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Abstract Background Several studies have validated capillary refill time (CRT) as a marker of tissue hypoperfusion, and recent guidelines recommend CRT monitoring during septic shock resuscitation. Therefore, it is relevant to further explore its kinetics of response to short-term hemodynamic interventions with fluids or vasopressors. A couple of previous studies explored the impact of a fluid bolus on CRT, but little is known about the impact of norepinephrine on CRT when aiming at a higher mean arterial pressure (MAP) target in septic shock. We designed this observational study to further evaluate the effect of a fluid challenge (FC) and a vasopressor test (VPT) on CRT in septic shock patients with abnormal CRT after initial resuscitation. Our purpose was to determine the effects of a FC in fluid-responsive patients, and of a VPT aimed at a higher MAP target in chronically hypertensive fluid-unresponsive patients on the direction and magnitude of CRT response. Methods Thirty-four septic shock patients were included. Fluid responsiveness was assessed at baseline, and a FC (500 ml/30 mins) was administered in 9 fluid-responsive patients. A VPT was performed in 25 patients by increasing norepinephrine dose to reach a MAP to 80–85 mmHg for 30 min. Patients shared a multimodal perfusion and hemodynamic monitoring protocol with assessments at at least two time-points (baseline, and at the end of interventions). Results CRT decreased significantly with both tests (from 5 [3.5–7.6] to 4 [2.4–5.1] sec, p = 0.008 after the FC; and from 4.0 [3.3–5.6] to 3 [2.6 -5] sec, p = 0.03 after the VPT. A CRT-response was observed in 7/9 patients after the FC, and in 14/25 pts after the VPT, but CRT deteriorated in 4 patients on this latter group, all of them receiving a concomitant low-dose vasopressin. Conclusions Our findings support that fluid boluses may improve CRT or produce neutral effects in fluid-responsive septic shock patients with persistent hypoperfusion. Conversely, raising NE doses to target a higher MAP in previously hypertensive patients elicits a more heterogeneous response, improving CRT in the majority, but deteriorating skin perfusion in some patients, a fact that deserves further research.

Background: Several studies have validated capillary refill time (CRT) as a marker of tissue hypoperfusion, and recent guidelines recommend CRT monitoring during septic shock resuscitation. Therefore, it is relevant to further explore its kinetics of response to short-term hemodynamic interventions with fluids or vasopressors. A couple of previous studies explored the impact of a fluid bolus on CRT, but little is known about the impact of norepinephrine on CRT when aiming at a higher mean arterial pressure (MAP) target in septic shock. We designed this observational study to further evaluate the effect of a fluid challenge (FC) and a vasopressor test (VPT) on CRT in septic shock patients with abnormal CRT after initial resuscitation. Our purpose was to determine the effects of a FC in fluid-responsive patients, and of a VPT aimed at a higher MAP target in chronically hypertensive fluid-unresponsive patients on the direction and magnitude of CRT response. Methods: Thirty-four septic shock patients were included. Fluid responsiveness was assessed at baseline, and a FC (500 ml/30 mins) was administered in 9 fluid-responsive patients. A VPT was performed in 25 patients by increasing norepinephrine dose to reach a MAP to 80–85 mmHg for 30 min. Patients shared a multimodal perfusion and hemodynamic monitoring protocol with assessments at at least two time-points (baseline, and at the end of interventions). Results: CRT decreased significantly with both tests (from 5 [3.5–7.6] to 4 [2.4–5.1] sec, p = 0.008 after the FC; and from 4.0 [3.3–5.6] to 3 [2.6 -5] sec, p = 0.03 after the VPT. A CRT-response was observed in 7/9 patients after the FC, and in 14/25 pts after the VPT, but CRT deteriorated in 4 patients on this latter group, all of them receiving a concomitant low-dose vasopressin. Conclusions: Our findings support that fluid boluses may improve CRT or produce neutral effects in fluid-responsive septic shock patients with persistent hypoperfusion. Conversely, raising NE doses to target a higher MAP in previously hypertensive patients elicits a more heterogeneous response, improving CRT in the majority, but deteriorating skin perfusion in some patients, a fact that deserves further research. [ABSTRACT FROM AUTHOR]

