Robotham James L
Department of Anesthesiology, University of Rochester, Rochester, New York, USA.
Crit Care. 2004 Oct;8(5):315-8. doi: 10.1186/cc2944. Epub 2004 Sep 1.
In a clinical investigation, Kumar and coworkers reported the hemodynamic events that accompany plasma volume expansion over 3 hours in healthy adult volunteers, and found that increases in stroke volume (SV) may be related to increases in left ventricular (LV)/right ventricular (RV) end-diastolic volume, as they expected, but also to decreases in LV/RV end-systolic volume. The latter finding suggests increased contractility and/or decreased afterload, which do not fit with their perception that clinicians ascribe increases in SV to increases in end-diastolic volume based on Starling's work. Increased ejection fraction and decreased vascular resistances were also observed. The same authors recently reported novel data suggesting that reduced blood viscosity may account for the observed reduction in vascular resistances with saline volume expansion. However, the variances in preload and afterload, along with uncertainty in estimates of contractility, substantially limit their ability to define a primary mechanism to explain decreases in LV end-systolic volume. A focus on using ejection fraction to evaluate the integrated performance of the cardiovascular system is provided to broaden this analytic perspective. Sagawa and colleagues described an approach to estimate the relationship, under clinical conditions, between ventricular and arterial bed elastances (i.e. maximal ventricular systolic elastance [Emax] and maximal arterial systolic elastance [Ea]), reflecting ventricular-arterial coupling. I used the mean data provided in one of the reports from Kumar and coworkers to calculate that LV Emax decreased from 1.09 to 0.96 mmHg/ml with saline volume expansion, while Ea decreased from 1.1 to 0.97 mmHg/ml and the SV increased (i.e. the increase in mean SV was associated with a decrease in mean afterload while the mean contractility decreased). The results reported by Kumar and coworkers invite further studies in normal and critically ill patients during acute saline-induced plasma volume expansion and hemodilution. If reduced viscosity decreases afterload, then this raises the questions by what mechanism, and what is the balance of benefit and harm associated with reduced blood viscosity affecting oxygen delivery? Why the mean Emax might decrease must be evaluated with respect to benefit in reducing ventricular work or a negative inotropic effect of saline.
在一项临床研究中，库马尔及其同事报告了健康成年志愿者在3小时内血浆容量扩张时伴随的血流动力学事件，发现正如他们所预期的，每搏输出量（SV）的增加可能与左心室（LV）/右心室（RV）舒张末期容积的增加有关，但也与LV/RV收缩末期容积的减少有关。后一个发现提示收缩力增加和/或后负荷降低，这与他们的认知不符，即临床医生基于斯塔林的研究将SV的增加归因于舒张末期容积的增加。还观察到射血分数增加和血管阻力降低。同一组作者最近报告了新的数据，表明血液粘度降低可能是盐水扩容时观察到的血管阻力降低的原因。然而，前负荷和后负荷的变化，以及收缩力估计的不确定性，极大地限制了他们确定解释LV收缩末期容积减少的主要机制的能力。文中提供了一种关注使用射血分数来评估心血管系统综合性能的方法，以拓宽这一分析视角。佐川及其同事描述了一种在临床条件下估计反映心室 - 动脉耦合的心室和动脉床弹性（即最大心室收缩弹性[Emax]和最大动脉收缩弹性[Ea]）之间关系的方法。我利用库马尔及其同事的一份报告中提供的平均数据计算得出，随着盐水扩容，LV Emax从1.09降至0.96 mmHg/ml，而Ea从1.1降至0.97 mmHg/ml，且SV增加（即平均SV的增加与平均后负荷的降低相关，而平均收缩力降低）。库马尔及其同事报告的结果促使人们对正常和重症患者在急性盐水诱导的血浆容量扩张和血液稀释期间进行进一步研究。如果粘度降低会降低后负荷，那么这就引发了以下问题：通过何种机制，以及血液粘度降低影响氧输送时利弊的平衡是怎样的？必须从减少心室做功的益处或盐水的负性肌力作用方面评估平均Emax可能降低的原因。
