帮忙看一下？谢谢

In a follow-on study Guarracino et al. recruited septic shock patients prior to initial resuscitation and measured Ea, Eesand a variety of other dynamic haemodynamic parameters sequentially during the initial course of sepsis resuscitation, based on the Surviving Sepsis Guidelines. Those guidelines treat all patients using a common protocol of 30 ml/kg crystalloids, followed by norepinephrine, if still hypotensive, and dobutamine if still unstable on norepinephrine. Although these current guidelines focus on the early resuscitation in order to restore haemodynamic stability providing an adequate CO and a sufficient mean arterial pressure to provide tissue perfusion, less is known about the treatment of the septic patients who are not responsive to the volume expansion. As multifactorial pathophysiologic mechanisms underlying the haemodynamic instability occur in septic shock, using a common approach, even in the initial resuscitation period may not be as effective as one guided by known pathophysiologic state and the degree of volume responsiveness with respect to the conventional functional haemodynamic monitoring [12]. Not surprisingly, many studies have documented a wide variability in the cardiovascular response to the volume expansion in septic shock patients. Guarracino et al. [3 &&] hypothesized that the pretreatment cardiovascular state (reserve, functionality) would accurately predict subsequent response to protocolized therapy. They submitted 55 septic shock patients to advanced haemodynamic monitoring and bedside echocardiographic assessment of Ea, Eesand the associated cardiovascular-derived dynamic parameters, like pulse pressure variation (PPV), SV variation (SVV) and dynamic arterial elastance (Eadyn), in order to achieve a deeper understanding of the underlying mechanisms of the haemodynamic instability and to investigate the further response to the recommended therapy. Eeswas calculated by the method of Chen et al. and Eawas calculated as 0.9 $ (systolic arterial pressure/SV). To get a further understanding of the role ventriculoarterial coupling would have on myocardial energetics, they also calculated LV efficiency estimated as the ratio of external work to total cardiac work during cardiac cycle, one of the main determinants of the cardiac performance, as shown in Fig. 1. Impressively, ventriculoarterial coupling was tightly correlated to LV efficiency, such that inefficiency was associated with ventriculoarterial uncoupling. The results of the study confirmed the wide variability of the cardiovascular system response to the treatment in the septic shock patients according to the Surviving Sepsis campaign recommendation. The majority of the septic patients increased their CO in response to the initial 30 ml/kg fluid bolus and also increased their mean arterial pressure (MAP) in proportion to the preresuscitation pulse pressure variation value, confirming the predictive value of the baseline PPV and SVV, as previously [13]. In these patients, the restoration of the circulating volume was sufficient to increase cardiac output and, although Eesis a load-independent determinant of LV contractility, both Eesand VAC improved. The reason why Eesimproved is unclear but probably because of reversing hypotension, increasing coronary perfusion pressure. Furthermore, the assessment of pretreatment VAC was correlated with the patients’ response to the use of norepinephrine in those patients who remained hypotensive after volume expansion. Regrettably, the increase in Ea induced by the norepinephrine administration lead to a restoration of ventriculoarterial uncoupling [14]. While, patients with high Ees and normal ventriculoarterial coupling tolerated the increase in LV afterload induced by norepinephrine infusion resulting in higher cardiac output [15]. The infusion of dobutamine induced an increase in cardiac output and improved ventriculoarterial coupling, with an effect on MAP emphasizing the role of inotropic support in septic shock patients. The conclusion was that the cardiovascular function and reserve of the critically septic shock patients examined prior to treatment can guide an individualized management of volume expansion in order to predict the response to the fluid resuscitation and the therapeutic approach to septic shock. Ventriculoarterial decoupling occurring in septic shock can depend on both Eaand Eeschanges, and Guarracino et al. [3 &&] demonstrated that ventriculoarterial decoupling can occur even in patients with normal LVEF, although the majority of the enrolled septic patients showed a low LVEF. Either preexisting cardiac dysfunction or sepsis-induced myocardial depression can affect the haemodynamic course in septic shock.

