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左侧心力衰竭伴与不伴静脉-动脉体外膜肺氧合支持的左右心室相互作用:一项模拟研究。

Right-Left Ventricular Interaction in Left-Sided Heart Failure With and Without Venoarterial Extracorporeal Membrane Oxygenation Support-A Simulation Study.

机构信息

From the Department of Intensive Care Medicine, University Medical Center Utrecht, Utrecht, the Netherlands.

Anaesthesiology and Intensive Care, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

出版信息

ASAIO J. 2021 Mar 1;67(3):297-305. doi: 10.1097/MAT.0000000000001242.

DOI:10.1097/MAT.0000000000001242
PMID:33627604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7908866/
Abstract

Left ventricular (LV) dilatation is commonly seen with LV failure and is often aggravated during venoarterial extracorporeal membrane oxygenation (VA ECMO). In this context, the intricate interaction between left and right heart function is considered to be of pivotal importance, yet mechanistically not well understood. We hypothesize that a preserved or enhanced right heart contractility causes increased LV loading both with and without VA ECMO. A closed-loop in-silico simulation model containing the cardiac chambers, the pericardium, septal interactions, and the pulmonary and systemic vascular systems with an option to connect a simulated VA ECMO circuit was developed. Right ventricular contractility was modified during simulation of severe LV failure with and without VA ECMO. Left atrial pressures increased from 14.0 to 23.8 mm Hg without VA ECMO and from 18.4 to 27.0 mm Hg under VA ECMO support when right heart contractility was increased between end-systolic elastance 0.1 and 1.0 mm Hg/ml. Left-sided end-diastolic volumes increased from 125 to 169 ml without VA ECMO and from 150 to 180 ml with VA ECMO. Simulations demonstrate that increased diastolic loading of the LV may be driven by increased right ventricular contractility and that left atrial pressures cannot be interpreted as a reflection of the degree of LV dysfunction and overload without considering right ventricular function. Our study illustrates that modelling and computer simulation are important tools to unravel complex cardiovascular mechanisms underlying the right-left heart interdependency both with and without mechanical circulatory support.

摘要

左心室(LV)扩张常见于 LV 衰竭,并在静脉-动脉体外膜肺氧合(VA ECMO)期间经常加重。在这种情况下,左右心功能之间的复杂相互作用被认为至关重要,但在机制上尚未得到很好的理解。我们假设右心收缩力的保留或增强会导致 LV 负荷增加,无论是在有 VA ECMO 还是没有 VA ECMO 的情况下。开发了一种包含心脏腔室、心包、间隔相互作用以及肺和全身血管系统的闭环仿真模型,并具有连接模拟 VA ECMO 回路的选项。在模拟严重 LV 衰竭时,右心室收缩力在有和没有 VA ECMO 的情况下发生变化。当右心室收缩力在终末期弹性 0.1 到 1.0 毫米汞柱/毫升之间增加时,左心房压力从 14.0 毫米汞柱增加到 23.8 毫米汞柱(无 VA ECMO),从 18.4 毫米汞柱增加到 27.0 毫米汞柱(有 VA ECMO 支持)。左心室舒张末期容积从 125 毫升增加到 169 毫升(无 VA ECMO),从 150 毫升增加到 180 毫升(有 VA ECMO)。模拟表明,LV 的舒张性负荷增加可能是由右心室收缩力增加引起的,并且如果不考虑右心室功能,就不能将左心房压力解释为 LV 功能障碍和过载程度的反映。我们的研究表明,建模和计算机模拟是揭示有和没有机械循环支持时右-左心相互依存的复杂心血管机制的重要工具。

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