Abstract Background Capillary refill time (CRT) is a valuable tool for triage and to guide resuscitation. However, little is known about CRT kinetics after fluid infusion. Methods We conducted a prospective observational study in a tertiary teaching hospital. First, we analyzed the intra-observer variability of CRT. Next, we monitored fingertip CRT in sepsis patients during volume expansion within the first 24 h of ICU admission. Fingertip CRT was measured every 2 min during 30 min following crystalloid infusion (500 mL over 15 min). Results First, the accuracy of repetitive fingertip CRT measurements was evaluated on 40 critically ill patients. Reproducibility was excellent, with an intra-class correlation coefficient of 99.5% (CI 95% [99.3, 99.8]). A CRT variation larger than 0.2 s was considered as significant. Next, variations of CRT during volume expansion were evaluated on 29 septic patients; median SOFA score was 7 [5–9], median SAPS II was 57 [45–72], and ICU mortality rate was 24%. Twenty-three patients were responders as defined by a CRT decrease > 0.2 s at 30 min after volume expansion, and 6 were non-responders. Among responders, we observed that fingertip CRT quickly improved with a significant decrease at 6–8 min after start of crystalloid infusion, the maximal improvement being observed after 10–12 min (−0.7 [−0.3;−0.9] s) and maintained at 30 min. CRT variations significantly correlated with baseline CRT measurements (R = 0.39, P = 0.05). Conclusions CRT quickly improved during volume expansion with a significant decrease 6–8 min after start of fluid infusion and a maximal drop at 10–12 min.

Abstract Although the administration of fluid is the first treatment considered in almost all cases of circulatory failure, this therapeutic option poses two essential problems: the increase in cardiac output induced by a bolus of fluid is inconstant, and the deleterious effects of fluid overload are now clearly demonstrated. This is why many tests and indices have been developed to detect preload dependence and predict fluid responsiveness. In this review, we take stock of the data published in the field over the past three years. Regarding the passive leg raising test, we detail the different stroke volume surrogates that have recently been described to measure its effects using minimally invasive and easily accessible methods. We review the limits of the test, especially in patients with intra-abdominal hypertension. Regarding the end-expiratory occlusion test, we also present recent investigations that have sought to measure its effects without an invasive measurement of cardiac output. Although the limits of interpretation of the respiratory variation of pulse pressure and of the diameter of the vena cava during mechanical ventilation are now well known, several recent studies have shown how changes in pulse pressure variation itself during other tests reflect simultaneous changes in cardiac output, allowing these tests to be carried out without its direct measurement. This is particularly the case during the tidal volume challenge, a relatively recent test whose reliability is increasingly well established. The mini-fluid challenge has the advantage of being easy to perform, but it requires direct measurement of cardiac output, like the classic fluid challenge. Initially described with echocardiography, recent studies have investigated other means of judging its effects. We highlight the problem of their precision, which is necessary to evidence small changes in cardiac output. Finally, we point out other tests that have appeared more recently, such as the Trendelenburg manoeuvre, a potentially interesting alternative for patients in the prone position.

