, previous "structural" cardiopathy, and, to a lesser extent, obesity were the main risk factors. When a treatment including fluid removal had changed preload-independence to preload-dependence, the following SBT was very likely to succeed.

Purpose of Review: Because of heart-lung interactions, weaning from mechanical ventilation induces strong hemodynamic changes that can lead to weaning-induced cardiac failure. Cardiac patients are particularly at risk for this complication. In this review, we will summarize the most recent advances concerning the mechanisms, diagnosis and treatment of weaning-induced cardiac failure., Recent Findings: The role of left ventricular diastolic abnormalities contributing to weaning-induced pulmonary edema has been recently emphasized. The most important recent findings concern the diagnostic tools that can be used as alternatives to the pulmonary artery catheter for detecting weaning-induced pulmonary edema during a spontaneous breathing trial, such as increase in estimates of left ventricular filling pressure with echocardiography, increase in B-type natriuretic peptide, increase in plasma protein and hemoglobin concentration and increase in extravascular lung water measured by transpulmonary thermodilution. Concerning the treatment, recent data suggest that fluid removal, which is often indicated in such instances, could be guided by the dosage of B-type natriuretic peptide., Summary: Nowadays, the diagnosis of weaning-induced pulmonary edema can be easily made. Identifying such an event is important as an appropriate treatment, guided by the suspected mechanisms leading to the cardiac failure, should hasten weaning from mechanical ventilation.

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.

Purpose of Review: The purpose of this review was to summarize recent findings concerning the consequences of cardiopulmonary interactions in acute cardiogenic pulmonary edema, weaning from mechanical ventilation and fluid-responsiveness assessment by respiratory variations of stroke volume., Recent Findings: The efficacy of continuous or bilevel positive airway pressure in patients with acute cardiogenic pulmonary edema was strongly suggested by two recent meta-analyses. There is growing evidence to suggest that weaning-induced cardiac dysfunction and acute cardiogenic pulmonary edema could explain a large amount of liberation failure from mechanical ventilation. Despite a potential role for echocardiography and plasma measurements of B-type natriuretic peptide in demonstrating a cardiac origin to weaning failure, the demonstration of a significant increase in pulmonary-artery occlusion pressure during the weaning trial remains the gold standard for this purpose. In patients with heart failure there is no evidence for revisiting the reliability of the respiratory variation of stroke-volume surrogates to predict fluid responsiveness., Summary: For clinical practice, the knowledge of cardiopulmonary interactions is of paramount importance in understanding the crucial role of mechanical ventilation for treating patients with heart failure and, by contrast, the deleterious cardiovascular effects of weaning in patients with overt or hidden cardiac failure.

The pulse oximetry plethysmographic signal resembles the peripheral arterial pressure waveform, and the degree of respiratory variation in the pulse oximetry wave is close to the degree of respiratory arterial pulse pressure variation. Thus, it is tempting to speculate that pulse oximetry can be used to assess preload responsiveness in mechanically ventilated patients. In this commentary we briefly review the complex meaning of the pulse oximetry plethysmographic signal and highlight the advantages, limitations and pitfalls of the pulse oximetry method. Future studies including volume challenge must be performed to test whether the pulse oximetry waveform can really serve as a nonivasive tool for the guidance of fluid therapy in patients receiving mechanical ventilation in intensive care units and in operating rooms.

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.