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 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.

Plasma Acid-base Changes in Chronic Renal Failure: A Stewart Analysis

2005 ◽  
Vol 28 (10) ◽  
pp. 961-965 ◽  
Author(s):  
D.A. Story ◽  
A. Tosolini ◽  
R. Bellomo ◽  
M. Leblanc ◽  
L. Bragantini ◽  
...  
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Chronic Renal Failure ◽  
Base Excess ◽  
Chloride Ions ◽  
Minor Role ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Failure Group ◽  
Stewart Approach

The bicarbonate centered approach to acid-base physiology involves complex explanations for the metabolic acidosis associated with chronic renal failure. We used the alternate Stewart approach to acid-base physiology to quantify the acid-base chemistry of patients with chronic renal failure. We examined the plasma and urine chemistry of 19 patients with chronic renal failure who were predialysis and 20 healthy volunteers. We compared the plasma strong-ion-difference due to sodium, potassium, and chloride ions as well as the weak acids albumin and phosphate. We used a simplified Fencl-Stewart approach to quantify the effects of sodium-chloride, albumin, and unmeasured ions on base-excess. The chronic renal failure group had a greater metabolic acidosis, with a base-excess that differed from the healthy group by a mean of −2.7 mmol/L, p= 0.04. This was associated with a strong ion acidosis due to both increased chloride and decreased sodium. The anion gap, strong-ion-gap, and base-excess effect of unmeasured ions were similar in both groups suggesting that unmeasured ions had only a minor role in the acid-base status in this group of patients.

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.

Impact of Continuous Veno-venous Hemofiltration on Acid-base Balance

2003 ◽  
Vol 26 (1) ◽  
pp. 19-25 ◽  
Author(s):  
J. Rocktäschel ◽  
H. Morimatsu ◽  
S. Uchino ◽  
C. Ronco ◽  
R. Bellomo
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Alkalosis ◽  
Base Excess ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Biophysical Analysis ◽  
Base Balance

Background Continuous veno-venous hemofiltration (CVVH) appears to have a significant and variable impact on acid-base balance. However, the pathogenesis of these acid-base effects remains poorly understood. The aim of this study was to understand the nature of acid-base changes in critically ill patients with acute renal failure during continuous veno-venous hemofiltration by applying quantitative methods of biophysical analysis (Stewart-Figge methodology). Methods We studied forty patients with ARF receiving CVVH in the intensive care unit. We retrieved the biochemical data from computerized records and conducted quantitative biophysical analysis. We measured serum Na+, K+, Mg2+, Cl-, HCO3-, phosphate, ionized Ca2+, albumin, lactate and arterial blood gases and calculated the following Stewart-Figge variables: Strong Ion Difference apparent (SIDa), Strong Ion Difference Effective (SIDe) and Strong Ion Gap (SIG). Results Before treatment, patients had mild acidemia (pH: 7.31) secondary to metabolic acidosis (bicarbonate: 19.8 mmol/L and base excess: −5.9 mEq/L). This acidosis was due to increased unmeasured anions (SIG: 12.3 mEq/L), hyperphosphatemia (1.86 mmol/L) and hyperlactatemia (2.08 mmol/L). It was attenuated by the alkalinizing effect of hypoalbuminemia (22.5 g/L). After commencing CVVH, the acidemia was corrected within 24 hours (pH 7.31 vs 7.41, p <0.0001). This correction was associated with a decreased strong ion gap (SIG) (12.3 vs. 8.8 mEq/L, p <0.0001), phosphate concentration (1.86 vs. 1.49 mmol/L, p <0.0001) and serum chloride concentration (102 vs. 98.5 mmol/L, p <0.0001). After 3 days of CVVH, however, patients developed alkalemia (pH: 7.46) secondary to metabolic alkalosis (bicarbonate: 29.8 mmol/L, base excess: 6.7 mEq/L). This alkalemia appeared secondary to a further decrease in SIG to 6.7 mEq/L (p <0.0001) and a further decrease in serum phosphate to 0.77 mmol/L (p <0.0001) in the setting of persistent hypoalbuminemia (21.0 g/L; p=0.56). Conclusions CVVH corrects metabolic acidosis in acute renal failure patients through its effect on unmeasured anions, phosphate and chloride. Such correction coupled with the effect of hypoalbuminemia, results in the development of a metabolic alkalosis after 72 hours of treatment.

Acid–base regulations a comparison of quantitative methods

1994 ◽  
Vol 72 (7) ◽  
pp. 818-826 ◽  
Author(s):  
John M. Kowalchuk ◽  
Barry W. Scheuermann
Keyword(s):  
Quantitative Methods ◽  
Linear Regression Analysis ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Weak Acids ◽  
Acid Base ◽  
Ramp Exercise ◽  
The Difference ◽  
Biological Solutions