Background: Capillary refill time (CRT) is a valuable tool for triage and to guide resuscitation. However, little is known about CRT kinetics after fluid infusion. Methods: We conducted a prospective observational study in a tertiary teaching hospital. First, we analyzed the intra-observer variability of CRT. Next, we monitored fingertip CRT in sepsis patients during volume expansion within the first 24 h of ICU admission. Fingertip CRT was measured every 2 min during 30 min following crystalloid infusion (500 mL over 15 min). Results: First, the accuracy of repetitive fingertip CRT measurements was evaluated on 40 critically ill patients. Reproducibility was excellent, with an intra-class correlation coefficient of 99.5% (CI 95% [99.3, 99.8]). A CRT variation larger than 0.2 s was considered as significant. Next, variations of CRT during volume expansion were evaluated on 29 septic patients; median SOFA score was 7 [5–9], median SAPS II was 57 [45–72], and ICU mortality rate was 24%. Twenty-three patients were responders as defined by a CRT decrease > 0.2 s at 30 min after volume expansion, and 6 were non-responders. Among responders, we observed that fingertip CRT quickly improved with a significant decrease at 6–8 min after start of crystalloid infusion, the maximal improvement being observed after 10–12 min (−0.7 [−0.3;−0.9] s) and maintained at 30 min. CRT variations significantly correlated with baseline CRT measurements (R = 0.39, P = 0.05). Conclusions: CRT quickly improved during volume expansion with a significant decrease 6–8 min after start of fluid infusion and a maximal drop at 10–12 min. [ABSTRACT FROM AUTHOR]

Abstract Background The end-expiratory occlusion (EEXPO) test detects preload responsiveness, but it is 15 s long and induces small changes in cardiac index (CI). It is doubtful whether the Starling bioreactance device, which averages CI over 24 s and refreshes the displayed value every 4 s (Starling-24.4), can detect the EEXPO-induced changes in CI (ΔCI). Our primary goal was to test whether this Starling device version detects preload responsiveness through EEXPO. We also tested whether shortening the averaging and refresh times to 8 s and one second, respectively, (Starling-8.1) improves the accuracy of the device in detecting preload responsiveness using EEXPO. Methods In 42 mechanically ventilated patients, during a 15-s EEXPO, we measured ∆CI through calibrated pulse contour analysis (CIpulse, PiCCO2 device) and using the Starling device. For the latter, we considered both CIStarling-24.4 from the commercial version and CIStarling-8.1 derived from the raw data. For relative ∆CIStarling-24.4 and ∆CIStarling-8.1 during EEXPO, we calculated the area under the receiver operating characteristic curve (AUROC) to detect preload responsiveness, defined as an increase in CIpulse ≥ 10% during passive leg raising (PLR). For both methods, the correlation coefficient vs. ∆CIpulse was calculated. Results Twenty-six patients were preload responders and sixteen non preload-responders. The AUROC for ∆CIStarling-24.4 was significantly lower compared to ∆CIStarling-8.1 (0.680 ± 0.086 vs. 0.899 ± 0.049, respectively; p = 0.027). A significant correlation was observed between ∆CIStarling-8.1 and ∆CIpulse (r = 0.42; p = 0.009), but not between ∆CIStarling-24.4 and ∆CIpulse. During PLR, both ∆CIStarling-24.4 and ∆CIStarling-8.1 reliably detected preload responsiveness. Conclusions Shortening the averaging and refresh times of the bioreactance signal to 8 s and one second, respectively, increases the reliability of the Starling device in detection of EEXPO-induced ∆CI. Trial registration: No. IDRCB:2018-A02825-50. Registered 13 December 2018.

Although the administration of fluid is the first treatment considered in almost all cases of circulatory failure, this therapeutic option poses two essential problems: the increase in cardiac output induced by a bolus of fluid is inconstant, and the deleterious effects of fluid overload are now clearly demonstrated. This is why many tests and indices have been developed to detect preload dependence and predict fluid responsiveness. In this review, we take stock of the data published in the field over the past three years. Regarding the passive leg raising test, we detail the different stroke volume surrogates that have recently been described to measure its effects using minimally invasive and easily accessible methods. We review the limits of the test, especially in patients with intra-abdominal hypertension. Regarding the end-expiratory occlusion test, we also present recent investigations that have sought to measure its effects without an invasive measurement of cardiac output. Although the limits of interpretation of the respiratory variation of pulse pressure and of the diameter of the vena cava during mechanical ventilation are now well known, several recent studies have shown how changes in pulse pressure variation itself during other tests reflect simultaneous changes in cardiac output, allowing these tests to be carried out without its direct measurement. This is particularly the case during the tidal volume challenge, a relatively recent test whose reliability is increasingly well established. The mini-fluid challenge has the advantage of being easy to perform, but it requires direct measurement of cardiac output, like the classic fluid challenge. Initially described with echocardiography, recent studies have investigated other means of judging its effects. We highlight the problem of their precision, which is necessary to evidence small changes in cardiac output. Finally, we point out other tests that have appeared more recently, such as the Trendelenburg manoeuvre, a potentially interesting alternative for patients in the prone position. [ABSTRACT FROM AUTHOR]

