Saline volume expansion and cardiovascular physiology novel observations, old explanations, and new questions 英文参考文献.docVIP
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Saline volume expansion and cardiovascular physiology novel observations, old explanations, and new questions 英文参考文献
Available online /content/8/5/315
Commentary
Saline volume expansion and cardiovascular physiology: novel
observations, old explanations, and new questions
James L Robotham
Professor and Chairman, Department of Anesthesiology, University of Rochester, Rochester, New York, USA
Corresponding author: James L Robotham, james_robotham@
Published online: 1 September 2004
Critical Care 2004, 8:315-318 (DOI 10.1186/cc2944)
This article is online at /content/8/5/315
? 2004 BioMed Central Ltd
Related to Research by Kumar et al., see issue 8.3, page 201
Abstract
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 ela
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