Acid–base regulations a comparison of quantitative methods

1994 ◽  
Vol 72 (7) ◽  
pp. 818-826 ◽  
Author(s):  
John M. Kowalchuk ◽  
Barry W. Scheuermann

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.

2009 ◽  
Vol 37 (3) ◽  
pp. 407-414 ◽  
Author(s):  
T. J. Morgan ◽  
M. Vellaichamy ◽  
D. M. Cowley ◽  
S. L. Weier ◽  
B. Venkatesh ◽  
...  

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.


2005 ◽  
Vol 98 (6) ◽  
pp. 2119-2125 ◽  
Author(s):  
Chris M. Anstey

Currently, three strong ion models exist for the determination of plasma pH. Mathematically, they vary in their treatment of weak acids, and this study was designed to determine whether any significant differences exist in the simulated performance of these models. The models were subjected to a “metabolic” stress either in the form of variable strong ion difference and fixed weak acid effect, or vice versa, and compared over the range 25 ≤ Pco2 ≤ 135 Torr. The predictive equations for each model were iteratively solved for pH at each Pco2 step, and the results were plotted as a series of log(Pco2)-pH titration curves. The results were analyzed for linearity by using ordinary least squares regression and for collinearity by using correlation. In every case, the results revealed a linear relationship between log(Pco2) and pH over the range 6.8 ≤ pH ≤ 7.8, and no significant difference between the curve predictions under metabolic stress. The curves were statistically collinear. Ultimately, their clinical utility will be determined both by acceptance of the strong ion framework for describing acid-base physiology and by the ease of measurement of the independent model parameters.


2006 ◽  
Vol 3 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger

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.


2009 ◽  
Vol 296 (3) ◽  
pp. R722-R727 ◽  
Author(s):  
Megan E. Preston ◽  
Dennis Jensen ◽  
Ian Janssen ◽  
John T. Fisher

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.


2001 ◽  
Vol 91 (3) ◽  
pp. 1364-1371 ◽  
Author(s):  
Peter D. Constable

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.


1997 ◽  
Vol 83 (1) ◽  
pp. 297-311 ◽  
Author(s):  
Peter D. Constable

Constable, Peter D. A simplified strong ion model for acid-base equilibria: application to horse plasma. J. Appl. Physiol. 83(1): 297–311, 1997.—The Henderson-Hasselbalch equation and Stewart’s strong ion model are currently used to describe mammalian acid-base equilibria. Anomalies exist when the Henderson-Hasselbalch equation is applied to plasma, whereas the strong ion model does not provide a practical method for determining the total plasma concentration of nonvolatile weak acids ([Atot]) and the effective dissociation constant for plasma weak acids ( K a). A simplified strong ion model, which was developed from the assumption that plasma ions act as strong ions, volatile buffer ions ([Formula: see text]), or nonvolatile buffer ions, indicates that plasma pH is determined by five independent variables:[Formula: see text], strong ion difference, concentration of individual nonvolatile plasma buffers (albumin, globulin, and phosphate), ionic strength, and temperature. The simplified strong ion model conveys on a fundamental level the mechanism for change in acid-base status, explains many of the anomalies when the Henderson-Hasselbalch equation is applied to plasma, is conceptually and algebraically simpler than Stewart’s strong ion model, and provides a practical in vitro method for determining [Atot] and K a of plasma. Application of the simplified strong ion model to CO2-tonometered horse plasma produced values for [Atot] (15.0 ± 3.1 meq/l) and K a(2.22 ± 0.32 × 10−7 eq/l) that were significantly different from the values commonly assumed for human plasma ([Atot] = 20.0 meq/l, K a = 3.0 × 10−7 eq/l). Moreover, application of the experimentally determined values for [Atot] and K a to published data for the horse (known [Formula: see text], strong ion difference, and plasma protein concentration) predicted plasma pH more accurately than the values for [Atot] and K a commonly assumed for human plasma. Species-specific values for [Atot] and K a should be experimentally determined when the simplified strong ion model (or strong ion model) is used to describe acid-base equilibria.


1998 ◽  
Vol 84 (5) ◽  
pp. 1740-1748 ◽  
Author(s):  
Peter Wilkes

The present study was a prospective, nonrandomized, observational examination of the relationship among hypoproteinemia and electrolyte and acid-base status in a critical care population of patients. A total of 219 arterial blood samples reviewed from 91 patients was analyzed for arterial blood gas, electrolytes, lactate, and total protein. Plasma strong-ion difference ([SID]) was calculated from [Na+] + [K+] − [Cl−] − [La−]. Total protein concentration was used to derive the total concentration of weak acid ([A]tot). [A]tot encompassed a range of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with [A]tot. The decline in [SID] was primarily attributable to an increase in [Cl−]. A direct correlation was also noted between[Formula: see text] and [SID], but not between [Formula: see text] and [A]tot. The decrease in [SID] and [Formula: see text] was such that neither [H+] nor [[Formula: see text]] changed significantly with [A]tot.


