scholarly journals Chloride content of solutions used for regional citrate anticoagulation might be responsible for blunting correction of metabolic acidosis during continuous veno-venous hemofiltration

2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Rita Jacobs ◽  
Patrick M. Honore ◽  
Marc Diltoer ◽  
Herbert D. Spapen
Keyword(s):  
Metabolic Acidosis ◽  
Chloride Content ◽  
Regional Citrate Anticoagulation ◽  
Strong Ion Difference ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Citrate Anticoagulation ◽  
Acid Base Equilibrium ◽  
Acid Base Status ◽  
Regional Anticoagulation

Abstract Background Citrate, the currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium. Methods The effect of 2 different citrate solutions on acid-base status was assessed according to the Stewart-Figge approach in two consecutive cohorts of critically ill adult patients. The first group received Prismocitrate 10/2 (PC10/2; 10 mmol citrate/L). The next group was treated with Prismocitrate 18/0 (PC18; 18 mmol citrate/L). Both groups received bicarbonate-buffered fluids in post-dilution. Results At similar citrate flow, the metabolic acidosis present at baseline in both groups was significantly attenuated in PC18 patients but persisted in PC10/2 patients after 24 h of treatment (median pH 7,42 vs 7,28; p = 0.0001). Acidosis in the PC10/2 group was associated with a decreased strong ion difference and an increased strong ion gap (respectively 43 vs. 51 mmol/L and 17 vs. 12 mmol/L, PC10/2 vs. PC18; both p = 0.001). Chloride flow was higher in PC10/2 than in PC18 subjects (25.9 vs 14.3 mmol/L blood; p < 0.05). Conclusion Correction of acidosis was blunted in patients who received 10 mmol citrate/L as regional anticoagulation during CVVH. This could be explained by differences in chloride flow between the applied citrate solutions inducing hyperchloremic acidosis.

Equivalent Metabolic Acidosis with Four Colloids and Saline on Ex Vivo Haemodilution

2009 ◽  
Vol 37 (3) ◽  
pp. 407-414 ◽  
Author(s):  
T. J. Morgan ◽  
M. Vellaichamy ◽  
D. M. Cowley ◽  
S. L. Weier ◽  
B. Venkatesh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Base Excess ◽  
Ex Vivo ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Acid Properties

Colloid infusions can cause metabolic acidosis. Mechanisms and relative severity with different colloids are incompletely understood. We compared haemodilution acid-base effects of 4% albumin, 3.5% polygeline, 4% succinylated gelatin (all weak acid colloids, strong ion difference 12 mEq/l, 17.6 mEq/l and 34 mEq/l respectively), 6% hetastarch (non-weak acid colloid, strong ion difference zero) and 0.9% saline (crystalloid, strong ion difference zero). Gelatin weak acid properties were tracked via the strong ion gap. Four-step ex vivo dilutions of pre-oxygenated human venous blood were performed to a final [Hb] near 50% baseline. With each fluid, base excess fell to approximately −13 mEq/l. Base excess/[Hb] relationships across dilution were linear and direct (R2 ≥0.96), slopes and intercepts closely resembling saline. Baseline strong ion gap was −0.3 (2.1) mEq/l. Post-dilution increases occurred in three groups: small with saline, hetastarch and albumin (to 3.5 (02) mEq/l, 4.3 (0.3) mEq/l, 3.3 (1.4) mEq/l respectively), intermediate with polygeline (to 12.2 (0.9) mEq/l) and greatest with succinylated gelatin (to 20.8 (1.4) mEq/l). We conclude that, despite colloid weak acid activity ranging from zero (hydroxyethyl starch) to greater than that of albumin with both gelatin preparations, ex vivo dilution causes a metabolic acidosis of identical severity to saline in each case. This uniformity reflects modifications to the albumin and gelatin saline vehicles, in part aimed at pH correction. By proportionally increasing the strong ion difference, these modifications counter deviations from pure saline effects caused by colloid weak acid activity. Extrapolation in vivo requires further investigation.

scholarly journals Buffer Therapy in Acute Metabolic Acidosis: Effects on Acid-Base Status and Glomerular Permeability

2019 ◽  
Author(s):  
Jan Schnapauff ◽  
David Piros ◽  
Anna Rippe ◽  
Peter Bentzer ◽  
Naomi Clyne ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Extracellular Fluid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Glomerular Permeability ◽  
Filtration Barrier ◽  
Bicarbonate Therapy ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis ◽  
Cellular Components

