Abstract

Background and ObjectivesUltrafiltration (UF) of excess fluid activates numerous compensatory mechanisms during hemodialysis (HD). The increase of both total peripheral and splanchnic vascular resistance is considered essential in maintaining hemodynamic stability. The aim of this study was to evaluate the extent of UF-induced changes in hepato-splanchnic blood flow and resistance in a group of maintenance HD patients during regular dialysis.Design, Setting, Participants, & MeasurementsHepato-splanchnic flow resistance index (RI) and hepato-splanchnic perfusion index (QI) were measured in 12 chronic HD patients using a modified, non-invasive Indocyaningreen (ICG) dilution method. During a midweek dialysis session we determined RI, QI, ICG disappearance rate (k ICG), plasma volume (V p), hematocrit (Hct), mean arterial blood pressure (MAP) and heart rate (HR) at four times in hourly intervals (t 1 to t 4). Dialysis settings were standardized and all patient studies were done in duplicate.ResultsIn the whole study group mean UF volume was 1.86 ± 0.46 L, V p dropped from 3.65 ± 0.77L at t1 to 3.40 ± 0.78L at t4, and all patients remained hemodynamically stable. In all patients RI significantly increased from 12.40 ± 4.21 mmHg∙s∙m2/mL at t1 to 14.94 ± 6.36 mmHg∙s∙m2/mL at t4 while QI significantly decreased from 0.61 ± 0.22 at t1 to 0.52 ± 0.20 L/min/m2 at t4, indicating active vasoconstriction. In diabetic subjects, however, RI was significantly larger than in non-diabetics at all time points. QI was lower in diabetic subjects.ConclusionsIn chronic HD-patients hepato-splanchnic blood flow substantially decreases during moderate UF as a result of an active splanchnic vasoconstriction. Our data indicate that diabetic HD-patients are particularly prone to splanchnic ischemia and might therefore have an increased risk for bacterial translocation, endotoxemia and systemic inflammation.

Highlights

  • In all patients resistance index (RI) significantly increased from 12.40 ± 4.21 mmHgÁsÁm2/mL at t1 to 14.94 ± 6.36 mmHgÁsÁm2/mL at t4 while QI significantly decreased from 0.61 ± 0.22 at t1 to 0.52 ± 0.20 L/min/m2 at t4, indicating active vasoconstriction

  • In chronic HD-patients hepato-splanchnic blood flow substantially decreases during moderate UF as a result of an active splanchnic vasoconstriction

  • Our data indicate that diabetic HD-patients are prone to splanchnic ischemia and might have an increased risk for bacterial translocation, endotoxemia and systemic inflammation

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Summary

Introduction

Ultrafiltration (UF) induced hypovolemia activates a variety of compensatory mechanisms to maintain hemodynamic stability during hemodialysis (HD). In hypovolemic states an active vasoconstriction of the splanchnic vascular bed increasing both vascular resistance and venous return is considered fundamental to maintain hemodynamic stability [2]. Results from early studies showing a decrease of splanchnic blood flow during HD-treatment are in support of this important compensatory response to hypovolemia [3] [4] [5]. Ultrafiltration (UF) of excess fluid activates numerous compensatory mechanisms during hemodialysis (HD). The increase of both total peripheral and splanchnic vascular resistance is considered essential in maintaining hemodynamic stability. The aim of this study was to evaluate the extent of UF-induced changes in hepato-splanchnic blood flow and resistance in a group of maintenance HD patients during regular dialysis

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