在后续研究中，Guarracino等人招募了初始复苏前的脓毒症休克患者，并根据现有脓毒症指南，在脓毒症初始复苏过程中依次测量了Ea、Ees和一系列其他动态的血流动力学参数。指南推荐使用30ml/kg晶体，然后是去甲肾上腺素(如果持续低血压)和多巴酚丁胺(如果去甲肾上腺素基础上仍不稳定)的通用方案治疗所有患者。虽然目前的指南侧重于早期复苏，以恢复血流动力学的稳定性，提供足够的心输出量和有效的平均动脉压力来保证组织灌注，但对那些对容量增加无反应的脓毒症患者知之甚少。由于脓毒性休克时血流动力学不稳定的多种病理生理机制存在，即使在初始复苏阶段采用一种方法，相比传统的功能性血流动力学监测而言，这也可能不是一种基于已知病理生理状态和容量反应程度的有效方法。不出所料，许多研究已经证明脓毒症休克患者心血管对容量扩张的反应存在广泛的变异性。Guarracino等人假设治疗前的心血管状态(储备状态、功能状态)可以准确预测后续程序化治疗的反应。为了更深入地理解血液动力学不稳定的潜在机制以及进一步探索对推荐治疗的反应，他们纳入了55例脓毒性休克患者，采用高级血流动力学监测和床旁超声心动图评估Ea、Ees以及相关的心血管派生的动态参数，如脉压变异度(PPV), 每搏量变异度（SVV)以及动态动脉弹性(Eadyn)。采用Chen法计算Ees，Ea计算为0.9*(收缩期动脉压/ SV)。为了加深心室动脉藕联对心肌功能影响的理解，他们还计算了左心室效率，估计为心动周期内外部做功与心脏总做功的比率，这是心脏功能的主要决定因素之一，如图1所示。值得注意的是，心室-动脉藕联与左室效率密切相关，低效率状态与心室-动脉失藕联有关。研究结果证实，根据脓毒症指南推荐，脓毒症休克患者的心血管系统对治疗的反应存在广泛的变异性。大多数脓毒症休克患者在初始的30ml/kg液体时增加了心输出量，也增加了平均动脉压(MAP)，成比例增加了复苏前脉搏压力变异值，确认了正如前面所说的基线PPV和SVV的预测价值。在这些患者中，循环容量的恢复足以增加心输出量，虽然Ees是一个左室收缩力的非压力依赖性指标，但Ees和VAC均有改善。Ees改善的原因尚不清楚，很可能是由于逆转了低血压，增加了冠状动脉灌注压。此外，在容量负荷后始终存在低血压的患者中，治疗前VAC的评估与患者对去甲肾上腺素的反应相关。遗憾的是，去甲肾上腺素引起的Ea增加促使心室动脉失藕联[14]的恢复，而高Ees患者和正常心室动脉藕联的患者可以耐受因去甲肾上腺素输注引起的左室后负荷增加而引起的心输出量增加。多巴酚丁胺的输注增加了心输出量，改善了心室动脉耦联，对MAP的影响强化了正性肌力药物在脓毒症休克患者中的作用。因此重症脓毒症休克患者治疗前检查心血管功能及储备情况，可指导个体化容量复苏管理，预测液体复苏的反应性及脓毒症休克的治疗策略。脓毒性休克时发生的心室动脉失藕联可能依赖于Ea和Ees的变化，Guarracino等证明，尽管大多数入组脓毒性休克患者存在较低的LVEF，但即使在LVEF正常的患者中，心室动脉失藕联也可能发生。脓毒症休克时，无论是先前存在的心功能障碍还是脓毒症引起的心肌抑制，都会影响血流动力学过程。

老师，患者有高的收缩期末期弹性阻力(Ees)和正常的心室动脉藕联，那么他的动脉弹性阻力(Ea)也应该是大的，为什么输注去甲肾上腺素还是可以增加心输出量呢？谢谢