Valerianova A, Mlcek M, Malik J, Grus T, Tejkl L, Kolosova B, Lejsek V, Kittnar O
3rd Department of Internal Medicine, General University Hospital in Prague and 1st Faculty of Medicine, Charles University, Prague, Czechia.
Institute of Physiology, 1st Faculty of Medicine, Charles University, Prague, Czechia.
Front Physiol. 2023 Jul 3;14:1180224. doi: 10.3389/fphys.2023.1180224. eCollection 2023.
A large arteriovenous fistula (AVF) is a low-resistant circuit that affects organ perfusion and systemic hemodynamics even in standard conditions. The extent of its' effect in critical states has not been elucidated yet. We used norepinephrine to create systemic vasoconstriction, dobutamine to create high cardiac output, and rapid right ventricle pacing as a model of acute heart failure in a porcine model of high-flow AVF circulation. The protocol was performed on nine domestic female pigs under general anesthesia. AVF was created by connecting two high-diameter ECMO cannulas inserted in the femoral artery and vein. Continuous hemodynamic monitoring was performed throughout the protocol. Three interventions were performed-moderate dose of norepinephrine (0.25 ug/kg/min), moderate dose of dobutamine (10 ug/kg/min) and rapid right ventricle pacing to simulate low cardiac output state with mean arterial pressure under 60 mmHg. Measurements were taken with opened and closed arteriovenous fistula. Continuous infusion of norepinephrine with opened AVF significantly increased mean arterial pressure (+20%) and total cardiac output (CO) (+36%), but vascular resistance remained virtually unchanged. AVF flow (Qa) rise correlated with mean arterial pressure increase (+20%; R = 0.97, = 0.0001). Effective cardiac output increased, leading to insignificant improvement in organ perfusion. Dobutamine substantially increased cardiac output with insignificant effect on AVF flow and mean arterial pressure. Carotid artery blood flow increased significantly after dobutamine infusion by approximately 30%, coronary flow velocity increased significantly only in closed AVF state. The effective cardiac output using the heart failure model leading to decrease of carotid artery flow and worsening of brain and peripheral tissue oximetry. AVF blood flow also dropped significantly and proportionally to pressure, but Qa/CO ratio did not change. Therefore, the effective cardiac output decreased. In abovementioned extreme hemodynamic conditions the AVF flow was always directly proportional to systemic perfusion pressure. The ratio of shunt flow to cardiac output depended on systemic vascular resistance. These experiments highlight the detrimental role of a large AVF in these critical conditions' models.
大型动静脉瘘（AVF）是一种低阻力循环，即使在标准条件下也会影响器官灌注和全身血流动力学。其在危急状态下的影响程度尚未阐明。我们使用去甲肾上腺素引起全身血管收缩，多巴酚丁胺产生高心输出量，并在高流量AVF循环的猪模型中进行快速右心室起搏作为急性心力衰竭的模型。该方案在9只雌性家猪全身麻醉下进行。通过连接插入股动脉和静脉的两个大口径体外膜肺氧合（ECMO）插管来创建AVF。在整个方案过程中进行连续血流动力学监测。进行了三项干预措施——中等剂量的去甲肾上腺素（0.25微克/千克/分钟）、中等剂量的多巴酚丁胺（10微克/千克/分钟）以及快速右心室起搏以模拟平均动脉压低于60毫米汞柱的低心输出量状态。在动静脉瘘开放和闭合的情况下进行测量。动静脉瘘开放时持续输注去甲肾上腺素可显著提高平均动脉压（+20%）和总心输出量（CO）（+36%），但血管阻力基本保持不变。AVF血流量（Qa）的增加与平均动脉压的升高相关（+20%；R = 0.97，P = 0.0001）。有效心输出量增加，导致器官灌注有不显著的改善。多巴酚丁胺显著增加心输出量，对AVF血流量和平均动脉压影响不显著。输注多巴酚丁胺后颈动脉血流量显著增加约30%，仅在动静脉瘘闭合状态下冠状动脉血流速度显著增加。使用心力衰竭模型导致有效心输出量下降，颈动脉血流减少，脑和外周组织血氧饱和度恶化。AVF血流量也显著下降且与压力成比例，但Qa/CO比值未改变。因此，有效心输出量下降。在上述极端血流动力学条件下，AVF血流量始终与全身灌注压成正比。分流流量与心输出量的比值取决于全身血管阻力。这些实验突出了大型AVF在这些危急状态模型中的有害作用。
