Estimation of body fluid changes during peritoneal dialysis by segmental bioimpedance analysis

Estimation of body fluid changes during peritoneal dialysis by segmental bioimpedance analysis.BackgroundCommonly used bioimpedance analysis (BIA) is insensitive to changes in peritoneal fluid volume. The purpose of this study was to show, to our knowledge for the first time, that a new segmental approach accurately measures extracellular fluid changes during peritoneal dialysis (PD).MethodsFourteen stable PD patients were studied during a standard exchange with fluids of known conductivity. Bioimpedance was continuously measured in the arm, trunk, and leg and from wrist to ankle. Volume changes were calculated using both a newly developed sum of segmental BIA (SBIA) and current wrist-to-ankle BIA (WBIA) and were compared with actual volume changes measured gravimetrically.ResultsWhen 2.19 ± 0.48 L were removed from the peritoneal cavity during draining, 95.2 ± 13.8% of this volume was detected by SBIA compared with only 12.5 ± 24.3% detected by WBIA. When 2.11 ± 0.20 L of fresh dialysate was infused into the peritoneal cavity during filling, 91.1 ± 19.6% of this volume was detected by SBIA compared with only 8.8 ± 21.1% detected by WBIA.ConclusionThe good agreement between measured and calculated data using SBIA was due to: (a) improved placement of electrodes, (b) estimation of trunk extracellular volume based on a new algorithm, and (c) consideration of changes in dialysate conductivity. Correct estimation of fluid volume in the trunk is a prerequisite for applications in which direct analysis of fluid changes cannot be performed such as with peritoneal equilibration tests and continuous flow PD

Selective transport of protein-bound uremic toxins in erythrocytes

To better understand the kinetics of protein-bound uremic toxins (PBUTs) during hemodialysis (HD), we investigated the distribution of hippuric acid (HA), indole-3-acetic acid (IAA), indoxyl sulfate (IS), and p-cresyl sulfate (pCS) in erythrocytes of HD patients. Their transport across the erythrocyte membrane was explored in the absence of plasma proteins in vitro in a series of loading and unloading experiments of erythrocytes from healthy subjects and HD patients, respectively. Furthermore, the impact of three inhibitors of active transport proteins in erythrocytes was studied. The four PBUTs accumulated in erythrocytes from HD patients. From loading and unloading experiments, it was found that (i) the rate of transport was dependent on the studied PBUT and increased in the following sequence: HA < IS < pCS < IAA and (ii) the solute partition of intra-to extra-cellular concentrations was uneven at equilibrium. Finally, inhibiting especially Band 3 proteins a ff ected the transport of HA (both in loading and unloading), and of IS and pCS (loading). By exploring erythrocyte transmembrane transport of PBUTs, their kinetics can be better understood, and new strategies to improve their dialytic removal can be developed

Protein-bound uremic toxin profiling as a tool to optimize hemodialysis

Aim : We studied various hemodialysis strategies for the removal of protein-bound solutes, which are associated with cardiovascular damage. Methods : This study included 10 patients on standard (3x4h/week) high-flux hemodialysis. Blood was collected at the dialyzer inlet and outlet at several time points during a midweek session. Total and free concentration of several protein-bound solutes was determined as well as urea concentration. Per solute, a two-compartment kinetic model was fitted to the measured concentrations, estimating plasmatic volume (V-1), total distribution volume (V-tot) and inter-compartment clearance (K-21). This calibrated model was then used to calculate which hemodialysis strategy offers optimal removal. Our own in vivo data, with the strategy variables entered into the mathematical simulations, was then validated against independent data from two other clinical studies. Results : Dialyzer clearance K, V-1 and V-tot correlated inversely with percentage of protein binding. All Ks were different from each other. Of all protein-bound solutes, K-21 was 2.7-5.3 times lower than that of urea. Longer and/or more frequent dialysis that processed the same amount of blood per week as standard 3x4h dialysis at 300mL/min blood flow showed no difference in removal of strongly bound solutes. However, longer and/or more frequent dialysis strategies that processed more blood per week than standard dialysis were markedly more adequate. These conclusions were successfully validated. Conclusion : When blood and dialysate flow per unit of time and type of hemodialyzer are kept the same, increasing the amount of processed blood per week by increasing frequency and/or duration of the sessions distinctly increases removal

