Abstract

In patients with acute circulatory failure, fluid administration represents a first-line therapeutic intervention for improving cardiac output. However, only approximately 50% of patients respond to fluid infusion with a significant increase in cardiac output, defined as fluid responsiveness. Additionally, excessive volume expansion and associated hyperhydration have been shown to increase morbidity and mortality in critically ill patients. Thus, except for cases of obvious hypovolaemia, fluid responsiveness should be routinely tested prior to fluid administration. Static markers of cardiac preload, such as central venous pressure or pulmonary artery wedge pressure, have been shown to be poor predictors of fluid responsiveness despite their widespread use to guide fluid therapy. Dynamic tests including parameters of aortic blood flow or respiratory variability of inferior vena cava diameter provide much higher diagnostic accuracy. Nevertheless, they are also burdened with several significant limitations, reducing the reliability, or even precluding their use in many clinical scenarios. This non-systematic narrative review aims to provide an update on the novel, less employed dynamic tests of fluid responsiveness evaluation in critically ill patients.

Highlights

  • Fluid administration represents a first-line therapeutic intervention in patients with acute circulatory failure [1]

  • The physiologic relationship among cardiac preload, contractility, and stroke volume is described by Frank–Starling law (Figure 1) and creates a scientific basis for the evaluation of fluid responsiveness, which is defined as a significant increase (10–15%) in cardiac output (CO) after intravascular volume expansion

  • By adding the absolute values of changes induced by end-expiratory occlusion test (EEOT) and end-inspiratory occlusion test (EIOT) separated by one minute, Jozwiak et al were able to increase the fluid responsiveness detection threshold from 4% to 11% of CO change monitored by pulse contour analysis [32]

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Summary

Introduction

Fluid administration represents a first-line therapeutic intervention in patients with acute circulatory failure [1]. The physiologic relationship among cardiac preload, contractility, and stroke volume is described by Frank–Starling law (Figure 1) and creates a scientific basis for the evaluation of fluid responsiveness, which is defined as a significant increase (10–15%) in CO after intravascular volume expansion Such fluid challenge has been achieved by the infusion of 500 mL of either crystalloid or colloid solution over a short period of time. That means that a large proportion of patients receive a significant amount of unnecessary fluid, which subsequently leads to hyperhydration with the development of interstitial and intracellular tissue oedema [7] Such fluid overload has been shown to adversely influence morbidity and survival in a wide range of critically ill patients due to compromised organ function [8,9,10,11,12]. It seems rational that fluid therapy should be tailored to individual patients’ needs with regard to their actual

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