Evaluation of fluid responsiveness in ventilated septic patients: Back to venous return

Abstract

Adequate tissue perfusion and oxygen delivery is the primary goal of the therapeutic management of patientswith circulatory failure. Cardiac output-a major determinant of oxygen delivery-is the result of the interaction between the cardiac pump and venous return. Since cardiac output must equal the volume of blood entering the heart, an increase in venous return will increase cardiac output, provided that the venous return curve intersects with the ascending limb of the cardiac function curve [1]. This defines the preload dependence of the heart. In contrast, a further increase in preload when the heart operates on the flat portion of its function curve fails to increase cardiac output and results in increased filling pressure with potential deleterious venous congestion. Importantly, there is no fluid responsiveness of the left ventricle (LV) without right ventricular (RV) preload dependence [2]. A pivotal clinical question frequently raised is, therefore, the evaluation of RV ability to increase its output significantly in response to a fluid challenge. Another clinical question even more challenging to address is to determine if the patient really needs a higher cardiac output to improve his current condition.