Basic concepts of fluid responsiveness

Abstract

Predicting fluid responsiveness, the response of stroke volume to fluid loading, is a relatively novel concept that aims to optimise circulation, and as such organ perfusion, while avoiding futile and potentially deleterious fluid administrations in critically ill patients. Dynamic parameters have shown to be superior in predicting the response to fluid loading compared with static cardiac filling pressures. However, in routine clinical practice the conditions necessary for dynamic parameters to predict fluid responsiveness are frequently not met. Passive leg raising as a means to alter biventricular preload in combination with subsequent measurement of the change in stroke volume can provide a fast and accurate way to guide fluid management in a broad population of critically ill patients.

Fig. 1

The cardiac function curve representing the relationship between right atrial pressure (RAP) and cardiac output. The shape of the cardiac function curve will move up with decreased afterload, increased contractility and increased heart rate. Similarly, the curve will move down with increased afterload, decreased contractility and decreased heart rate. Furthermore, when cardiac performance is enhanced, the location of the curve will move leftward by generating a decrease in RAP through a further reduction in the systolic x-wave known from the venous pulse. Similarly, RAP will rise when cardiac performance is decreased and the location of the curve will move to the right. It should be noted that although there is no descending limb illustrated beyond the ‘flat’ part of the curve since actin-myosin myofibrils cannot be disengaged, the secondary effects of increased RAP and preload are not taken into account. For instance, increased preload resulting in ventricular distension with increased wall tension leading to a reduction in coronary perfusion pressure and oxygen delivery could potentially decrease ventricular contractility causing a descending limb in the cardiac function curve

Fig. 2

The venous return curve representing the relationship between right atrial pressure (RAP) and venous return. Baseline venous return curve: RAP becomes equal to mean systemic filling pressure (MSFP) in the absence of flow. Therefore MSFP can be determined at the intercept of the venous return curve with the x-axis. Lowering RAP increases venous return until reaching the critical pressure (Pcrit) at which the great veins at the thoracic inlet start to collapse preventing a further increase in venous return. Increased MSFP: Fluid loading will shift the baseline curve upwards and to the right as MSFP increases more than the rise in RAP with a subsequent increase in venous return. Decreased venous resistance (Rv): Venodilatation will theoretically increase venous return assuming unchanged MSFP, but the expected concomitant decrease in MSFP in practice makes the effect on venous return unpredictable

Fig. 3

Venous return curves (Fig. 2) superimposed on cardiac function curves (Fig. 1) where the cardiac output and right atrial pressure (RAP) are determined at the junction of the curves assuming a theoretical steady state; in reality, there are fluctuations for instance in RAP with respiration and atrial contractions. Three cardiac function curves are illustrated with different cardiac performances and two venous return curves are depicted with different mean systemic filling pressures (MSFP) obtained by fluid loading. In the curve representing decreased cardiac performance, point I corresponds to a cardiac output which is barely increased by raising MSFP through fluid loading as evidenced by point II signifying fluid unresponsiveness. Point III is reached by increasing cardiac performance not only moving the cardiac function curve upwards resulting in an increase in cardiac output but lowering RAP as well with subsequent increase in venous return without which no increase in cardiac output can be accomplished. Below the critical pressure no increase in cardiac output can be obtained through increasing contractility since no further increase in venous return can be obtained (point IV). Instead cardiac output can be augmented by increasing MSFP (point V)

Fig. 4

Passive leg raising (PLR) can be performed by elevating the limbs while placing the patient in the supine position to transfer blood both from the lower limbs as from the abdominal compartment creating a sufficient venous return to significantly elevate biventricular preload. Alternatively, classic PLR can be performed by merely elevating the legs with the patient in supine position