2005 ◽  
Vol 98 (3) ◽  
pp. 856-865 ◽  
Author(s):  
Benjamin F. Miller ◽  
Michael I. Lindinger ◽  
Jill A. Fattor ◽  
Kevin A. Jacobs ◽  
Paul J. LeBlanc ◽  
...  

An emerging technique used for the study of metabolic regulation is the elevation of lactate concentration with a sodium-lactate infusion, the lactate clamp (LC). However, hematological and acid-base properties affected by the infusion of hypertonic solutions containing the osmotically active strong ions sodium (Na+) and lactate (Lac−) are a concern for clinical and research applications of LC. In the present study, we characterized the hematological and plasma acid-base changes during rest and prolonged, light- to moderate-intensity (55% V̇o2 peak) exercise with and without LC. During the control (Con) trial, subjects were administered an isotonic, isovolumetric saline infusion. During LC, plasma lactate concentration ([Lac−]) was elevated to 4 meq/l during rest and to 4–7 meq/l during exercise. During LC at rest, there were rapid and transient changes in plasma, erythrocyte, and blood volumes. LC resulted in decreased plasma [H+] (from 39.6 to 29.6 neq/l) at the end of exercise while plasma [HCO3−] increased from 26 to 32.9 meq/l. Increased plasma strong ion difference [SID], due to increased [Na+], was the primary contributor to decreased [H+] and increased [HCO3−]. A decrease in plasma total weak acid concentration also contributed to these changes, whereas Pco2 contributed little. The infusion of hypertonic LC caused only minor volume, acid-base, and CO2 storage responses. We conclude that an LC infusion is appropriate for studies of metabolic regulation.


1982 ◽  
Vol 101 (1) ◽  
pp. 255-264 ◽  
Author(s):  
RAYMOND P. HENRY ◽  
JAMES N. CAMERON

When transferred from 865 to 250 m-osmol salinity, the blue crab C. sapidus maintains its blood Na+ and Cl− concentrations significantly above those in the medium. When branchial carbonic anhydrase is inhibited by acetazolamide, ion regulation fails and the animals do not survive the transfer. An alkalosis occurs in the blood at low salinity, indicated by an increase in HCO3− and pH at constant PCO2. The alkalosis is closely correlated with an increase in the Na+-Cl− difference, a convenient indicator of the overall strong ion difference. The contribution of changes in PCO2 to acid-base changes was negligible, but the change in the total weak acid (proteins) may be important. It is suggested that the change in blood acidbase status with salinity is related to an increase in the strong ion difference, which changes during the transition from osmoconformity to osmoregulation in the blue crab, and which is related to both carbonic anhydrase and ionactivated ATPases. Note:


1988 ◽  
Vol 255 (1) ◽  
pp. R97-R104 ◽  
Author(s):  
J. W. Anderson ◽  
D. B. Jennings

Arterial PCO2, arterial [H+] ([H+]a), electrolytes, and osmolality, as well as rectal temperature (Tre), were monitored in six awake dogs over sequential 12- or 13-day periods in which their NaCl intake was first less than 5 meq/day, then approximately 120 meq/day, and finally less than 5 meq/day. Water intake was maintained constant at 77 ml.kg-1.day-1 throughout. During low-NaCl periods, decreases in body and plasma water, indicated by weight loss did not prevent lower arterial [Na+] ([Na+]a), arterial [Cl-] ([Cl-]a), and osmolality relative to the high-NaCl period. During high dietary NaCl, the arterial strong ion difference [[SID]a = ([Na+]a + [K+]a) - (arterial [lactate-] + [Cl-]a)] was lower. From physicochemistry, this lowered [SID]a results in a higher [H+]a. However, independent of NaCl intake, [H+]a was positively correlated with plasma osmolality; moreover, [H+]a, relative to plasma osmolality, was higher at lower Tre than at higher Tre. We speculate that this spectrum of plasma osmolality and body temperature may contribute to the creation of an appropriate protein pK to match plasma [H+]a. We also found that the difference between plasma [protein] (measured by the biuret test) and [ATOT]a (an estimation of plasma protein as total weak acid from physicochemistry) was related to plasma osmolality, [SID]a, and [Na+]a. These latter relations may reflect the effect of plasma water concentration (osmolality) and strong ions on the pK of plasma proteins.


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