Cardiovascular Center, Na Homolce Hospital, Roentgenova 2, 15000, Prague, Czech Republic.
Department of Physiology, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.
Sci Rep. 2022 Oct 12;12(1):17076. doi: 10.1038/s41598-022-21501-z.
Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Eight female swine (45 kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure-volume catheter. Data are expressed as median (interquartile range). Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9-3.1) L/min and LV ejection fraction to 15.2% (10.5-19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2-34.9) to 56.0 (51.9-73.3) mmHg (P ˂ 0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2-40.0) to 19.1 (15.2-29.0) mmHg (P ˂ 0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0-53.4) to 72.5 (51.4-77.1) mmHg (P ˂ 0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7-19.1) to 20.8 (16.3-25.6) mmHg (P ˂ 0.01). Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.
体外膜肺氧合（VA-ECMO）在治疗心源性休克（CS）患者中被广泛应用。然而，增加 VA-ECMO 血流量（EBF）可能会显著损害左心室（LV）功能。本研究的目的是在猪模型中评估 VA-ECMO 在伴有严重主动脉瓣狭窄（AS）或二尖瓣反流（MR）的急性 CS 中对 LV 功能的影响。8 只雌性猪（45kg）在全身麻醉和机械通气下植入 VA-ECMO。通过全球心肌缺氧诱导急性 CS。随后，通过阻塞主动脉瓣模拟严重 AS，通过机械破坏二尖瓣诱导严重 MR。使用动脉和静脉导管、肺动脉导管和 LV 压力-容积导管，在不同的 EBF 速率（1 至 4 L/min）下测量血流动力学和 LV 功能变量。数据表示为中位数（四分位数范围）。心肌缺氧导致心输出量降至 2.7（1.9-3.1）L/min 和 LV 射血分数降至 15.2%（10.5-19.3%）。在严重 AS 中，将 EBF 从 1 增加到 4 L/min 与平均动脉压（MAP）的显著升高相关，从 33.5（24.2-34.9）mmHg 升高到 56.0（51.9-73.3）mmHg（P < 0.01）。然而，LV 容积（舒张末期、收缩末期、冲程）保持不变，LV 舒张末期压（LVEDP）从 24.9（21.2-40.0）mmHg 显著降低到 19.1（15.2-29.0）mmHg（P < 0.01）。在严重 MR 中，将 EBF 增加导致 MAP 从 49.0（28.0-53.4）mmHg 显著升高到 72.5（51.4-77.1）mmHg（P < 0.01）；LV 容积保持稳定，LVEDP 从 17.1（13.7-19.1）mmHg 升高到 20.8（16.3-25.6）mmHg（P < 0.01）。本研究结果表明，瓣膜性心脏病的存在可能减轻 CS 中 VA-ECMO 对 LV 功能的负面影响。严重 AS 完全防止 LV 过载，并且在严重 MR 中也检测到部分保护，尽管这是以增加 LVEDP 为代价的，因此肺水肿的风险更高。