Increased Hepato-Splanchnic Vasoconstriction in Diabetics during Regular Hemodialysis

BACKGROUND AND OBJECTIVES: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. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:Hepato-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 (kICG), plasma volume (Vp), hematocrit (Hct), mean arterial blood pressure (MAP) and heart rate (HR) at four times in hourly intervals (t1 to t4). Dialysis settings were standardized and all patient studies were done in duplicate. RESULTS:In the whole study group mean UF volume was 1.86 ± 0.46 L, Vp 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. CONCLUSIONS: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 particularly prone to splanchnic ischemia and might therefore have an increased risk for bacterial translocation, endotoxemia and systemic inflammation

Feasibilty of Transcutaneous pCO2 Monitoring During Immediate Transition After Birth\u2014A Prospective Observational Study

Background: According to recommendations, non-invasive monitoring during neonatal resuscitation after birth includes heart rate (HR) and oxygen saturation (SpO2). Continuous transcutaneous monitoring of carbon dioxide partial pressure (tcpCO2) may further offer quantitative information on neonatal respiratory status. Objective: We aimed to investigate feasibility of tcpCO2 measurements in the delivery room during immediate neonatal transition and to compare the course of tcpCO2 between stable term and preterm infants. Methods: Neonates without need for cardio-respiratory intervention during immediate transition after birth were enrolled in a prospective observational study. In these term and preterm neonates, we measured HR and SpO2 by pulse oximetry on the right wrist and tcpCO2 with the sensor applied on the left hemithorax during the first 15 min after birth. Courses of tcpCO2 were analyzed in term and preterm neonates and groups were compared. Results: Fifty-three term (gestational age: 38.8 \ub1 0.9 weeks) and 13 preterm neonates (gestational age: 34.1 \ub1 1.5 weeks) were included. First tcpCO2 values were achieved in both groups at minute 4 after birth, which reached a stable plateau after the equilibration phase at minute 9. Mean tcpCO2 values 15 min after birth were 46.2 (95% CI 34.5\u201357.8) mmHg in term neonates and 48.5 (95%CI 43.0\u201354.1) mmHg in preterm neonates. Preterm and term infants did not show significant differences in the tcpCO2 values at any time point. Conclusion: This study demonstrates that tcpCO2 measurement is feasible during immediate neonatal transition after birth and that tcpCO2 values were comparable in stable term and preterm neonates

Impact of bradycardia and hypoxemia on oxygenation in preterm infants requiring respiratory support at birth

Aim of the study: Analysis of the impact of bradycardia and hypoxemia on the course of cerebral and peripheral oxygenation parameters in preterm infants in need for respiratory support during foetal-to-neonatal transition. Methods: The first 15 min after birth of 150 preterm neonates in need for respiratory support born at the Division of Neonatology, Graz (Austria) were analyzed. Infants were divided into different groups according to duration of bradycardia exposure (no Bradycardia, brief bradycardia &lt;2 min, and prolonged bradycardia 652 min) and to systemic oxygen saturation (SpO2) value at 5 min of life (&lt;80% or 6580%). Analysis was performed considering the degree of bradycardia alone (step 1) and in association with the presence of hypoxemia (step 2). Results: In step 1, courses of SpO2 differed significantly between bradycardia groups (p = 0.002), while courses of cerebral regional oxygen saturation (crStO2) and cerebral fractional tissue oxygen extraction (cFTOE) were not influenced (p = 0.382 and p = 0.878). In step 2, the additional presence of hypoxemia had a significant impact on the courses of SpO2 (p &lt; 0.001), crStO2 (p &lt; 0.001) and cFTOE (p = 0.045). Conclusion: Our study shows that the degree of bradycardia has a significant impact on the course of SpO2 only, but when associated with the additional presence of hypoxemia a significant impact on cerebral oxygenation parameters was seen (crStO2, cFTOE). Furthermore, the additional presence of hypoxemia has a significant impact on FiO2 delivered. Our study emphasizes the importance of HR and SpO2 during neonatal resuscitation, underlining the relevance of hypoxemia during the early transitional phase

