Physicochemical properties of abnormal blood acid-base buffering

Area of Science:

• Physicochemical modeling
• Blood acid-base balance
• Physiology

Background:

• Existing models of blood acid-base balance are often limited to single compartments and lack crucial constraints.
• Understanding the physicochemical basis of blood buffering is essential for diagnosing and managing acid-base disorders.

Purpose of the Study:

• To develop and validate a two-compartment physicochemical model of blood acid-base state.
• To investigate the impact of altered protein concentrations (hypoproteinemia and hyperalbuminemia) on blood buffering.
• To identify novel parameters for characterizing blood acid-base status.

Main Methods:

• Development of two-compartment physicochemical models based on in vitro experiments with normal blood.
• Manipulation of blood protein levels (hypoproteinemia and hyperalbuminemia) and equilibration with varying CO2 concentrations.
• Evaluation of physicochemical factors using buffer curve linearized slope (βH+) and [H+] at 40 mmHg ([H+]40).

Main Results:

• Hypoproteinemia with hypoalbuminemia led to alkalemia, while severe hyperalbuminemia caused acidemia and compromised buffering.
• Hemoglobin's electrical charge changes due to Pco2 were identified as key to buffering in altered protein states.
• Strong-ion gap (SIG) was confirmed as a Pco2-independent characteristic of blood acid-base status.

Conclusions:

• The developed model provides a more comprehensive physicochemical representation of blood acid-base dynamics.
• New parameters (βH+, [H+]40, and SIG) offer a more informative and intuitive characterization of blood buffering properties.
• The findings highlight the critical role of protein concentration and Pco2 in maintaining blood pH homeostasis.