Predicting the Need for Fluid Therapy-Does Fluid Responsiveness Work?

Abstract

Fluid overdose can be harmful in critically ill patients. Since central venous pressure (CVP) is currently considered to be an inappropriate indicator of preload, much attention is being given to predicting fluid responsiveness, i.e., the response of stroke volume (SV) or cardiac output (CO) to fluid challenge. However, when fluid responsiveness was evaluated in critically ill patients, including sepsis, only 40-50% of the patients responded. Moreover, most fluid responders do not show significant hemodynamic improvement after fluid administration. In this review, we discuss why fluid responsiveness based on the Starling mechanism did not work well in the clinical setting. According to the Starling mechanism, a patient whose SV/CO significantly increases after a fluid challenge is considered to be a fluid responder and judged to need fluid therapy. However, the currently recommended fluid challenge dose of crystalloid 250-500 mL has little effect on increasing blood volume and is not sufficient to increase the preload of the Starling curve. Especially in septic patients, due to their vascular hyperpermeability, increase in blood volume is even smaller. Furthermore, Infusion induced hemodilution is known to reduce blood viscosity and hematocrit, as a result, decreasing afterload. This indicates that the increased SV/CO after fluid challenge is caused not only by increased preload but also by decreased afterload. For these reasons, fluid responsiveness with small crystalloid challenge is questionable as a clinical indicator of fluid therapy.

Keywords: Afterload; Cardiac output; Colloid; Crystalloid; Fluid challenge; Fluid responsiveness; Fluid therapy; Preload; Starling mechanism; Starling’s law; Stroke volume; Systemic vascular resistance.

Fig. 1

Starling curve and left ventricular function: the relationship between SV and preload. a If fluid challenge adequately improves SV, a patient is considered hypovolemic (responder). b If fluid was given at the plateau of Starling curve, SV will not increase, and a patient is considered normovolemic (non-responder). c For decreased left ventricular function cases, SV response after fluid loading cannot be observed even in hypovoelia, as Starling curve is flatter than the normal cardiac function cases. SV stroke volume

Fig. 2

Starling curve and respiratory variation of SV. At the point where the ascending limb of Starling curve, respiratory variation in the stroke volume is significant (a) and judged as a large preload reserve. While at the point where the Starling curve is nearly flat, the respiratory variation is minimal (b) with a small preload reserve. SV stroke volume

Fig. 3

The relation between percent change in blood volume and cardiac output (CO) after volume preload with 1.5 L lactated Ringer’s solution (〇), 0.5 L hydroxyethylstarch solution, 6% (●), and 1.0 L hydroxyethylstarch solution, 6% (×) in parturients at term. [15]. Exponential increase in CO was observed after volume preloading

Fig. 4

Schematic illustration of the hypothetical Starling curve after fluid administration. Infusion beyond normovolemia may exponential increase SV until the onset of heart failure. The maximum increase in SV against preload change (δSV/δP) may observe at hypervolemic state