Schneditz D. Reactive hyperemia in the human liver

We tested whether hepatic blood flow is altered following central hypovolemia caused by simulated orthostatic stress. After 30 min of supine rest, hemodynamic, plasma density, and indocyanine green (ICG) clearance responses were determined during and after release of a 15-min 40 mmHg lower body negative pressure (LBNP) stimulus. Plasma density shifts and the time course of plasma ICG concentration were used to assess intravascular volume and hepatic perfusion changes. Plasma volume decreased during LBNP (Ϫ10%) as did cardiac output (Ϫ15%), whereas heart rate (ϩ14%) and peripheral resistance (ϩ17%) increased, as expected. On the basis of ICG elimination, hepatic perfusion decreased from 1.67 Ϯ 0.32 (pre-LBNP control) to 1.29 Ϯ 0.26 l/min (Ϫ22%) during LBNP. Immediately after LBNP release, we found hepatic perfusion 25% above control levels (to 2.08 Ϯ 0.48 l/min, P ϭ 0.0001). Hepatic vascular conductance after LBNP was also significantly higher than during pre-LBNP control (21.4 Ϯ 5.4 vs. 17.1 Ϯ 3.1 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 , P Ͻ 0.0001). This indicates autoregulatory vasodilatation in response to relative ischemia during a stimulus that has cardiovascular effects similar to normal orthostasis. We present evidence for physiological post-LBNP reactive hyperemia in the human liver. Further studies are needed to quantify the intensity of this response in relation to stimulus duration and magnitude, and clarify its mechanism. hepatic; indocyanine green; orthostasis; splanchnic blood flow; autoregulation; lower body negative pressure CENTRAL HYPOVOLEMIA, AS CAUSED by blood redistribution (e.g., orthostasis) or blood loss (e.g., trauma) can be simulated by application of negative pressure to the body from the iliac crest downward (lower body &quot;negative&quot; pressure, LBNP), as this leads to peripheral blood pooling while avoiding additional hydrostatic effects of upright posture (14). Driven by decreased load on cardiopulmonary and eventually arterial baroreceptors, neurohumoral readjustments occur. The splanchnic vascular bed is a major regulatory target because it represents a large regional vascular conductance and constitutes the primary blood reserve in cardiovascular &quot;emergency&quot; situations (11) Even low (Յ20 mmHg) levels of LBNP suffice to induce sympathetic activation and reduce splanchnic perfusion (17), whereas higher stimulus levels (e.g., 50 mmHg) lower splanchnic vascular conductance as well, by as much as Ϸ30% (6, 33). Reduced perfusion has local metabolic consequences. Vascular &quot;escape&quot; from sympathetic influence (9, 34) and the general concept of &quot;reactive hyperemia&quot; (20, 31) and autoregulation (38) are well established, but hepatic reactive hyperemia as such has not yet been reported. Splanchnic ischemia is connected to hypotensive episodes especially under prolonged hypovolemic stress such as hemodialysis and ultrafiltration of excess body fluid (12, 36). We speculated whether a much shorter perturbation such as standard LBNP would also induce ischemia. We measured hepatic clearance of ICG as a surrogate for splanchnic perfusion before, during, and after LBNP and hypothesized that after LBNP-induced vasoconstriction, hepatic perfusion would not only return to but also actually exceed pre-LBNP control levels, owing to local effects of relative hypoperfusion induced metabolite accumulation that occurred during LBNP. METHODS The study was done in 14 healthy, male volunteers of moderate physical fitness, free from cardiovascular, renal, hepatic, and pulmonary diseases and not on any medication. The subjects abstained from use of tobacco, caffeine, alcohol, and heavy exercise for at least 48 h preceding each investigation and the subjects were their own controls. The Graz Medical University Research Ethics Committee approved the study protocol, and written, informed consent was obtained from each subject. Before the study, LBNP sham runs without blood sampling were carried out for familiarization to the study (24). Protocols were conducted between 9 and 12 AM to minimize circadian influences on hemodynamic variables (29). The subjects were fasting and emptied the bladder before each study. An antecubital vein was cannulated, for blood sampling and administration of ICG. Experiments were carried out in a semidark, quiet room maintained at 24°C and humidity at 55%. A padded pair of tightly connected chains was used to stabilize and maintain an exact sealing position at the exact level of the iliac crest within the LBNP box (14). The box was equipped with a footrest that was individually adjusted before LBNP was commenced. A pillow supported the head to avoid stimulation of the otolith organs, which has been reported to increase muscle sympathetic nerve activity and calf vascular resistance (21). Baseline data were collected for 30 min in the supine position, with the seal in place, before LBNP to allow for reequilibration of gravityrelated fluid shifts (16). Pressure within the box was lowered electronically by a pump within 10 s and monitored by an electronic gauge (24). LBNP (Ϫ40 mmHg) lasted for 15 min because any longer period affects LBNP tolerance (15). During LBNP the subjects were instructed to avoid movements of the lower limbs and to breathe normally. The post-LBNP observation period lasted another 15 min. The time course of the experimental protocol is shown in Blood volume and hepatic perfusion. ICG (25 mg) was injected at two times, 20 min before and 7 min into LBNP, with sufficient time between injections for ICG to be completely cleared from the blood stream. Whereas the ICG disappearance following the first injectio