ABSTRACTBackground:Correction of acute metabolic acidosis using sodium bicarbonate is effective, but has been hypothesized to exacerbate intra-cellular acidosis causing cellular dysfunction. The effects of acidemia and bicarbonate therapy on the cellular components of the glomerular filtration barrier, crucial for the integrity of the renal filter, are as yet unknown. Controversy persists regarding the most appropriate method to assess acid-base status: the “Stewart approach” or the “Siggaard-Andersen approach” using the standard base excess (SBE).Methods:Here we performed physiological studies in anesthetized Sprague-Dawley rats during severe metabolic acidosis (HCl iv 6 mmol kg-1) and following bicarbonate (2.5 mmol kg-1) administration. We assessed glomerular permeability using sieving coefficients of polydisperse fluorescein isothiocyanate (FITC)-Ficoll 70/400. Acid-base status was evaluated using SBE, standard bicarbonate, total CO2, the Stewart-Fencl strong ion difference (ΔSID = Na – Cl – 38) and a theoretical model of plasma and erythrocyte strong ion difference.Results:Our data show that neither acidosis nor its correction with NaHCO3altered glomerular permeability. We identified ΔSID as a strong estimator of plasma base excess (as assessed using the Van Slyke equation).In silicomodeling indicates that changes in the strong ion difference in erythrocytes would explain their buffering effect by means of a shift of anions from the extracellular fluid.Conclusion:These data demonstrate a remarkable tolerance of the glomerular filter to severe acute acidosis and bicarbonate therapy. Our results also cast light on the buffer mechanism in erythrocytes and the ability of different acid-base parameters to evaluate the extent of an acid-base disorder.IMPORTANCE STATEMENTMetabolic acidosis is a frequent complication of acute kidney injury in critically ill patients and is associated with a high risk of mortality. Correction of acidosis using sodium bicarbonate is simple and effective, but could possibly induce intracellular acidosis causing cellular dysfunction. The effects of acidemia and subsequent bicarbonate treatment on the cellular components of the glomerular filtration barrier, crucial for the integrity of the renal filter, are unknown. We show that neither severe acidemia nor bicarbonate therapy appear to have negative effects on glomerular permeability. Our analysis also highlights the buffering effects of erythrocytes, which appear to be mediated by a shift of strong anions into the red cells, increasing the strong ion difference in the extracellular fluid.

scholarly journals Acid-Base Effects of a Bicarbonate-Balanced Priming Fluid during Cardiopulmonary Bypass: Comparison with Plasma-Lyte 148. A Randomised Single-Blinded Study

2008 ◽  
Vol 36 (6) ◽  
pp. 822-829 ◽  
Author(s):  
T. J. Morgan ◽  
G Power ◽  
B. Venkatesh ◽  
M. A. Jones
Keyword(s):  
Metabolic Acidosis ◽  
Cardiopulmonary Bypass ◽  
Base Excess ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Elective Cardiac Surgery ◽  
Standard Base Excess ◽  
Acid Base Status ◽  
Standard Base ◽  
Normal Acid

Fluid-induced metabolic acidosis can be harmful and can complicate cardiopulmonary bypass. In an attempt to prevent this disturbance, we designed a bicarbonate-based crystalloid circuit prime balanced on physico-chemical principles with a strong ion difference of 24 mEq/l and compared its acid-base effects with those of Plasma-Lyte 148, a multiple electrolyte replacement solution containing acetate plus gluconate totalling 50 mEq/l. Twenty patients with normal acid-base status undergoing elective cardiac surgery were randomised 1:1 to a 2 litre prime of either bicarbonate-balanced fluid or Plasma-Lyte 148. With the trial fluid, metabolic acid-base status was normal following bypass initiation (standard base excess 0.1 (1.3) mEq/l, mean, SD), whereas Plasma-Lyte 148 produced a slight metabolic acidosis (standard base excess -2.2 (2.1) mEq/l). Estimated group difference after baseline adjustment was 3.6 mEq/l (95% confidence interval 2.1 to 5.1 mEq/l, P=0.0001). By late bypass, mean standard base excess in both groups was normal (0.8 (2.2) mEq/l vs. -0.8 (1.3) mEq/l, P=0.5). Strong ion gap values were unaltered with the trial fluid, but with Plasma-Lyte 148 increased significantly on bypass initiation (15.2 (2.5) mEq/l vs. 2.5 (1.5) mEq/l, P <0.0001), remaining elevated in late bypass (8.4 (3.4) mEq/l vs. 5.8 (2.4) mEq/l, P <0.05). We conclude that a bicarbonate-based crystalloid with a strong ion difference of 24 mEq/l is balanced for cardiopulmonary bypass in patients with normal acid-base status, whereas Plasma-Lyte 148 triggers a surge of unmeasured anions, persisting throughout bypass. These are likely to be gluconate and/or acetate. Whether surges of exogenous anions during bypass can be harmful requires further study.

