Masi Paul, Tchatat Wangueu Lionel, Bagate François, Plesa Alexandra, Folliguet Thierry, Mekontso Dessap Armand
AP-HP, Hôpitaux Universitaires Henri-Mondor, Service de Médecine Intensive Réanimation, 94010, Créteil, France.
Univ Paris Est Créteil, CARMAS, 94010, Créteil, France.
Cardiovasc Drugs Ther. 2024 Dec 30. doi: 10.1007/s10557-024-07650-5.
Hypoxemia is a risk factor for mortality and long-term neuropsychological impairment during severe acute respiratory distress syndrome (ARDS). Veno-venous extracorporeal membrane oxygenation (VV-ECMO) is a potential treatment for such cases but may not suffice. We aimed to evaluate the effects of pharmacological interventions for cardiac output (CO) control using ivabradine or beta-blockers for refractory hypoxemia during VV-ECMO.
The study involved retrospective analysis of consecutive patients with severe ARDS who underwent VV-ECMO at a tertiary university hospital between March 2020 and May 2022. Patients with refractory hypoxemia under VV-ECMO were included. Pharmacological interventions included ivabradine and/or short half-life beta-blockers. The primary endpoint was the change in ECMO flow/CO ratio and secondary endpoints were changes in macrocirculation (mean arterial pressure), oxygenation [arterial saturation (SaO) and oxygen transport (DO)] and tissue hypoxia (lactate levels).
Out of 70 patients on VV-ECMO, ten had refractory hypoxemia under VV-ECMO and received pharmacological interventions to control CO. The ECMO flow/CO ratio significantly increased with pharmacological intervention overall (from 60% [50-66] to 69% [61-81], p = 0.02), as well as with beta-blockers or ivabradine individually. However, DO decreased, especially with beta-blockers and to some extent with ivabradine. There were no reported immediate adverse events, and lactate levels remained below the anaerobic threshold.
Ivabradine and beta-blockers were clinically well-tolerated and improved the ECMO flow/CO ratio in patients with refractory hypoxemia during VV-ECMO. However, the improvement of arterial oxygenation was associated with decreased DO.
低氧血症是严重急性呼吸窘迫综合征（ARDS）患者死亡及长期神经心理功能障碍的危险因素。静脉-静脉体外膜肺氧合（VV-ECMO）是此类病例的一种潜在治疗方法，但可能并不充分。我们旨在评估使用伊伐布雷定或β受体阻滞剂进行心输出量（CO）控制的药物干预对VV-ECMO期间难治性低氧血症的影响。
本研究对2020年3月至2022年5月在一家三级大学医院接受VV-ECMO治疗的连续性重症ARDS患者进行回顾性分析。纳入VV-ECMO期间出现难治性低氧血症的患者。药物干预包括伊伐布雷定和/或半衰期短的β受体阻滞剂。主要终点是体外膜肺氧合（ECMO）流量/心输出量（CO）比值的变化，次要终点是体循环（平均动脉压）、氧合[动脉血氧饱和度（SaO）和氧输送（DO）]及组织缺氧（乳酸水平）的变化。
在接受VV-ECMO治疗的70例患者中，有10例在VV-ECMO期间出现难治性低氧血症并接受了控制CO的药物干预。总体而言，药物干预使ECMO流量/CO比值显著增加（从60%[50-66]增至69%[61-81]，p=0.02），单独使用β受体阻滞剂或伊伐布雷定时也有同样效果。然而，DO下降，尤其是使用β受体阻滞剂时，伊伐布雷定在一定程度上也会导致DO下降。未报告即时不良事件，乳酸水平仍低于无氧阈值。
伊伐布雷定和β受体阻滞剂在临床上耐受性良好，可改善VV-ECMO期间难治性低氧血症患者的ECMO流量/CO比值。然而，动脉氧合的改善与DO降低相关。