Acid base and metabolic parameters of the umbilical cord blood and cerebral oxygenation immediately after birth

ObjectiveAim was to investigate whether acid-base and metabolic parameters obtained from arterial umbilical cord blood affect cerebral oxygenation after birth in preterm neonates with respiratory support and in term neonates without respiratory support.Study designThis was a post-hoc analysis of secondary outcome parameters of a prospective observational study including preterm neonates with and term neonates without respiratory support. Non-asphyxiated neonates with cerebral oxygenation measured with near-infrared spectroscopy during the first 15 min and with blood gas analyses from arterial umbilical cord blood were included. Arterial oxygen saturation (SpO2) and heart rate (HR) were monitored with pulse oximetry. Potential correlations were investigated between acid-base and metabolic parameters (pH-value, bicarbonate, base-excess, and lactate) and crSO2/cFTOE 5 min after birth.ResultsSeventy-seven neonates were included: 14 preterm neonates with respiratory support (mean gestational age [GA] 31.4 ± 4.1 weeks; mean birth weight [BW] 1,690 ± 640 g) and 63 term neonates without respiratory support (GA 38.7 ± 0.8 weeks; BW 3,258 ± 443 g). Mean crSO2 5 min after birth was 44.0% ± 24.2% in preterm and 62.2% ± 20.01% in term neonates. Mean cFTOE 5 min after birth was 0.46 ± 0.06 in preterm and 0.27 ± 0.19 in term neonates. In preterm neonates with respiratory support higher lactate was significantly associated with lower crSO2 and SpO2 and tended to be associated with higher cFTOE. In term neonates without respiratory support no significant correlations were found.ConclusionIn non-asphyxiated preterm neonates with respiratory support, lactate levels were negatively associated with crSO2 and SpO2, whereas in term neonates without respiratory support no associations were observed