Acute Response to Acid-base Stress

2021

ASAIO Journal

This study contrasts the abilities and mechanisms of two physicochemical, mathematical models to predict experimental bicarbonate kinetics, hence, buffer transport, during a hemodialysis (HD) treatment in chronic renal failure patients. The existing Sargent model assumes that the body fluids can be described as a single, homogeneous extracellular fluid (EC) compartment whose volume decreases because of a constant ultrafiltration rate during HD. Bicarbonate and acetate transport between HD fluid and the EC compartment are by convection and diffusion with acetate metabolized in that compartment. The new model formulated in this study assumes the same conditions as Sargent et al., but constrains ion concentrations in the EC to be electrically neutral at all times. This constraint requires inclusion in the EC of other transportable small ions, Na+, K+, Cl− and unidentified, anionic organic acids in addition to an electrical charge on impermeable albumin. The findings are that the new electroneutrality model predicts plasma bicarbonate-concentration kinetics as closely as the Sargent model, but bicarbonate transport is an unlikely mechanism. Rather, the findings are better explained by rapid interconversion of CO2 and bicarbonate in this simplified EC compartment model. The results of this study bring into question the ability of the Sargent et al. hypothesized H+-mobilization model to explain buffer-transport kinetics during HD.

mentioning

confidence: 99%

Mechanisms of Acid-Base Kinetics During Hemodialysis: a Mathematical-Model Study

2021

ASAIO Journal

A comprehensive, computer-model-based approach for diagnosis and treatment of complex acid–base disorders in critically-ill patients

DeLand

2011

J Clin Monit Comput

We have developed a computer-model-based approach to quantitatively diagnose the causes of metabolic acid-base disorders in critically-ill patients. We use an interstitial-plasma-erythrocyte (IPE) model that is sufficiently detailed to accurately calculate steady-state changes from normal in fluid volumes and electrolyte concentrations in a given patient due to a number of causes of acid-base disorders. Normal fluid volumes for each patient are determined from their sex, height and weight using regression equations derived from measured data in humans. The model inputs (electrolyte masses and volumes) are altered to simulate the laboratory chemistry of each critically-ill patient. In this process, the model calculates changes in body-fluid volumes, osmolality and yields the individual values of IPE base excess (BE(IPE)) attributed to changes due to: (1) fluid dilution/contraction, (2) gain or loss of Cl(-), (3) hyper- or hypoalbuminemia, (4) presence of unmeasured ions, (5) gain of lactate, (6) gain or loss of phosphate, (7) gain or loss of calcium and magnesium, (8) gain or loss of potassium and (9) gain or loss of sodium. We use critically-ill patient data to show how our new approach is more informative and much simpler to interpret as compared to the approaches of Siggaard-Andersen or Stewart. We demonstrate how the model can be used at the bedside to diagnose acid-base disorders and suggest appropriate treatment. Hence, this new approach gives clinicians a new tool for diagnosing disorders and specifying fluid-therapy options for critically-ill patients.

Comprehensive diagnosis of whole-body acid–base and fluid-electrolyte disorders using a mathematical model and whole-body base excess

2014

J Clin Monit Comput

A mathematical model of whole-body acid-base and fluid-electrolyte balance was used to provide information leading to the diagnosis and fluid-therapy treatment in patients with complex acid-base disorders. Given a set of measured laboratory-chemistry values for a patient, a model of their unique, whole-body chemistry was created. This model predicted deficits or excesses in the masses of Na(+), K(+), Cl(-) and H2O as well as the plasma concentration of unknown or unmeasured species, such as ketoacids, in diabetes mellitus. The model further characterized the acid-base disorder by determining the patient's whole-body base excess and quantitatively partitioning it into ten components, each contributing to the overall disorder. The results of this study showed the importance of a complete set of laboratory measurements to obtain sufficient accuracy of the quantitative diagnosis; having only a minimal set, just pH and PCO2, led to a large scatter in the predicted results. A computer module was created that would allow a clinician to achieve this diagnosis at the bedside. This new diagnostic approach should prove to be valuable in the treatment of the critically ill.