To the Editor:
In the recent issue of Anesthesiology there is an article1 and an accompanying editorial2 that provide us with somewhat contradictory conclusions. The study1 did not find any difference in outcome of intermediate risk orthopedic surgery between the patients who received goal-directed hemodynamic therapy or usual treatment determined by an anesthesiologist in charge of the case. Maheshwari and Sessler2 correctly stated that future studies should include patients who undergo surgery requiring more severe volume changes than patients in the reported study did,1 possibly implying that such group of patients would do well regardless of the goal-directed hemodynamic therapy.
Despite no differences in outcome the patients who were treated with goal-directed hemodynamic therapy received 1.5 times more fluid than the patients in the controlled group.1 Basic physiology of venous system helps to elucidate the possible reason for the difference.
The blood within the venous vasculature may be under zero pressure (unstressed volume) or under pressure above zero (stressed volume).3,4 It is important to keep in mind that the stressed volume and unstressed volume are virtual volumes; they are not separated by a membrane, they are different only by being under pressure above zero or not. When a fluid infusion starts, the infused fluid “enters” the unstressed volume because transmural pressure there is lower than in the stressed volume, by definition. Infused fluid gradually increases unstressed volume that eventually reaches “the point of conversion of unstressed volume-to-stressed volume.” The unstressed volume does not affect hemodynamics, whereas stressed volume does (stressed volume is one of the main determinants of flow within the venous vasculature). Therefore, the amount of fluid infused before the point of conversion of the unstressed volume-to-stressed volume does not affect hemodynamics, is not needed, and may represent overloading at that time. When the point of conversion of unstressed volume-to-stressed volume is reached, the whole blood in that chamber (that part of venous vasculature), together with the infused fluid, constitutes the stressed volume that increases preload affecting the hemodynamics. Any vasodilating insults that occur before the points of conversion of unstressed volume-to-stressed volume increase the unstressed volume that does not affect hemodynamics but may be associated with an increase in the amount of infused fluid and represent overloading at that moment. Clinicians have to remember that the unstressed volume represents the reservoir of volume that can be partially mobilized within seconds by converting the unstressed volume to stressed volume.
Small doses of a vasoconstrictor constrict mainly veins, not arteries, and therefore do not jeopardize tissue perfusion.4 However, they decrease the unstressed volume, thereby decreasing the amount of overload during goal-directed hemodynamic therapy. Two clinical studies5,6 are in agreement with the speculations above. Moreover, the study by Nakamoto et al.6 showed that a vasopressor increases the responsiveness to fluid challenge. This is apparently attributable to a decrease in unstressed volume (induced by a vasopressor), leading to sooner conversion of the unstressed volume to stressed volume and thereby decreasing the amount of fluid infused before the point of conversion of unstressed volume-to-stressed volume.7
Thus, the goal-directed hemodynamic therapy per se helps to prevent underfilling, whereas small doses of a vasopressor may effectively diminish overloading of the vasculature.
The author declares no competing interests.