Preload Dependence and Microcirculation Relationship: Reply

I would like to thank the authors of the letter for reminding us that the notion of preload dependence is not synonymous with hypovolemia. As mentioned in the article,¹  preload dependence is defined as a state in which increases in right ventricular and/or left ventricular end-diastolic volume result in an increase in stroke volume.²  Changes in preload could be due to hypovolemia and/or a decrease in venous tone with increased venous capacity. Having a preload dependence does not give any indication of the state of the microcirculation. Indeed, microcirculation can be preserved up to a certain level of venous return decline, but can then be altered if the venous return decline is greater. For this reason, it is essential to have an assessment of microcirculation in order to titrate perioperative fluid and correctly administrate vasopressors.

With this in mind, our study highlights that the occurrence of preload dependence was associated with reduced sublingual microcirculation during major abdominal surgery. This shows that decreases in venous return during anesthesia for major abdominal surgery, regardless of cause, are sufficient to alter sublingual microcirculation. In these circumstances, sublingual microcirculation was not protected by self-regulatory mechanisms during venous return decreases. This should encourage us to correct the preload dependency episodes that may occur during surgery in order to avoid these microvascular alterations. As mentioned in the article,¹  the fact that fluid challenge was able to restore microcirculatory alterations pleads for hypovolemia. Fluid administration may have corrected an absolute hypovolemia due to a loss of blood volume or a relative hypovolemia due to a decrease in venous tone. In any case, correcting preload dependency remains a priority considering the risk of failure to treat an alteration of the microcirculation. Static (pulmonary artery occlusion pressure, central venous pressure, global end-diastolic volume, flow time of aortic flow) and dynamic (pulse pressure variation, stroke volume variations, vena cava diameter variations) hemodynamic variables have their own limits and their gray zone to guide fluid administration. Especially, pulse pressure variations cannot be used during arrhythmia, when tidal volumes are less than 8 ml/kg of ideal body weight, when spontaneous breathing occurs, or when pulse pressure variation value is in the gray zone (between 9 and 13%). Microvascular sublingual measurements could be an additional tool in the future to support the decision to administer fluids or vasopressors. It is clear that we must continue to develop techniques to analyze the behavior of microcirculation because the ultimate goal of hemodynamic optimization is the optimization of microcirculation and tissue oxygenation.

The author declares no competing interests.