Abstract
ObjectivesThis study aims to test the hypothesis that fluid loading with sodium chloride (150 mmol Na and 150 mmol Cl) or sodium octanoate (150 mmol Na, 100 mmol Cl, and 50 mmol octanoate) would lead to different acid–base changes.DesignWe performed a double-blind crossover experimental study.SettingThe study was done at a University Physiology Laboratory.SubjectsEight Merino ewes were used as subjects.Measurements and main resultsWe randomly assigned animals to a rapid intravenous infusion (1 L over 30 min) of either normal saline (NS) or sodium octanoate solution (OS). We collected blood samples at 0.5, 1, 2, 4, and 6 h after the start of the infusion for blood gas analyses and biochemistry. We calculated strong ion difference apparent (SIDa), effective strong ion difference, and strong ion gap (SIG). Animals in the NS group developed metabolic acidification immediately after fluid administration (pH 7.49 to 7.42, base excess 3.0 to -1.6 mEq/L), while the OS group did not (pH 7.47 to 7.51, base excess 1.1 to 1.4 mEq/L; P < 0.001). Additionally, the OS group had higher SIDa (36.2 vs. 33.2 mEq/L) and SIG (7.4 vs. 6.2 mEq/L) at the end of the infusion.ConclusionsOur findings provide further evidence that acidification induced by intravenous fluid loading is dependent on fluid composition and challenges the paradigm of the so-called dilutional acidosis.Electronic supplementary materialThe online version of this article (doi:10.1186/2197-425X-1-4) contains supplementary material, which is available to authorized users.
Highlights
Large-volume infusion of normal saline (NS) has been repeatedly associated with metabolic acidosis [1,2,3,4]
Our findings provide further evidence that acidification induced by intravenous fluid loading is dependent on fluid composition and challenges the paradigm of the so-called dilutional acidosis
The following day, the animal was assigned to the other fluid in a crossover design, such that those animals first assigned to sodium chloride received sodium octanoate the day and those first assigned to sodium octanoate received sodium chloride the day
Summary
Large-volume infusion of normal saline (NS) has been repeatedly associated with metabolic acidosis [1,2,3,4]. The correctness of this view has been challenged by the lack of significant acid–base change after infusion of equivalent volumes of socalled balanced fluids such as Ringer's lactate, sodium acetate, and other solutions [3,8,9] and the emergence of the Stewart approach to acid–base physiology This approach argues that a change in the strong ion difference (SID) [10,11] is most likely responsible for the acidosis of saline administration. This controversy is difficult to resolve because balanced fluids with an in vivo physiological SID contain substances like lactate or acetate or gluconate, which are believed to immediately enter the citric acid cycle and become a source of bicarbonate.
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