Mathieu Jozwiak1,2, Sandrine Millasseau3, Christian Richard1,2, Xavier Monnet1,2, Pablo Mercado1,2, François Dépret1,2, Jean-Emmanuel Alphonsine1,2, Jean-Louis Teboul1,2, Denis Chemla2,4. 1. AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, service de réanimation médicale, Le Kremlin-Bicêtre, F-94270 France. 2. Inserm UMR S_999, Univ Paris-Sud, Le Kremlin-Bicêtre, F-94270 France. 3. Pulse Wave Consulting, Saint Leu La Foret, F-95320 France. 4. AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, service de physiologie, Le Kremlin-Bicêtre, F-94270 France.
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.
OBJECTIVES: First, to validate bedside estimates of effective arterial elastance = end-systolic pressure/stroke volume in critically illpatients. 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 illpatients, 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.
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