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Longrois, D.

Publications and source records attributed to Longrois, D..

2 recordsLinked to original sources

Mapping general anesthesia states based on electro-encephalogram transition phases

Cortical electro-encephalography (EEG) has become the clinical reference for monitoring unconsciousness during general anesthesia. The current EEG-based monitors classify general anesthesia states simply as underdosed, adequate, or overdosed, with no transition phases among these states, and therefore no predictive power. To address the issue of transition phases, we analyzed EEG signal of isoflurane-induced general anesthesia in mice. We adopted a data-driven approach and utilized signal processing to track{theta} - and{delta} - band dynamics as well as iso-electric suppressions. By combining this approach with machine learning, we developed a fully-automated algorithm. We found that the dampening of the{delta} -band occurred several minutes before significant iso-electric suppression episodes. Additionally, we observed a distinct{gamma} -frequency oscillation that persisted for several minutes during the recovery phase following isoflurane-induced overdose. Finally, we constructed a map summarizing multiple states and their transitions which can be utilized to predict and prevent overdose during general anesthesia. The transition phases we identified and algorithm we developed may allow clinicians to prevent inadequate anesthesia, and thus individually tailor anesthetic regimens. 1 Significance statementIn human patients, overdosing during general anesthesia can lead to cognitive impairment. Cortical electro-encephalograms are used to measure the depth of anesthesia. They allow for correction, but not prevention, of overdose. However, data-driven approaches open new possibilities to predict the depth of anesthesia. We established an electro-encephalogram signalprocessing pipeline, and constructed a predictive map representing an ensemble of gradual sedation states during general anesthesia in mice. In particular, we identified key electroencephalogram patterns which anticipate signs of overdose several minutes before they occur. Our results bring a novel paradigm to the medical community, allowing for the development of individually tailored and predictive anesthetic regimens.

neuroscience↗

Ventriculo-arterial uncoupling is associated with VO2 dependency in cardiac surgical patients

BackgroundThe clinical relevance of V-A (un)coupling in critically ill patients is under investigation. In this study we measured the association between V-A coupling and oxygen consumption (VO2) response in patients with acute circulatory instability following cardiac surgery.\n\nMethods and resultsSixty-one cardio-thoracic ICU patients who received fluid challenge or norepinephrine infusion were included. Arterial pressure, cardiac output (CO), heart rate (HR), arterial (EA), and ventricular elastances (EV), total indexed peripheral resistance (TPRi) were assessed before and after hemodynamic interventions. VO2 responders were defined as VO2 increase > 15 %. V-A coupling was evaluated by the ratio EA/EV. Left ventricle stroke work (SW) to pressure volume area (PVA) ratio was calculated. In the overall population, 24 patients (39%) were VO2 responders and 48 patients were uncoupled (i.e., EA/EV ratio > 1.3): 1.9 (1.6-2.4). Most of the uncoupled patients were classified as VO2 responders (28 of 31 patients, p=0.031). Changes in VO2 were correlated with those of TPRi, EA, EA/EV and CO. EA/EV ratio predicted VO2 increase with an AUC of 0.76 [95 % CI: 0.62-0.87]; p=0.001. In multivariate and principal component analyses, EA/EV and SW/PVA ratios were independently associated (P < 0.05) with VO2 response following interventions.\n\nConclusionsVO2 responders were characterized by baseline V-A uncoupling due to high EA and low EV. Baseline EA/EV and SW/PVA ratios were associated with VO2 changes independently of the hemodynamic intervention used. These results further underline the pathophysiological significance of V-A uncoupling in patients with hemodynamic instability.

physiology↗