Resuscitation
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Randomized Controlled Trial
Mechanical Active Compression-Decompression versus Standard Mechanical Cardiopulmonary Resuscitation: A Randomised Haemodynamic Out-of-Hospital Cardiac Arrest Study.
Active compression-decompression cardiopulmonary resuscitation (ACD-CPR) utilises a suction cup to lift the chest-wall actively during the decompression phase (AD). We hypothesised that mechanical ACD-CPR (Intervention), with AD up to 30 mm above the sternal resting position, would generate better haemodynamic results than standard mechanical CPR (Control). ⋯ ClinicalTrials.gov identifier (NCT number): NCT02479152. The Haemodynamic Effects of Mechanical Standard and Active Chest Compression-decompression During Out-of-hospital CPR.
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Accurate and timely prognostication of patients with out-of-hospital cardiac arrest (OHCA) who achieved the return of spontaneous circulation (ROSC) is crucial in clinical decision-making, resource allocation, and communications with next-of-kins. We aimed to develop the Survival After ROSC in Cardiac Arrest (SARICA), a practical clinical decision tool to predict survival in OHCA patients who attained ROSC. ⋯ We developed and internally validated the SARICA score to accurately predict survival of OHCA patients with ROSC at the time of admission. SARICA is clinically practical and developed using an interpretable machine-learning framework. SARICA has unknown generalizability pending external validation studies.
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Whole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the post-cardiac arrest syndrome. Previous studies on the inflammatory effect on circulatory failure after cardiac arrest have either investigated a selected patient group or a limited part of the inflammatory mechanisms. We examined the association between cardiac arrest characteristics and inflammatory biomarkers, and between inflammatory biomarkers and circulatory failure after cardiac arrest, in an unselected patient cohort. ⋯ Inflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.