Circulation, Vol 80, 178-188, Copyright © 1989 by American Heart Association
I Belenkie, R Dani, ER Smith and JV Tyberg
Volume loading is used to treat hemodynamically compromised patients with
acute pulmonary embolism despite data to suggest that volume loading after
embolism might cause a leftward shift of the ventricular septum with a
subsequent decrease in left ventricular (LV) end- diastolic volume and
stroke work. We studied 10 closed-chest, anesthetized, and ventilated dogs
to assess the effects of volume loading after pulmonary embolism caused by
autologous clot. LV, right ventricular, and right atrial pressures as well
as LV anteroposterior, septum-to-right ventricular, and septum-to-LV free
wall diameters (sonomicrometry) were measured. Pericardial pressure was
measured with flat, liquid-containing balloons. The effects of volume
loading were assessed before embolism, after one episode of embolization,
and after repeated embolizations. The LV area index (as a reflection of LV
volume) increased during volume loading before embolism (2,870 +/- 430 to
3,080 +/- 520 mm2; p less than 0.05), did not change significantly during
infusion of fluid after one embolization (2,850 +/- 470 to 2,860 +/- 500
mm2; p = NS), and decreased significantly during volume expansion after
repeated embolizations (2,760 +/- 440 to 2,660 +/- 420 mm2; p less than
0.01). An index of LV stroke work increased (188 +/- 85 to 260 +/- 101 mm
Hg x mm2; p less than 0.05), did not change significantly (188 +/- 39 to
203 +/- 52 mm Hg x mm2; p = NS), and decreased markedly (133 +/- 64 to 45
+/- 27 mm Hg x mm2; p less than 0.001) before embolism, after one
embolization, and after repeated embolizations, respectively. The decrease
in LV area index during volume loading after repeated embolizations was
associated with an increase in septum-to-right ventricular free wall
diameter (31 +/- 8 to 34 +/- 8 mm; p = 0.001) and a decrease in the
septum-to-LV free wall diameter (44 +/- 5 to 42 +/- 5 mm; p less than
0.001), whereas the LV anteroposterior diameter did not change (62 +/- 5 to
63 +/- 5 mm; p = NS). This is compatible with a leftward septal shift being
partially responsible for the decrease in LV end-diastolic volume; such a
shift would be expected with the observed decrease in transseptal end-
diastolic pressure gradient (-3 +/- 2 to -5 +/- 2 mm Hg; p = 0.001). In
addition, after repeated embolizations, LV transmural pressure decreased in
response to the volume load reflecting a marked increase in pericardial
pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Effects of volume loading during experimental acute pulmonary embolism
Department of Medicine, Faculty of Medicine, University of Calgary, Alberta, Canada.
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