Abstract Background We performed a systematic review and meta-analysis of studies assessing the end-expiratory occlusion test (EEXPO test)-induced changes in cardiac output (CO) measured by any haemodynamic monitoring device, as indicators of preload responsiveness. Methods MEDLINE, EMBASE and Cochrane Database were screened for original articles. Bivariate random-effects meta-analysis determined the Area under the Summary Receiver Operating Characteristic (AUSROC) curve of EEXPO test-induced changes in CO to detect preload responsiveness, as well as pooled sensitivity and specificity and the best diagnostic threshold. Results Thirteen studies (530 patients) were included. Nine studies were performed in the intensive care unit and four in the operating room. The pooled sensitivity and the pooled specificity for the EEXPO test-induced changes in CO were 0.85 [0.77–0.91] and 0.88 [0.83–0.91], respectively. The AUSROC curve was 0.91 [0.86–0.94] with the best threshold of CO increase at 5.1 ± 0.2%. The accuracy of the test was not different when changes in CO were monitored through pulse contour analysis compared to other methods (AUSROC: 0.93 [0.91–0.95] vs. 0.87 [0.82–0.96], respectively, p = 0.62). Also, it was not different in studies in which the tidal volume was ≤ 7 mL/kg compared to the remaining ones (AUSROC: 0.96 [0.92–0.97] vs. 0.89 [0.82–0.95] respectively, p = 0.44). Subgroup analyses identified one possible source of heterogeneity. Conclusions EEXPO test-induced changes in CO reliably detect preload responsiveness. The diagnostic performance is not influenced by the method used to track the EEXPO test-induced changes in CO. Trial registration The study protocol was prospectively registered on PROSPERO: CRD42019138265.

Abstract Background Volume expansion is aimed at increasing cardiac output (CO), but this variable is not always directly measured. We assessed the ability of changes in arterial pressure, pulse pressure variation (PPV) and heart rate (HR) or of a combination of them to detect a positive response of cardiac output (CO) to fluid administration. Methods We retrospectively included 491 patients with circulatory failure. Before and after a 500-mL normal saline infusion, we measured CO (PiCCO device), HR, systolic (SAP), diastolic (DAP), mean (MAP) and pulse (PP) arterial pressure, PPV, shock index (HR/SAP) and the PP/HR ratio. Results The fluid-induced changes in HR were not correlated with the fluid-induced changes in CO. The area under the receiver operating characteristic curve (AUROC) for changes in HR as detectors of a positive fluid response (CO increase ≥ 15%) was not different from 0.5. The fluid-induced changes in SAP, MAP, PP, PPV, shock index (HR/SAP) and the PP/HR ratio were correlated with the fluid-induced changes in CO, but with r

