Hemodynamic improvement after continuous renal replacement therapies: Not only immunomodulation

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Abstract

Hemodynamically unstable patients under continuous renal replacement therapies (CRRT) frequently show an improvement in hemodynamic parameters and a reduction in vasopressor agents. Different mechanisms have been proposed to explain this effect. A high rate of fluid exchange between interstitial and intravascular compartments seems to contribute to the therapeutic effect of CRRT. Other mechanism that seems to play a role is cooling; a raise in BP and SVR will follow a moderate heat loss but this effect will be accompanied by a decrement in oxygen delivery that can be detrimental and, when the cooling is severe, a shock can theoretically be precipitated. Metabolic acidosis, usually present when RRT is started, is a proinflammatory stimulus and conditions vasopressor unresponsiveness; the efficient control provided by CRRT can explain in part a positive hemodynamic response. Ionized calcium may have a role based on a potential effect on cardiac function and has been used in some studies in high concentration but there are limited in vivo data supporting this effect. The role of sodium concentration as a factor influencing hemodynamic tolerance has been reported for IHD but for CRRT has not been studied so far. Clearance of cytokines is the central key factor proposed as a mechanism for hemodynamic improvement but we have conflicting data regarding elimination. The volume of fluid exchange involved is a critical factor in order to reach an effective clearance but at this point we lack a proven theory for the way CCRT works. In this review we aim to explore possible mechanisms involved in the hemodynamic effect of CRRT on critically ill unstable patients.

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