Validation and Critical Evaluation of the Effective Arterial Elastance in Critically Ill Patients

Abstract

Objectives: First, to validate bedside estimates of effective arterial elastance = end-systolic pressure/stroke volume in critically ill patients. Second, to document the added value of effective arterial elastance, which is increasingly used as an index of left ventricular afterload. Design: Prospective study. Setting: Medical ICU. Patients: Fifty hemodynamically stable and spontaneously breathing patients equipped with a femoral (n = 21) or radial (n = 29) catheter were entered in a “comparison” study. Thirty ventilated patients with invasive hemodynamic monitoring (PiCCO-2; Pulsion Medical Systems, Feldkirchen, Germany), in whom fluid administration was planned were entered in a “ dynamic” study. Interventions: In the “dynamic” study, data were obtained before/after a 500 mL saline administration. Measurements and Main Results: According to the “cardiocentric” view, end-systolic pressure was considered the classic index of left ventricular afterload. End-systolic pressure was calculated as 0.9 × systolic arterial pressure at the carotid, femoral, and radial artery level. In the “comparison” study, carotid tonometry allowed the calculation of the reference effective arterial elastance value (1.73 ± 0.62 mm Hg/mL). The femoral estimate of effective arterial elastance was more accurate and precise than the radial estimate. In the “dynamic” study, fluid administration increased stroke volume and end-systolic pressure, whereas effective arterial elastance (femoral estimate) and systemic vascular resistance did not change. Effective arterial elastance was related to systemic vascular resistance at baseline (r = 0.89) and fluid-induced changes in effective arterial elastance and systemic vascular resistance were correlated (r = 0.88). In the 15 fluid responders (cardiac index increases ≥ 15%), fluid administration increased end-systolic pressure and decreased effective arterial elastance and systemic vascular resistance (each p < 0.05). In the 15 fluid nonresponders, end-systolic pressure increased (p < 0.05), whereas effective arterial elastance and systemic vascular resistance remained unchanged. Conclusions: In critically ill patients, effective arterial elastance may be reliably estimated at bedside (0.9 × systolic femoral pressure/stroke volume). We support the use of this validated estimate of effective arterial elastance when coupled with an index of left ventricular contractility for studying the ventricular-arterial coupling. Conversely, effective arterial elastance should not be used in isolation as an index of left ventricular afterload.

Volume status and volume responsiveness in postoperative cardiac surgical patients: An observational, multicentre cohort study

“…The VRdP and CP vol demonstrated an AUROC and threshold values associated with volume responsiveness close to previous studies 11,12 . The reduced effective arterial elastance, E a , following a fluid bolus in responders suggested that the lumped steady and pulsatile arterial load was reduced, consistent with the findings of a recent methodological study on E a 19 . Volume responsive patients by a dichotomous definition thus exhibited the dual benefits of increased left ventricular end‐diastolic filling as well as reduced afterload.…”

“…An integrative measure of the hydraulic pumping ability of the heart, cardiac power (CP) 17 , is provided by the product of CO and MAP indexed to P msa, describing the heart performance at a particular volume state, CP vol 11,18 . Effective arterial elastance ( E a ) was calculated as 0.9 × systolic arterial pressure/SV 19 . The left ventricular end‐diastolic volume was set to the y‐axis intercept of the E a line.…”

Changes in dynamic arterial elastance induced by volume expansion and vasopressor in the operating room: a prospective bicentre study

“…Arterial resistance ( R ) was calculated as the ratio between mean arterial pressure and cardiac output. Arterial elastance was calculated using these two formulas: Ea SAP = (systolic arterial pressure × 0.9)/stroke volume and Ea MAP = mean arterial pressure/stroke volume [22, 23].…”

Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

“…Both E a and E ES can be altered by a variety of physiological and pharmacological interventions that affect ventricular performance and vasomotor tone, which thereby will alter the ventricular-vascular coupling ratio, which, under optimal conditions, ranges between 0.6 and 1.2 in humans (1,13,38,60). Recently, E a has been used as a diagnostic assessment measure of ventricular-vascular coupling and ventricular afterload (10,18,19,44,72,74). In healthy individuals and canines, E a increases in response to exercise in parallel with the rise in ventricular performance, which maintains an optimal stroke work (19,68,72,73).…”