Background: The end-expiratory occlusion (EEXPO) test detects preload responsiveness, but it is 15 s long and induces small changes in cardiac index (CI). It is doubtful whether the Starling bioreactance device, which averages CI over 24 s and refreshes the displayed value every 4 s (Starling-24.4), can detect the EEXPO-induced changes in CI (ΔCI). Our primary goal was to test whether this Starling device version detects preload responsiveness through EEXPO. We also tested whether shortening the averaging and refresh times to 8 s and one second, respectively, (Starling-8.1) improves the accuracy of the device in detecting preload responsiveness using EEXPO. Methods: In 42 mechanically ventilated patients, during a 15-s EEXPO, we measured ∆CI through calibrated pulse contour analysis (CIpulse, PiCCO2 device) and using the Starling device. For the latter, we considered both CIStarling-24.4 from the commercial version and CIStarling-8.1 derived from the raw data. For relative ∆CIStarling-24.4 and ∆CIStarling-8.1 during EEXPO, we calculated the area under the receiver operating characteristic curve (AUROC) to detect preload responsiveness, defined as an increase in CIpulse ≥ 10% during passive leg raising (PLR). For both methods, the correlation coefficient vs. ∆CIpulse was calculated. Results: Twenty-six patients were preload responders and sixteen non preload-responders. The AUROC for ∆CIStarling-24.4 was significantly lower compared to ∆CIStarling-8.1 (0.680 ± 0.086 vs. 0.899 ± 0.049, respectively; p = 0.027). A significant correlation was observed between ∆CIStarling-8.1 and ∆CIpulse (r = 0.42; p = 0.009), but not between ∆CIStarling-24.4 and ∆CIpulse. During PLR, both ∆CIStarling-24.4 and ∆CIStarling-8.1 reliably detected preload responsiveness. Conclusions: Shortening the averaging and refresh times of the bioreactance signal to 8 s and one second, respectively, increases the reliability of the Starling device in detection of EEXPO-induced ∆CI. Trial registration: No. IDRCB:2018-A02825-50. Registered 13 December 2018. [ABSTRACT FROM AUTHOR]

Abstract Background Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic after a positive response to fluid challenge (FC). Methods Three groups of patients were studied if they increased stroke volume (SV) > 10% after 250 or 500 ml of crystalloids: control group: patients free of comorbidity anesthetized for orthopedic surgery; sepsis group: patients with severe sepsis or septic shock (classic definition); brain injury (BI) group: trauma brain jury or hemorrhagic stroke with no detectable systemic inflammation. The measurements before and after FC were mean arterial blood pressure (MAP) (radial catheter); SV and cardiac output (CO; transesophageal Doppler); bilateral middle cerebral artery (MCAv) velocity with peak systolic (PSV) and end diastolic (EDV) values (transcranial Doppler); end-tidal CO2. The role of MAP increase was investigated by an arbitrarily threshold increase of 5%, called responder in CO and MAP (RR). The remaining patients were call responders in CO and non-responders in MAP (RnR). Nonparametric tests were used for statistical analysis. Results Among the 86 screened patients, 66 have completed the protocol: 17 in control group; 38 in sepsis group; and 11 in BI group. All patients increased SV > 10% after FC. Only the sepsis group increased MAP [+ 12 (2–25%), p baseline median MAP had similar MCAv. Conclusions After a FC-induced increase in SV, MCAv (PSV and EDV) increased only in septic group, mostly independently from MAP increase and from baseline MAP level. Cerebral perfusion becomes passively dependent on systemic blood flow, suggesting a modification of the control of cerebrovascular tone in sepsis-induced systemic inflammation. This information has been considered in the clinical management of septic patients.

Abstract Many efforts have been made to predict, before giving fluid, whether it will increase cardiac output. Nevertheless, after fluid administration, it is also essential to assess the therapeutic efficacy and to look for possible adverse effects. Like for any drug, this step should not be missed. Basically, volume expansion is aimed at improving tissue oxygenation and organ function. To assess this final result, clinical signs are often unhelpful. The increase in urine output in case of acute kidney injury is a poor marker of the kidney perfusion improvement. Even if oxygen delivery has increased with fluid, the increase in oxygen consumption is not constant. Assessing this response needs to measure markers such as lactate, central/mixed venous oxygen saturation, or carbon dioxide-derived indices. If tissue oxygenation did not improve, one should check that cardiac output has actually increased with fluid administration. To assess this response, changes in arterial pressure are not reliable enough, and direct measurements of cardiac output are required. In cases where cardiac output did not increase with fluid, one should check that it was not due to an insufficient volume of fluid administered. For this purpose, volume markers of cardiac preload sometimes lack precision. The central venous pressure, in theory at least, should not augment to a large extent in fluid responders. The worst adverse effect of fluids is the increase in the cumulative fluid balance. In patients with acute respiratory distress syndrome (ARDS), the risk of aggravating pulmonary oedema should be systematically assessed by looking for increases in extravascular lung water, or, more indirectly, increases in central venous or pulmonary artery occlusion pressure. In ARDS patients receiving fluid, one should always keep in mind the risk of inducing/aggravating right ventricular dilation, which should be confirmed through echocardiography. The risk of increasing the intra-abdominal pressure should be carefully sought in patients at risk. Finally, fluid-induced haemodilution should not be neglected. Like for any drug which has inconsistent effectiveness and may exert significant harm, the correct fluid management should include a cautious and comprehensive assessment of fluid-induced benefits and side effects.

