BackgroundIn mechanically ventilated patients, an increase in cardiac index during an end-expiratory-occlusion test predicts fluid responsiveness. To identify this rapid increase in cardiac index, continuous and instantaneous cardiac index monitoring is necessary, decreasing its feasibility at the bedside. Our study was designed to investigate whether changes in velocity time integral and in peak velocity obtained using transthoracic echocardiography during an end-expiratory-occlusion maneuver could predict fluid responsiveness.MethodsThis single-center, prospective study included 50 mechanically ventilated critically ill patients. Velocity time integral and peak velocity were assessed using transthoracic echocardiography before and at the end of a 12-sec end-expiratory-occlusion maneuver. A third set of measurements was performed after volume expansion (500 mL of saline 0.9% given over 15 minutes). Patients were considered as responders if cardiac output increased by 15% or more after volume expansion.ResultsTwenty-eight patients were responders. At baseline, heart rate, mean arterial pressure, cardiac output, velocity time integral and peak velocity were similar between responders and non-responders. End-expiratory-occlusion maneuver induced a significant increase in velocity time integral both in responders and non-responders, and a significant increase in peak velocity only in responders. A 9% increase in velocity time integral induced by the end-expiratory-occlusion maneuver predicted fluid responsiveness with sensitivity of 89% (95% CI 72% to 98%) and specificity of 95% (95% CI 77% to 100%). An 8.5% increase in peak velocity induced by the end-expiratory-occlusion maneuver predicted fluid responsiveness with sensitivity of 64% (95% CI 44% to 81%) and specificity of 77% (95% CI 55% to 92%). The area under the receiver operating curve generated for changes in velocity time integral was significantly higher than the one generated for changes in peak velocity (0.96 ± 0.03 versus 0.70 ± 0.07, respectively, P = 0.0004 for both). The gray zone ranged between 6 and 10% (20% of the patients) for changes in velocity time integral and between 1 and 13% (62% of the patients) for changes in peak velocity.ConclusionsIn mechanically ventilated and sedated patients in the neuro Intensive Care Unit, changes in velocity time integral during a 12-sec end-expiratory-occlusion maneuver were able to predict fluid responsiveness and perform better than changes in peak velocity.

No abstract

No abstract

Background There is insufficient evidence to guide ventilatory targets in acute brain injury (ABI). Recent studies have shown associations between mechanical power (MP) and mortality in critical care populations. We aimed to describe MP in ventilated patients with ABI, and evaluate associations between MP and clinical outcomes. Methods In this preplanned, secondary analysis of a prospective, multi-center, observational cohort study (ENIO, NCT03400904), we included adult patients with ABI (Glasgow Coma Scale ≤ 12 before intubation) who required mechanical ventilation (MV) ≥ 24 h. Using multivariable log binomial regressions, we separately assessed associations between MP on hospital day (HD)1, HD3, HD7 and clinical outcomes: hospital mortality, need for reintubation, tracheostomy placement, and development of acute respiratory distress syndrome (ARDS). Results We included 1217 patients (mean age 51.2 years [SD 18.1], 66% male, mean body mass index [BMI] 26.3 [SD 5.18]) hospitalized at 62 intensive care units in 18 countries. Hospital mortality was 11% (n = 139), 44% (n = 536) were extubated by HD7 of which 20% (107/536) required reintubation, 28% (n = 340) underwent tracheostomy placement, and 9% (n = 114) developed ARDS. The median MP on HD1, HD3, and HD7 was 11.9 J/min [IQR 9.2–15.1], 13 J/min [IQR 10–17], and 14 J/min [IQR 11–20], respectively. MP was overall higher in patients with ARDS, especially those with higher ARDS severity. After controlling for same-day pressure of arterial oxygen/fraction of inspired oxygen (P/F ratio), BMI, and neurological severity, MP at HD1, HD3, and HD7 was independently associated with hospital mortality, reintubation and tracheostomy placement. The adjusted relative risk (aRR) was greater at higher MP, and strongest for: mortality on HD1 (compared to the HD1 median MP 11.9 J/min, aRR at 17 J/min was 1.22, 95% CI 1.14–1.30) and HD3 (1.38, 95% CI 1.23–1.53), reintubation on HD1 (1.64; 95% CI 1.57–1.72), and tracheostomy on HD7 (1.53; 95%CI 1.18–1.99). MP was associated with the development of moderate-severe ARDS on HD1 (2.07; 95% CI 1.56–2.78) and HD3 (1.76; 95% CI 1.41–2.22). Conclusions Exposure to high MP during the first week of MV is associated with poor clinical outcomes in ABI, independent of P/F ratio and neurological severity. Potential benefits of optimizing ventilator settings to limit MP warrant further investigation.

Background Hyperoxia is associated with increased morbidity and mortality in the intensive care unit. Classical noninvasive measurements of oxygen saturation with pulse oximeters are unable to detect hyperoxia. The Oxygen Reserve Index (ORI) is a continuous noninvasive parameter provided by a multi-wave pulse oximeter that can detect hyperoxia. Primary objective was to evaluate the diagnostic accuracy of the ORI for detecting arterial oxygen tension (PaO2) > 100 mmHg in neurocritical care patients. Secondary objectives were to test the ability of ORI to detect PaO2 > 120 mmHg and the ability of pulse oximetry (SpO2) to detect PaO2 > 100 mmHg and PaO2 > 120 mmHg. Methods In this single-center study, we collected ORI and arterial blood samples every 6 h for 3 consecutive days. Diagnostic performance was estimated using the area under the receiver operating characteristic curve (AUROC). Results There were 696 simultaneous measurements of ORI and PaO2 in 62 patients. Considering the repeated measurements, the correlation between ORI and PaO2 was r = 0.13. The area under the receiver operating characteristic curve (AUROC), obtained to test the ability of ORI to detect PaO2 > 100 mmHg, was 0.567 (95% confidence interval = 0.566–0.569) with a sensitivity of 0.233 (95%CI = 0.230–0.235) and a specificity of 0.909 (95%CI = 0.907–0.910). The AUROC value obtained to test the ability of SpO2 to detect a PaO2 > 100 mmHg was 0.771 (95%CI = 0.770–0.773) with a sensitivity of 0.715 (95%CI = 0.712–0.718) and a specificity of 0.700 (95%CI = 0.697–0.703). The diagnostic performance of ORI and SpO2 for detecting PaO2 > 120 mmHg was AUROC = 0.584 (95%CI = 0.582–0.586) and 0.764 (95%CI = 0.762–0.766), respectively. The AUROC obtained for SpO2 was significantly higher than that for ORI (p < 0.01). Diagnostic performance was not affected by sedation, norepinephrine infusion, arterial partial pressure of carbon dioxide, hemoglobin level and perfusion index. Conclusion In a specific population of brain-injured patients hospitalized in a neurointensive care unit, our results suggest that the ability of ORI to diagnose hyperoxia is relatively low and that SpO2 provides better detection.