Circulation, Vol 78, 761-768, Copyright © 1988 by American Heart Association
I Belenkie, R Dani, ER Smith and JV Tyberg
Although stroke volume may decrease markedly after acute pulmonary
embolism, left ventricular end-diastolic pressure (LVEDP) usually changes
very little, which suggests that compliance or contractility or both are
reduced. To test the hypothesis that the altered LV function during
pulmonary embolism is primarily due to reduced preload mediated by
increased pericardial constraint, hemodynamics and chamber dimensions
(measured by sonomicrometry) were assessed in seven anesthetized dogs
during control volume loading, after pulmonary embolism (with autologous
blood clot), and after repeated pulmonary embolism in the volume-loaded
state. The correlation between LVEDP and an index of LVED volume (LVED area
index) throughout a wide range of LVEDP before and after embolism was poor
(mean r = 0.42; range, 0- 0.82). However, the correlation between
transmural LVEDP (LVEDP- directly measured pericardial pressure) and LVED
area index (mean r = 0.78; range, 0.61-0.94) was significantly higher (p =
0.03). Similarly, an index of stroke work (LV area stroke work) correlated
less well (p less than 0.01) with LVEDP (mean r = 0.43; range, 0.07-0.77)
than with transmural LVEDP (mean r = 0.82; range, 0.68-0.92). LV area
stroke work also correlated well with the LV area index (mean r = 0.84;
range, 0.70- 0.95). These data indicate that neither compliance nor
contractility is substantially altered during acute pulmonary embolism. The
altered LV performance is due to reduced LV preload as reflected by a
decrease in transmural LVEDP. This study also demonstrates that LVEDP is a
poor index of LV preload during pulmonary embolism, whereas transmural
LVEDP accurately reflects LVED dimensions.
ARTICLES
Ventricular interaction during experimental acute pulmonary embolism
Department of Medicine, University of Calgary, Alberta, Canada.
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