Background: We performed a systematic review and meta-analysis of studies assessing the end-expiratory occlusion test (EEXPO test)-induced changes in cardiac output (CO) measured by any haemodynamic monitoring device, as indicators of preload responsiveness. Methods: MEDLINE, EMBASE and Cochrane Database were screened for original articles. Bivariate random-effects meta-analysis determined the Area under the Summary Receiver Operating Characteristic (AUSROC) curve of EEXPO test-induced changes in CO to detect preload responsiveness, as well as pooled sensitivity and specificity and the best diagnostic threshold. Results: Thirteen studies (530 patients) were included. Nine studies were performed in the intensive care unit and four in the operating room. The pooled sensitivity and the pooled specificity for the EEXPO test-induced changes in CO were 0.85 [0.77–0.91] and 0.88 [0.83–0.91], respectively. The AUSROC curve was 0.91 [0.86–0.94] with the best threshold of CO increase at 5.1 ± 0.2%. The accuracy of the test was not different when changes in CO were monitored through pulse contour analysis compared to other methods (AUSROC: 0.93 [0.91–0.95] vs. 0.87 [0.82–0.96], respectively, p = 0.62). Also, it was not different in studies in which the tidal volume was ≤ 7 mL/kg compared to the remaining ones (AUSROC: 0.96 [0.92–0.97] vs. 0.89 [0.82–0.95] respectively, p = 0.44). Subgroup analyses identified one possible source of heterogeneity. Conclusions: EEXPO test-induced changes in CO reliably detect preload responsiveness. The diagnostic performance is not influenced by the method used to track the EEXPO test-induced changes in CO. Trial registration The study protocol was prospectively registered on PROSPERO: CRD42019138265. [ABSTRACT FROM AUTHOR]

Background: Volume expansion is aimed at increasing cardiac output (CO), but this variable is not always directly measured. We assessed the ability of changes in arterial pressure, pulse pressure variation (PPV) and heart rate (HR) or of a combination of them to detect a positive response of cardiac output (CO) to fluid administration. Methods: We retrospectively included 491 patients with circulatory failure. Before and after a 500-mL normal saline infusion, we measured CO (PiCCO device), HR, systolic (SAP), diastolic (DAP), mean (MAP) and pulse (PP) arterial pressure, PPV, shock index (HR/SAP) and the PP/HR ratio. Results: The fluid-induced changes in HR were not correlated with the fluid-induced changes in CO. The area under the receiver operating characteristic curve (AUROC) for changes in HR as detectors of a positive fluid response (CO increase ≥ 15%) was not different from 0.5. The fluid-induced changes in SAP, MAP, PP, PPV, shock index (HR/SAP) and the PP/HR ratio were correlated with the fluid-induced changes in CO, but with r < 0.4. The best detection was provided by increases in PP, but it was rough (AUROC = 0.719 ± 0.023, best threshold: increase ≥ 10%, sensitivity = 72 [66–77]%, specificity = 64 [57–70]%). Neither the decrease in shock index nor the changes in other indices combining changes in HR, shock index, PPV and PP provided a better detection of a positive fluid response than changes in PP. Conclusion: A positive response to fluid was roughly detected by changes in PP and not detected by changes in HR. Changes in combined indices including the shock index and the PP/HR ratio did not provide a better diagnostic accuracy. [ABSTRACT FROM AUTHOR]