Acid-base effects of altering plasma protein concentration in human blood in vitro

Abstract

We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2-83% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.

The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime

“…In such studies, the albumin concentration of the pump prime was approximately half that of normal blood. Because albumin is a weak acid, hypoalbuminaemia alkalinises blood [12]. The decrease in serum albumin concentration in our patients was responsible for the subtraction of approximately 4 mEq/l of acid from the circulation, a change almost entirely offset by the anionic contribution of polygeline.…”

The strong ion gap does not have prognostic value in critically ill patients in a mixed medical/surgical adult ICU

“…All of these measures give an insight into the derangement, but they give little information as to the source of the problem. The significance of these variables in quantifying the degree of acid-base disturbance is dependent upon normal plasma composition [3,4,5,6]. When electrolyte and protein abnormalities are present, simplistic clinical interpretation of acid-base derangements may be misleading.…”

Usefulness of serum fibrin degradation products and D‐dimer levels as biomarkers to predict return of spontaneous circulation in patients with cardiopulmonary arrest on arrival: comparison with acid–base balance

“…In particular, hypoalbuminemia, a common disturbance in hospitalized patients, can mask an increased concentration of gap anions by lowering the value of AG. 8,10 Hatherill and colleagues 5 insisted that ACAG was a more appropriate screening tool for the diagnosis of metabolic acidosis in the intensive care unit and ACAG should be calculated to screen for occult tissue anions in children with shock. Morris et al 11 proposed ACAG-based techniques for bedside use in critically ill patients.…”