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 (βH+) and [H+] curve shift at 40 mmHg ([H+]40). Model findings were: 1) In severe hypoproteinemia, hemoglobin enhances buffering (decreases βH+), whereas albumin compromises it, resulting in an almost unchanged βH+; [H+]40 decreases (alkalemia) due to hypoalbuminemia. 2) Severe hyperalbuminemia greatly increases both βH+ and [H+]40, hence, compromising buffering and causing a severe acidemia, 3) PCO2-induced changes in the electrical-charge concentration of hemoglobin is 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, βH+, [H+]40 and SIG, derived from a [H+] vs PCO2 perspective, are a more informative and intuitive way to characterize blood acid-base state.