Why the study?
Does plasma volume expansion with dextran characterize the left ventricular diastolic capacity and pressure-volume relationship in humans?
Does plasma volume expansion with dextran characterize the left ventricular diastolic capacity and pressure-volume relationship in humans?
The study demonstrates that the human left ventricle has a finite diastolic capacity, with minimal volume increases occurring once end-diastolic pressure exceeds 20 mm Hg.
Answers are grounded in this paper and cite their sources.
May limit volume responsiveness once LVEDP exceeds 20 mm Hg; leaves open validation in disease states and clinical decision-making.
Plasma volume expansion with 500 ml of low-molecular-weight dextran was used in 27 patients (nine normal subjects, 13 patients with ischemic heart disease, four with aortic stenosis and one with cardiomyopathy) to increase left ventricular end-diastolic pressure (LVEDP) from a control value of 12.4 +/- 7.0 mm Hg (mean +/- SD) to 23.3 +/- 7.0 mm Hg and end-diastolic volume (EDV) from 84.0 +/- 23.8 ml/m2 to 97.6 +/- 22.9 ml/m2. EDV-LVEDP curves constructed for 12 patients from multiple angiograms at progressively increasing LVEDPs during plasma volume expansion showed an initial part where EDV increased in parallel with LVEDP and a final steep or perpendicular part where EDV increased minimally or not at all as LVEDP exceeded 20 mm Hg. Exponential equations were used to fit diastolic volume-pressure data obtained with catheter-tip manometers in seven patients: the exponential constant, k, was 0.012-0.044 ml-1 and was inversely related to EDV (Spearman's rank correlation coefficient = -1). For comparable EDV, there were no differences in k values between normal subjects and patients with a variety of heart diseases.
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Flessas et al. (1982) studied this question.
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