Predicting and measuring fluid responsiveness with echocardiography

Abstract

Echocardiography is ideally suited to guide fluid resuscitation in critically ill patients. It can be used to assess fluid responsiveness by looking at the left ventricle, aortic outflow, inferior vena cava and right ventricle. Static measurements and dynamic variables based on heart-lung interactions all combine to predict and measure fluid responsiveness and assess response to intravenous fluid resuscitation. Thorough knowledge of these variables, the physiology behind them and the pitfalls in their use allows the echocardiographer to confidently assess these patients and in combination with clinical judgement manage them appropriately.

Keywords: echocardiography; guidelines; haemodynamics; ultrasound protocols; ventricular function.

© 2016 The authors.

Figures

Figure 1

The Frank–Starling curve. Lower on the curve a given change in preload results in a large change in stroke volume. On the higher, flatter portion, the same preload change has minimal effect on stroke volume.

Figure 2

Stressed volume and venous return. (A) The fluid below the outlet is unstressed venous volume and does not contribute to flow out of the tank. The additional fluid in the tank is stressed volume, which drives venous return. Lowering RAP or increasing MSP in isolation would increase VR. (B) The proportion of the circulation that is stressed volume can be increased by giving fluid (attenuated somewhat by reflex venodilatation) or reducing the size of the tank (giving a vasopressor to convert unstressed to stressed volume).

Figure 3

The physiology of respiratory-induced flow and pressure changes during positive pressure ventilation without additional respiratory effort. The inspiratory rise in intrathoracic pressure is transmitted, at least in part, to the pericardium and causes increased transmural pressure across the RV wall, plethora within the IVC and compression of the SVC. The RV stroke volume immediately falls. Concurrently, the pulmonary vasculature is compressed, forcing blood into the LV causing an initial increase in LV stroke volume. After the pulmonary transition time, the LV receives less blood and its stroke volume falls. This effect is exaggerated in states of low circulating volume and attenuated in the overloaded system or when either ventricle is failing. PP pulse pressure, IVC D inferior vena cava diameter, SVC D superior vena cava diameter.

Figure 4

PW Doppler of MV inflow demonstrating high LV filling pressure.

Figure 5

PLAX view optimized for measuring the LVOT diameter.

Figure 6

Tracing the PWD waveform to get the VTI value.

Figure 7

(A) PWD in the LV outflow tract. VTI measurement of the smallest and largest envelope within the respiratory cycle. (B) Measuring Vmax variation with appropriate sweep speed.

Figure 8

IVC measurement just distal to the hepatic vein. M-mode (A) can be used if the vessel is perpendicular to the ultrasound incidence; however, 2D measurements (B) are often more reliable.

Figure 9

RV dilatation and septal flattening is evident in this PSAX view. LV filling is being impaired.

Figure 10

A typical ROC curve for the power of echocardiography to predict fluid responsiveness. The ‘optimum’ threshold is neither the most sensitive nor specific.

Figure 11

The ‘grey zone’ approach to flow variation assessment means that when the result is around the threshold value, further corroborating evidence should be sort from other modalities (e.g. IVC evaluation).

Figure 12

An algorithm to guide fluid resuscitation using echocardiography.