Journal of critical care · 2026
Impact of fluid expansion on ventriculo-arterial coupling during circulatory failure.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Bagate François, Masi Paul, Cicetti Marta, Lapenta Cristina, Mekontso Dessap Armand
Аннотация
BACKGROUND: While the effects of fluid expansion (FE) on preload are well established, its impact on cardiac afterload and ventriculo-arterial coupling (VAC) remains less defined. This study aimed to assess the effects of FE on VAC and its components-arterial elastance (Ea) and left ventricular end-systolic elastance (Ees)-and to evaluate the influence of preload responsiveness.
METHODS: In this prospective observational study conducted in a French ICU, patients with acute circulatory failure requiring FE (500 mL crystalloid bolus) were included. Transthoracic echocardiography was performed before and after FE to estimate VAC, Ea, and Ees using the single-beat method. Fluid responsiveness was defined as an increase ≥10% in the velocity-time integral of the left ventricular outflow tract.
RESULTS: Thirty-eight patients were enrolled; 17 (45%) were fluid responders. At baseline, responders had higher Ea and Ees than non-responders, while VAC was comparable between groups. In the overall population, FE did not significantly modify VAC or its components. In responders, Ea decreased (1.63 [1.19-2.05] to 1.46 [1.10-1.96], p = 0.0007), whereas it increased in non-responders (1.31 [0.99-1.67] to 1.37 [1.02-1.78], p = 0.003). Ees remained unchanged. VAC improved significantly in responders (1.26 [0.82-1.63] to 1.09 [0.79-1.43], p = 0.03). Conclusion In acute circulatory failure, the effects of FE on VAC depend on preload responsiveness. Responders exhibit improved VAC driven by reduced Ea, while non-responders show increased Ea without significant VAC modification. Ees remains unaffected in both groups.
METHODS: In this prospective observational study conducted in a French ICU, patients with acute circulatory failure requiring FE (500 mL crystalloid bolus) were included. Transthoracic echocardiography was performed before and after FE to estimate VAC, Ea, and Ees using the single-beat method. Fluid responsiveness was defined as an increase ≥10% in the velocity-time integral of the left ventricular outflow tract.
RESULTS: Thirty-eight patients were enrolled; 17 (45%) were fluid responders. At baseline, responders had higher Ea and Ees than non-responders, while VAC was comparable between groups. In the overall population, FE did not significantly modify VAC or its components. In responders, Ea decreased (1.63 [1.19-2.05] to 1.46 [1.10-1.96], p = 0.0007), whereas it increased in non-responders (1.31 [0.99-1.67] to 1.37 [1.02-1.78], p = 0.003). Ees remained unchanged. VAC improved significantly in responders (1.26 [0.82-1.63] to 1.09 [0.79-1.43], p = 0.03). Conclusion In acute circulatory failure, the effects of FE on VAC depend on preload responsiveness. Responders exhibit improved VAC driven by reduced Ea, while non-responders show increased Ea without significant VAC modification. Ees remains unaffected in both groups.