Out-of-Hospital Cardiac Arrest Detection by Machine Learning Based on the Phonetic Characteristics of the Caller's Voice.

INTRODUCTION: Out-of-hospital cardiac arrest (OHCA) is a major public health issue. The prognosis is closely related to the time from collapse to return of spontaneous circulation. Resuscitation efforts are frequently initiated at the request of emergency call center professionals who are specifically trained to identify critical conditions over the phone. However, 25% of OHCAs are not recognized during the first call. Therefore, it would be interesting to develop automated computer systems to recognize OHCA on the phone. The aim of this study was to build and evaluate machine learning models for OHCA recognition based on the phonetic characteristics of the caller's voice. METHODS: All patients for whom a call was done to the emergency call center of Rennes, France, between 01/01/2017 and 01/01/2019 were eligible. The predicted variable was OHCA presence. Predicting variables were collected by computer-automatized phonetic analysis of the call. They were based on the following voice parameters: fundamental frequency, formants, intensity, jitter, shimmer, harmonic to noise ratio, number of voice breaks, and number of periods. Three models were generated using binary logistic regression, random forest, and neural network. The area under the curve (AUC) was the primary outcome used to evaluate each model performance. RESULTS: 820 patients were included in the study. The best model to predict OHCA was random forest (AUC=74.9, 95% CI=67.4-82.4). CONCLUSION: Machine learning models based on the acoustic characteristics of the caller's voice can recognize OHCA. The integration of the acoustic parameters identified in this study will help to design decision-making support systems to improve OHCA detection over the phone.

New considerations on pathways involved in acute traumatic coagulopathy: the thrombin generation paradox.

Background: An acute traumatic coagulopathy (ATC) is observed in about one third of severely traumatized patients. This early, specific, and endogenous disorder is triggered by the association of trauma and hemorrhage. The early phase of this condition is characterized by the expression of a bleeding phenotype leading to hemorrhagic shock and the late phase by a prothrombotic profile leading to multiple organ failure. The physiopathology of this phenomenon is still poorly understood. Hypotheses of disseminated intravascular coagulation, activated protein C-mediated fibrinolysis, fibrinogen consumption, and platelet functional impairment were developed by previous authors and continue to be debated. The objective of this study was to observe general hemostasis disorders in case of ATC to confront these hypotheses. Method: Four groups of 15 rats were compared: C, control; T, trauma; H, hemorrhage; and TH, trauma and hemorrhage. Blood samples were drawn at baseline and 90 min. Thrombin generation tests, platelet aggregometry, and standard hemostasis tests were performed. Results: Significant differences were observed between the baseline and TH groups for aPTT (17.9 ± 0.8 s vs 24.3 ± 1.4 s, p < 0.001, mean ± SEM), MAP (79.7 ± 1.3 mmHg vs 43.8 ± 1.3 mmHg, p < 0.001, mean ± SEM), and hemoglobin (16.5 ± 0.1 g/dL vs 14.1 ± 0.3 g/dL, p < 0.001, mean ± SEM), indicating the presence of an hemorrhagic shock due to ATC. Compared to all other groups, coagulation factor activities were decreased in the TH group, but endogenous thrombin potential was (paradoxically) higher than in group C (312 ± 17 nM/min vs. 228 ± 23 nM/min; p = 0.016; mean ± SEM). We also observed a subtle decrease in platelet count and function in case of ATC and retrieved an inversed linear relationship between fibrinogen concentration and aPTT (intercept, 26.53 ± 3.16; coefficient, - 3.40 ± 1.26; adjusted R2: 0.1878; p = 0.0123). Conclusions: The clinical-biological profile that we observed, combining normal thrombin generation, fibrinogen depletion, and a hemorrhagic phenotype, reinforced the hypothesis of activated protein C mediated-fibrinolysis. The key role of fibrinogen, but not of the platelets, was confirmed in this study. The paradoxical preservation of thrombin generation suggests a protective mechanism mediated by rhabdomyolysis in case of major trauma. Based on these results, we propose a new conception concerning the pathophysiology of ATC.