A simplified strong ion model for acid-base equilibria: application to horse plasma

Abstract

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 (Ka). A simplified strong ion model, which was developed from the assumption that plasma ions act as strong ions, volatile buffer ions (HCO-3), or nonvolatile buffer ions, indicates that plasma pH is determined by five independent variables: PCO2, 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 Ka 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 Ka (2.22 +/- 0.32 x 10(-7) eq/l) that were significantly different from the values commonly assumed for human plasma ([Atot] = 20.0 meq/l, Ka = 3.0 x 10(-7) eq/l). Moreover, application of the experimentally determined values for [Atot] and Ka to published data for the horse (known PCO2, strong ion difference, and plasma protein concentration) predicted plasma pH more accurately than the values for [Atot] and Ka commonly assumed for human plasma. Species-specific values for [Atot] and Ka should be experimentally determined when the simplified strong ion model (or strong ion model) is used to describe acid-base equilibria.

Effect of Intravenous Small‐Volume Hypertonic Sodium Bicarbonate, Sodium Chloride, and Glucose Solutions in Decreasing Plasma Potassium Concentration in Hyperkalemic Neonatal Calves with Diarrhea

“…In addition to the traditional Henderson‐Hasselbalch acid‐base model, the simplified quantitative physicochemical strong ion approach33 was used to allow a more comprehensive assessment of acid‐base status of calves of this study population. The strong ion difference in mEq/L calculated from the plasma concentrations of sodium, potassium, and chloride (SID 3 ) was obtained as follows2:…”

Physicochemical Approach to Determine the Mechanism for Acid–Base Disorders in 793 Hospitalized Foals

“…and unmeasured strong ion difference (SID um ) calculated as:19 ${\text{SID}}_{\mathrm{normalum}}=S\times {\mathrm{normalp}}_{\mathrm{normala}}{\text{CO}}_2\times {10}^{(\mathrm{pH}-\mathrm{pK}{1}^{\prime })}-\frac{A_{\mathrm{tot}}}{[false(1+{10}^{false(\mathrm{normalpKa}-\mathrm{normalpH}false)}false]}-{\text{SID}}_{\mathrm{normalm}}$ …”

“…Strong ion gap was calculated by rearranging the above equation and substituting SID um for SIG as:19 $\text{SIG}=\frac{[A_{\mathrm{normaltot}}]}{[false(1+{10}^{false(\mathrm{pKa}-\mathrm{pH})}false]}-\text{AG}$ …”

“…where pK a (6.65) is the effective dissociation constant of equine plasma weak acids19 and total plasma concentration of weak acids ( A tot ) was calculated as: $A_{\mathrm{normaltot}}false(\text{mmol/L}false)=false[0.22\times \text{(TP)}false]$ …”

“…Neither the base excess nor the bicarbonate can explain the cause of a disturbance, only its existence and severity 16, 17. The quantitative physicochemical approach emphasizes the importance of strong ion difference (SID) which is the difference between the charge of plasma strong cations (Na + , K + ,Ca 2+ , Mg 2+ and anions (Cl − , l ‐lactate − , sulfate, and ketoacids), p a CO 2 , and total plasma protein concentration ( A tot ) in determining plasma pH and [${\text{HCO}}_3^{-}$] 18, 19. This approach is mechanistic and provides a more in‐depth insight into the pathophysiology of acid–base imbalances 18.…”