Physicochemical properties of abnormal blood acid-base buffering

This paper describes two new features 1) development of physicochemically based, two-compartment models describing acid-base-state changes in normal and abnormal blood and 2) use of model results to view and describe physicochemical properties of blood, in terms of Pco₂ as the causative independent variable and effected [H⁺] changes as the dependent variable. Models were derived from an in vitro experimental study, where normal blood was made both hypoproteinemic and hyperalbuminemic and then equilibrated with CO₂. Strong-ion gap (SIG) values were selected to match model and experimental pH. The effect of individual physicochemical factors affecting blood acid-base-state were evaluated from their induced changes on buffer curve linearized slope (β_H+) and [H⁺] curve shift at 40 mmHg ([H]₄₀). Model findings were: 1) in severe hypoproteinemia, hemoglobin enhances buffering (decreases β_H+), whereas albumin compromises it, resulting in an almost unchanged β_H+; [H]₄₀ decreases (alkalemia) due to hypoalbuminemia. 2) Severe hyperalbuminemia greatly increases both β_H+ and [H]₄₀, hence, compromising buffering and causing a severe acidemia. 3) Pco₂-induced changes in the electrical-charge concentration of hemoglobin are the principal factor responsible for maintaining normal buffering characteristics in hypoproteinemia and hyperalbuminemia. 4) SIG values are a third Pco₂-independent characteristic of blood acid-base state and 5) the quantities, β_H+, [H]₄₀, and SIG, derived from a [H⁺] vs. Pco₂ perspective, are a more informative and intuitive way to characterize blood acid-base state.NEW & NOTEWORTHY This study represents the most up-to-date, physicochemical, multi-compartment computer model of the processes involved in determining the acid-base buffering state of blood. Previous models lack this capability, notably by being single compartment and/or lacking electroneutrality and osmotic constraints. Model results, analyzed from a different perspective of dependent [H⁺] changes resulting from independent Pco₂ changes, provide a new set of Pco₂-independent parameters, characteristic of blood buffering properties.