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CLINICAL APPLICATION OF VENTRICULAR END‐SYSTOLIC ELASTANCE AND THE VENTRICULAR PRESSURE‐VOLUME DIAGRAM

The ability to clinically assess myocardial contractility in a load-independent fashion facilitates the selection of appropriate inotropes, when needed, during shock resuscitation. Within the framework of the ventricular pressure-volume diagram, the slope of the ventricular end-systolic pressure-volume relationship (expressed as ventricular end-systolic elastance, Ees), has been shown to accurately reflect ventricular inotropic state, and to be insensitive to loading conditions. It has not, however, been widely used at the bedside. Our goal was to evaluate the clinical utility of Ees and the ventricular pressure-volume diagram as bedside methods of hemodynamic assessment. We performed a prospective study of 123 hemodynamic interventions in 100 trauma patients during shock resuscitation in which contractility (Ees), preload (left ventricular end-diastolic volume index), and afterload (effective arterial elastance) were calculated before and after addition of inotropes, fluid bolus, and afterload reduction. Mean values of each variable were compared before and after each type intervention using the paired t test. The ventricular pressure-volume diagram was used to predict changes in the studied variables, and the experimental results were compared with predicted changes. Ees (mmHg/mL/m2) increased significantly with inotropes (4.7 ± 32 to 10 ± 8.7, p < .0001), but was not affected by clinically significant fluid administration (7.0 ± 4.7 to 8.3 ± 8.0, p = .10) or afterload reduction (9.6 ± 5.2 to 9.2 ± 4.7, p = .72). Left ventricular end-diastolic volume index (mL/m2) improved with fluid administration (54 ± 8.9 to 62 ± 9.8, p < .0001) and effective arterial elastance (mmHg/mL/m2) decreased with afterload reduction (3.3 ± .9 to 2.6 ± .7, p < .0001). We conclude that Ees is a load-independent measure of contractility, which is measurable at the bedside. The pressure-volume diagram is a useful method of monitoring hemodynamic changes associated with interventions during shock resuscitation.