scholarly journals Acid-base status in canine babesiosis caused by Babesia canis

2020 ◽  
Vol 90 (6) ◽  
pp. 603-610
Author(s):  
Marin Torti ◽  
◽  
Josipa Kuleš ◽  
Vesna Matijatko ◽  
Mirna Brkljačić ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Strong Ion Difference ◽  
Canine Babesiosis ◽  
Acid Base ◽  
Mixed Acid ◽  
Naturally Occurring ◽  
Base Disorder ◽  
Acid Base Status ◽  
Healthy Dogs

Acid-base disturbances have been reported in severe canine babesiosis caused by Babesia rossi (B. rossi), but they have not been studied in babesiosis caused by B. canis. The objective of this study was to determine the acid-base status, blood gases and electrolyte concentrations in naturally occurring canine babesiosis caused by B. canis, and to compare the results to those in healthy dogs. Two groups of animals were used: group 1 consisted of 10 healthy dogs, and group 2 consisted of 14 dogs naturally infected with B. canis. The following acid-base disturbances occurred in the dogs with naturally occurring babesiosis: half of the dogs had a mixed acid-base disorder, and the other half a simple acid-base disorder. The most common mixed disorder was metabolic acidosis with metabolic alkalosis. It may be said that a variety of acid-base disorders occurs in canine babesiosis. The dogs in the present study had metabolic acidosis due to hyperlactemia and hyperchloremia, metabolic alkalosis due to hypochloremia and hypoalbuminemia, and respiratory alkalosis due to hypoxemia. With the use of the strong-ion difference approach clearer recognition of mixed acid-base disorders and their better understanding is possible.

scholarly journals Effects of two different regional citrate anticoagulation CVVH protocols on acid-base status and phosphate supplementation

Critical Care ◽  
2013 ◽  
Vol 17 (S2) ◽  
Author(s):  
S Morabito ◽  
V Pistolesi ◽  
V Pistolesi ◽  
L Tritapepe ◽  
L Tritapepe ◽  
...  
Keyword(s):  
Regional Citrate Anticoagulation ◽  
Acid Base ◽  
Citrate Anticoagulation ◽  
Acid Base Status ◽  
Phosphate Supplementation

scholarly journals Comparison between bicarbonate-based and Stewart methods to assess metabolic acid-base disorders in internistic patients. A pilot study

2017 ◽  
Vol 5 (2) ◽  
pp. 234
Author(s):  
Valenti Maria ◽  
Bruno Francesca ◽  
Demma Shirin ◽  
Bruno Cosimo Marcello
Keyword(s):  
Metabolic Acidosis ◽  
Traditional Method ◽  
Metabolic Alkalosis ◽  
Metabolic Disorders ◽  
Albumin Concentration ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Chi Square ◽  
Significant Difference ◽  
Acid Base Status

Aim: To assess the acid-base status in a cohort of internistic patients, using traditional and “modern” methods, to compare their different sensitivity to detect metabolic disorders and to evaluate a possible relationship between classical and alternative parameters.Patients and Methods: 143 assessment of acid-base and electrolytes balance on 121 internistic patients (76 males and 45 females, mean age 73.9 ± 10,8 years) were examined according to bicarbonate-based and Stewart methods.Results: The traditional method detected 81 cases (56.6 %) of metabolic alkalosis and 15 cases (10.4 %) of metabolic acidosis. The Stewart method detected 92 cases (64.3 %) of metabolic alkalosis and 22 cases (15.3%) of metabolic acidosis.Traditional method failed to detect 11 cases of metabolic alkalosis (chi square = 1.443; p = 0.226), and 7 cases of metabolic acidosis (chi square = 1.118; p = 0.290) when compared to Stewart's method. A significant relationship was observed between Strong Ion Gap (SIG) and Anion Gap corrected for albumin concentration (AGcorr) (r= 0.53; p <0.001).Conclusions: Our result showed that traditional method is useful to assess acid-base status in internistic clinical setting as well as Stewart's method because no significant difference was found between the two approaches. Nevertheless, the light disagreement observed between the two methods suggests that in a small percentage of cases the traditional method can fail to detect metabolic acid-base abnormalities.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

scholarly journals Complications of Regional Citrate Anticoagulation for Continuous Renal Replacement Therapy: An Observational Study

