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

Jozwiak, Mathieu MD, PhD1,2; Millasseau, Sandrine PhD3; Richard, Christian MD1,2; Monnet, Xavier MD, PhD1,2; Mercado, Pablo MD1,2; Dépret, François MD1,2; Alphonsine, Jean-Emmanuel MD1,2; Teboul, Jean-Louis MD, PhD1,2; Chemla, Denis MD, PhD2,4

doi: 10.1097/CCM.0000000000003645
Online Clinical Investigations

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.

1AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, service de réanimation médicale, Le Kremlin-Bicêtre, F-94270 France.

2Inserm UMR S_999, Univ Paris-Sud, Le Kremlin-Bicêtre, F-94270 France.

3Pulse Wave Consulting, Saint Leu La Foret, F-95320 France.

4AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, service de physiologie, Le Kremlin-Bicêtre, F-94270 France.

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Drs. Jozwiak and Chemla received travel grants from ALAM Medical for scientific meeting, outside the submitted work. Dr. Millasseau received personal fees from ALAM Medical, outside the submitted work. Drs. Monnet and Teboul are members of the Medical Advisory Board of Pulsion Medical Systems. Dr. Teboul received funding from Getinge (Germany). The remaining authors have disclosed that they do not have any potential conflicts of interest.

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