The [H+] and [HCO3−] of biological solutions is determined by the [Formula: see text], the concentration of strong ions (mainly Na+, K+, Ca2+, Cl−, lactate−), and the concentration of weak acids (mainly proteins, phosphates). Two mathematical models are available that use a quantitative approach to describe the acid–base behaviour of plasma, but which differ in their treatment of the weak acid component: Stewart model (using [Formula: see text], strong ion difference (SID = [Na+ + K+ + Ca2+] − [Cl− + lactate−]) and [protein]TOT); Fencl model (using [Formula: see text], SID, [albumin], and [Pi]TOT). The present study compared measured and estimated [H+] and [HCO3−] in whole-blood samples collected from eight subjects during two double-ramp exercise protocols to the limit of tolerance to assess the accuracy with which each of the quantitative models predicts measured values. Arterialized-venous blood was analyzed for [H+], [Formula: see text], [protein]TOT, [albumin], [Pi]TOT, and SID (= [Na+ + K+ + Ca2+] − [Cl− + lactate−]), and these independent variables were then substituted into the appropriate mathematical model to estimate [H+] and [HCO3−]. Analysis showed that the [H+] and [HCO3−] estimated using either model provided a good estimate of the [H+] (Stewart model, r = 0.81; Fencl model, r = 0.81) and [HCO3−] (Stewart model, r = 0.93; Fencl model, r = 0.93) measured in plasma; linear regression analysis demonstrated that the slopes and intercepts for each of die relationships were not different (p > 0.05) from the line of identity. Differences between estimated and measured values were small, averaging < 3 nmol∙L−1 for [H+] and < 2 mmol∙L−1 for [HCO3−]. However, in the case of plasma [H+], the difference between estimated and measured values became skewed (i.e., [H+]M < [H+]Est) above [H+]M ≈ 55 nmol∙L−1, or at [SID] ≤ 35 mequiv.∙L−1. Reasons for the difference between measured and estimated values are discussed, with attention given to the [SID] and weak acid components.Key words: quantitative acid–base chemistry, strong ion difference, weak acids, strong ions, lactate, hydrogen ion, bicarbonate.

Acid-base analysis during experimental anemia in rats

2000 ◽  
Vol 78 (10) ◽  
pp. 774-780 ◽  
Author(s):  
J Pesquero ◽  
V Alfaro ◽  
L Palacios
Keyword(s):  
Base Excess ◽  
Respiratory Alkalosis ◽  
Physicochemical Analysis ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Experimental Conditions ◽  
Physiological Relevance ◽  
Base Analysis ◽  
Acid Base Status

The present study evaluated the acid-base status of anemic rats by using two approaches of acid-base analysis: one based on the base excess (BE) calculation and the other based on Stewart's physicochemical analysis. Two sets of experimental data, derived from two different methods of inducing anemia, were used: repetitive doses of phenylhydrazine (PHZ) and bleeding (BL). A significant uncompensated respiratory alkalosis was found in both groups of anemic rats. BE increased slightly, whereas strong ion difference ([SID]) and weak acid buffers ([ATOT]) remained unchanged in anemic rats. The reasons for the absence of compensation for hypocapnia and the differences in the behaviour of acid-base variables are discussed. BE increase was considered paradoxical; its calculation was affected by the experimental conditions and BE had little physiological relevance during anemia. The absence of metabolic renal compensation in anemic rats could be due to a lower pH in the kidney due to anemic hypoxia. Finally, the changes in buffer strength related to low Hb and low Pc02 might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.Key words: anemia, phenylhydrazine, bleeding, base excess, strong ion difference, non-carbonic buffers.

Daily variation in plasma electrolyte and acid–base status in fasted horses over a 25 h period of rest

2006 ◽  
Vol 3 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger
Keyword(s):  
Time Course ◽  
Daily Variation ◽  
Venous Blood ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Night Time ◽  
Plasma Protein Concentration ◽  
Plasma Electrolyte ◽  
Acid Base Status

AbstractMeasurement and interpretation of acid–base status are important in clinical practice and among racing jurisdictions to determine if horses have been administered alkalinizing substances for the purpose of enhancing performance. The present study used the physicochemical approach to characterize the daily variation in plasma electrolytes and acid–base state that occurs in horses in the absence of feeding and exercise. Jugular venous blood was sampled every 1–2 h from two groups (n=4 and n=5) of Standardbred horses over a 25 h period where food and exercise were withheld. One group of horses was studied in October and one in December. The time course and magnitude of circadian responses differed between the two groups, suggesting that subtle differences in environment may manifest in acid–base status. Significant daily variation occurred in plasma weak acid concentration ([Atot]) and strong ion difference ([SID]), [Cl−], [K+], [Na+] and [lactate−], which contributed to significant changes in [H+] and TCO2. The night-time period was associated with a mild acidosis, marked by increases in plasma [H+] and decreases in TCO2, compared with the morning hours. The night-time acidosis resulted from an increased plasma [Atot] due to an increased plasma protein concentration ([PP]), and a decreased [SID] due to increases in [Cl−] and decreases in [Na+]. An increased plasma [K+] during the night-time had a mild alkalotic effect. There were no differences in pCO2. It was concluded that many equine plasma electrolyte and acid–base parameters exhibit fluctuations in the absence of feeding and exercise, and it is likely that some of these changes are due to daily variation.

