Department of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Department of Anaesthesiology and Intensive Care Medicine, Institute of Clinical Sciences at the Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Shock. 2019 May;51(5):650-658. doi: 10.1097/SHK.0000000000001197.
Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is gaining widespread use in the treatment of severe cardiorespiratory failure. Blood volume expansion is commonly used to increase ECMO flow (QECMO), with risk of positive fluid balance and worsening prognosis. We studied the effects of vasoconstriction on recruitment of blood volume as an alternative for increasing QECMO, based on the concepts of venous return.
In a closed chest, centrally cannulated porcine preparation (n = 9) in ventricular fibrillation and VA-ECMO with vented left atrium, mean systemic filling pressure (MSFP), and venous return driving pressure (VRdP) were determined in Euvolemia, during Vasoconstriction (norepinephrine 0.05, 0.125, and 0.2 μg/kg/min) and after Volume Expansion (3 boluses of 10 mL/kg Ringer's lactate). Maximum achievable QECMO was examined.
Vasoconstriction and Volume Expansion both increased maximum achievable QECMO, delivery of oxygen (DO2), and MSFP, but right atrial pressure increased in parallel. VRdP did not change. The vascular elastance curve was shifted to the left by Vasoconstriction, with recruitment of stressed volume. It was shifted to the right by Volume Expansion with direct expansion of stressed volume. Volume Expansion decreased resistance to venous return and pump afterload.
In a circulation completely dependent on ECMO support, maximum achievable flow directly depended on the vascular factors governing venous return-i.e., closing conditions, stressed vascular volume and the elastance and resistive properties of the vasculature. Both treatments increased maximum achievable ECMO flow at stable DO2, via increases in stressed volume by different mechanisms. Vascular resistance and pump afterload decreased with Volume Expansion.
静脉-动脉体外膜肺氧合（VA-ECMO）在治疗严重心肺衰竭方面的应用越来越广泛。为了增加 ECMO 流量（QECMO），通常会进行血容量扩充，但这存在正液平衡和预后恶化的风险。我们基于静脉回流的概念，研究了血管收缩对血量募集的影响，以替代增加 QECMO 的方法。
在胸部闭合、中心插管的猪模型（n = 9）中，模型处于心室颤动和 VA-ECMO 状态，左心房通气，在正常血容量、血管收缩（去甲肾上腺素 0.05、0.125 和 0.2 μg/kg/min）和血容量扩充（3 次 10 mL/kg 林格氏乳酸盐）期间，测定平均全身充盈压（MSFP）和静脉回流驱动压（VRdP）。研究最大可实现 QECMO。
血管收缩和血容量扩充都增加了最大可实现 QECMO、氧输送（DO2）和 MSFP，但右心房压力也相应增加。VRdP 没有变化。血管弹性曲线因血管收缩而向左移位，募集了应激容积。血容量扩充直接扩充了应激容积，使曲线向右移位。血容量扩充降低了静脉回流和泵后负荷的阻力。
在完全依赖 ECMO 支持的循环中，最大可实现流量直接取决于控制静脉回流的血管因素，即关闭条件、应激血管容积以及脉管系统的弹性和阻力特性。这两种治疗方法通过不同的机制增加了最大可实现的 ECMO 流量，同时保持稳定的 DO2。血容量扩充降低了血管阻力和泵后负荷。
