理解的对吗？

Both Eaand Eesmay change in septic shock. Myocardial depression impairing both diastolic compliance and contractility are well described. Pathological vasodilation, referred to as vasoplegia, often is a hall mark of septic shock. Presumably this is because of primary alterations signally between the vascular endothelium and smooth muscle cells as endogenous catecholamine levels are usually high. Both adrenergic receptors down regulation. Smooth muscle cell hyperpolarization and loss of endogenous vasopressin have been implemented in the pathophysiological process of septic vasoplegia. However, the most common haemodynamic profile of septic shock in treated critically ill patients is an increase in Ea, usually consequently to the pharmacological vasoconstriction induced by the infusion of exogenous vasoactive drugs, and an associated decrease in Ees, because of septic cardiomyopathy. Although in the majority of the septic shock patients, Ea/Eesis greater than 1 and the system is uncoupled, some patients show a normal Ea/Ees because of either an appropriate therapeutic approach restored this coupling or the presence of a normal cardiac function despite sepsis [2]. In this context, the assessment of ventriculoarterial coupling in septic shock is useful not only to evaluate the underlying pathophysiology of the haemodynamic failure, but to also predict the response therapy and to assess the effectiveness of the therapeutic strategies once given.

脓毒症休克时Ea和Ees均可发生改变。心肌抑制对舒张期顺应性和收缩力均有影响。病理性血管扩张，或称为血管麻痹，通常是脓毒症休克的一个显著特征。这可能是因为当内源性儿茶酚胺水平通常较高时，血管内皮细胞和平滑肌细胞之间发生了显著的原发性改变。两种肾上腺素能受体都下调。平滑肌细胞超极化和内源性血管加压素的丢失已经在脓毒症血管***病理生理过程中体现。然而，在治疗危重病人时最常见的脓毒性休克血流动力学特征是增加了Ea，往往是由于输注了外源性血管活性药物而引起药理性血管收缩的结果，而由于脓毒性心肌病则引起了相应Ees下降。

由于输注了外源性血管活性药物而引起药理性血管收缩    从而   增加了Ea(动脉弹性)，而脓毒性心肌病引起了相应Ees（左室(LV)收缩期末期弹性）下降？对吗？谢谢