Effect of menopause on the chemical control of breathing and its relationship with acid-base status

2009 ◽  
Vol 296 (3) ◽  
pp. R722-R727 ◽  
Author(s):  
Megan E. Preston ◽  
Dennis Jensen ◽  
Ian Janssen ◽  
John T. Fisher
Keyword(s):  
Venous Blood ◽  
Premenopausal Women ◽  
Weak Acid ◽  
Control Of Breathing ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Serum Progesterone ◽  
Sex Steroid Hormone ◽  
Peripheral Chemoreflex

This study examined the role of alterations in the chemoreflex control of breathing, acid-base balance, and their interaction in postmenopausal ventilatory adaptations. A modified iso-oxic hyperoxic and hypoxic CO2-rebreathing procedure was employed to evaluate central and peripheral chemoreflex drives to breathe, respectively, in 15 healthy postmenopausal and 20 premenopausal women of similar age. Arterialized venous blood samples were collected at rest for the estimation of arterial Pco2 (PaCO2) and H+ concentration ([H+]), plasma strong ion difference ([SID]) and total weak acid ([A]tot) concentrations, and serum progesterone ([P4]) and 17β-estradiol ([E2]) concentrations. In post- compared with premenopausal women, PaCO2, [SID], and the central chemoreflex ventilatory recruitment threshold for Pco2 (VRTco2) were higher, whereas [P4] and [E2] were lower (all P < 0.05), with no significant change in central or peripheral chemoreflex sensitivity, peripheral chemoreflex VRTco2, and [A]tot. The acidifying effect of an increased PaCO2 was offset by the alkalizing effect of an increased [SID], such that [H+] was preserved in post- compared with premenopausal women. PaCO2 correlated positively with the central chemoreflex VRTco2 ( r = 0.67, P < 0.01), which in turn correlated positively with [SID] ( r = 0.53, P < 0.01) within the pooled data. In conclusion, the relative alveolar hypoventilation and attendant arterial hypercapnia in healthy post- compared with premenopausal women could be explained, in part, by the interaction of 1) reduced central, but not peripheral, chemoreflex VRTco2, 2) increased [SID], and 3) reduced circulating female sex steroid hormone concentrations.

Total weak acid concentration and effective dissociation constant of nonvolatile buffers in human plasma

2001 ◽  
Vol 91 (3) ◽  
pp. 1364-1371 ◽  
Author(s):  
Peter D. Constable
Keyword(s):  
Dissociation Constant ◽  
Human Plasma ◽  
Total Concentration ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Horse Plasma ◽  
Using Data ◽  
Species Specific

The strong ion approach provides a quantitative physicochemical method for describing the mechanism for an acid-base disturbance. The approach requires species-specific values for the total concentration of plasma nonvolatile buffers (Atot) and the effective dissociation constant for plasma nonvolatile buffers ( K a), but these values have not been determined for human plasma. Accordingly, the purpose of this study was to calculate accurate Atot and K a values using data obtained from in vitro strong ion titration and CO2tonometry. The calculated values for Atot (24.1 mmol/l) and K a (1.05 × 10−7) were significantly ( P < 0.05) different from the experimentally determined values for horse plasma and differed from the empirically assumed values for human plasma (Atot = 19.0 meq/l and K a = 3.0 × 10−7). The derivatives of pH with respect to the three independent variables [strong ion difference (SID), Pco 2, and Atot] of the strong ion approach were calculated as follows: [Formula: see text] [Formula: see text], [Formula: see text]where S is solubility of CO2 in plasma. The derivatives provide a useful method for calculating the effect of independent changes in SID+, Pco 2, and Atot on plasma pH. The calculated values for Atot and K a should facilitate application of the strong ion approach to acid-base disturbances in humans.

scholarly journals Intestinal Permeability Assays: a Review

2021 ◽  
Vol 31 (1) ◽  
pp. 20-30
Author(s):  
A. A. Iakupova ◽  
S. R. Abdulkhakov ◽  
R. K. Zalyalov ◽  
A. G. Safin ◽  
R. A. Abdulkhakov
Keyword(s):  
Intestinal Permeability ◽  
Ex Vivo ◽  
Venous Blood ◽  
Intestinal Barrier ◽  
Intestinal Lumen ◽  
Alcoholic Fatty Liver ◽  
Key Points ◽  
Assessment Techniques ◽  
Portal Venous Blood

Aim. A literature review of intestinal permeability assessment techniques.Key points. The intestinal barrier is a functional entity separating the intestinal lumen and internal body, and intestinal permeability is a measure of the barrier functionality. The intestinal barrier integrity and permeability assays differ by the application setting (in vivo or ex vivo), subject (human or animal), marker molecules used to assess permeability (ions, various size carbohydrates, macromolecules, antigens, bacterial products and bacteria), biomaterial for the marker concentration assays (peripheral blood, portal venous blood, urine, stool). Despite a great variety of methods for assessing intestinal permeability, their clinical application requires further studies due to a lack of standardisation, the complexity of selected techniques and occasional limited reliability of results.Conclusion. Further investigation and improvement of intestinal permeability assays is required. The assay and result standardisation will facilitate practice in functional and organic intestinal diseases, as well as allergies, diabetes mellitus, non-alcoholic fatty liver disease and some other illnesses.

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