Decreased right ventricle (RV) output results in decreased left ventricle e
nd-diastolic volume (LVEDV) and output by series interaction. Direct ventri
cular interaction may also have a major effect on LV function. Thus, decrea
sed LVEDV caused by reduced RV output may be further reduced by a leftward
septal shift and pericardial constraint. This has been shown to be true in
acute and chronic pulmonary hypertension and is now also apparent in severe
congestive heart failure. The use of intracavitary LV end-diastolic pressu
re (LVEDP) to assess LVEDV is inappropriate if pressure surrounding the LV
is increased: the surrounding pressure should be subtracted from LVEDP to c
alculate the effective distending (transmural) pressure which governs prelo
ad. If the surrounding pressure increases more than LVEDP, transmural LVEDP
and LVEDV will decrease despite the increased LVEDP. Thus, the use of fill
ing pressure to reflect changes in LVEDV has led to erroneous conclusions r
egarding changes in myocardial compliance and contractility. It is now clea
r that volume loading may reduce LVEDV and stroke work in pulmonary embolis
m, chronic lung disease and severe congestive heart failure despite increas
ed LVEDP, The decreased stroke work is a result of reduced LV preload, not
decreased contractility as would be suggested if filling pressure is used t
o reflect preload.