2020 ◽  
Vol 49 (5) ◽  
pp. 567-575 ◽  
Author(s):  
Nathan Axel Bianchi ◽  
Marco Altarelli ◽  
Philippe Eckert ◽  
Antoine Guillaume Schneider
Keyword(s):  
Renal Replacement Therapy ◽  
Continuous Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Real Life ◽  
Regional Citrate Anticoagulation ◽  
Acid Base ◽  
Metabolic Complications ◽  
Citrate Anticoagulation ◽  
Randomized Controlled ◽  
Heparin Anticoagulation

Introduction: Regional citrate anticoagulation (RCA) is the recommended anticoagulation modality for continuous renal replacement therapy (CRRT). RCA was associated with a low rate of complications in randomized controlled trials. However, little is known about the type and rate of complications in real life. We sought to describe complications associated with RCA in comparison with those associated with heparin anticoagulation. Methods: In our institution, RCA has been the default anticoagulation modality for CRRT in all patients without contraindications since 2013. We have retrospectively reviewed all consecutive patients who received CRRT between January and December 2016 in our institution. For each CRRT session, we have assessed circuit duration, administered dose, as well as therapy-associated complications. Those parameters were compared according to whether the circuit was run in continuous veno-venous hemodialysis (CVVHD) mode with RCA or continuous veno-venous hemofiltration (CVVH) mode with heparin anticoagulation. Results: We analyzed 691 CRRT sessions in 121 patients. Of those 400 (57.9%) were performed in CVVHD-RCA mode and 291 (42.1%) in CVVH-Heparin Mode. Compared with ­CVVH-Heparin mode, CVVHD-RCA mode was associated with a longer circuit lifespan (median duration 54.9 interquartile range [IQR 44.6] vs. 15.3 h [IQR 22.4], p < 0.0001). It was associated with a higher rate of metabolic acidosis 77 (20.2%) vs. 18 (7.2%), (p < 0.0001), alkalosis 186 (48.7%) vs. 43 (17.1%), (p= 0.0001), and hypocalcemia 96 (25.07%) vs. 26 events (10.79%), p < 0.0001. However, the majority of these alterations were of benign or moderate severity. Only one possible citrate intoxication was observed. Conclusions: CVVHD-RCA was associated with a much longer circuit life but an increased rate of minor metabolic complications, in particular acid-base derangements. Some of these complications might have been prevented by therapy adaptation. Medical and nursing staff education is of major importance in the implementation of an RCA protocol.

Role of endothelin-1 in renal regulation of acid-base equilibrium in acidotic humans

2012 ◽  
Vol 303 (7) ◽  
pp. F991-F999 ◽  
Author(s):  
Alexandra Pallini ◽  
Henry N. Hulter ◽  
Jurgen Muser ◽  
Reto Krapf
Keyword(s):  
Metabolic Acidosis ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Endothelin 1 ◽  
Plasma Bicarbonate ◽  
Human Volunteers ◽  
Acid Base Equilibrium ◽  
Normal Human ◽  
Mineralocorticoid Activity

Endothelin-1 inhibits collecting duct sodium reabsorption and stimulates proximal and distal tubule acidification in experimental animals both directly and indirectly via increased mineralocorticoid activity. Diet-induced acid loads have been shown to increase renal endothelin-1 activity, and it is hypothesized that increased dietary acid-induced endothelin-1 activity may be a causative progression factor in human renal insufficiency and that this might be reversed by provision of dietary alkali. We sought to clarify, in normal human volunteers, the role of endothelin-1 in renal acidification and to determine whether the effect is dependent on dietary sodium chloride. Acid-base equilibrium was studied in seven normal human volunteers with experimentally induced metabolic acidosis [NH4Cl 2.1 mmol·kg body weight (BW)−1·day−1] with and without inhibition of endogenous endothelin-1 activity by the endothelin A/B-receptor antagonist bosentan (125 BID p.o./day) both during dietary NaCl restriction (20 mmol/day) and NaCl repletion (2 mmol NaCl·kg BW−1·day−1). During NaCl restriction, but not in the NaCl replete state, bosentan significantly increased renal net acid excretion in association with stimulation of ammoniagenesis resulting in a significantly increased plasma bicarbonate concentration (19.0 ± 0.8 to 20.1 ± 0.9 mmol/l) despite a decrease in mineralocorticoid activity and an increase in endogenous acid production. In pre-existing human metabolic acidosis, endothelin-1 activity worsens acidosis by decreasing the set-point for renal regulation of plasma bicarbonate concentration, but only when dietary NaCl provision is restricted.

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