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Detecting uptake or production of "metabolic acid" by a given tissue is often of interest. [Base excess] ([BE]) is the change in [strong acid] or [strong base] needed to restore pH to normal at normal PCO2. However, [BE] seems to have the potential for minor inaccuracy during hypercarbia, and venous blood is hypercarbic relative to arterial. Another approach is [strong ion difference] ([SID]), where a strong ion is one that is always dissociated in solution, and where [SID] = [strong cation] - [strong anion]. The hypothesis was tested that a-v [SID]p might be used to detect metabolic acid uptake or production by tissue. A computer simulation of O2-CO2 exchange was performed, using the Siggaard-Andersen [BE] equations, which provide an existing conceptual template. It was assumed that a change in [BE] = a change in [SID] (Adv. Exp. Med. Biol., in press). (A-v) [SID]p decreased linearly with decreasing [HbO2] during equimolar O2-CO2 exchange (delta mEq [SID]p.l-1 per delta gHbO2.dl-1 = 0.6, r2 = 1.0), and erythrocyte [BE] ([BE]e) and [SID]e decreased commensurately, such that [BE]WB remained constant. These changes represent ion exchanges between erythrocyte and plasma, governed by the Gibbs-Donnan equilibrium. It is concluded that a-v [SID]p may be used to examine a-v differences in [metabolic acid], based in [BE] concepts. The concentration of "metabolic acid" ([metabolic acid]) in blood increases during endotoxemia, exercise and shock. To identify organ(s) responsible, it is necessary to measure arteriovenous [strong acid]. Two methods are available. Whole blood base excess ([BE]WB), is the change in [strong acid]WB or [strong base]WB needed to restore plasma pH (pHp) to 7.4 at PCO2 of 40 torr, and is an excellent method for distinguishing "respiratory," from "metabolic" acidosis in arterial blood. However, while [BE] is most helpful conceptually, use of [BE] in venous blood presents two problems. First, [BE]WB may employ in vitro assumptions that are slightly inaccurate during hypercarbia in vivo, and venous blood is hypercarbic relative to arterial. The problem seems to be that [BE] assumes greater [hemoglobin] ([Hb]) than is actually effective in vivo, where Hb is diluted in the extracellular volume. The "Van Slyke" version of the [BE]WB equation is: BE]WB = ¿[HCO3-]p - 24.4 + (2.3 x [Hb] + 7.7) x (pHp - 7.4)¿ x (1-0.023 x [Hb]) (1) This equation may be thought of conceptually as: [BE] = ([HCO3-] + [A-]) - (normal [HCO3-] + normal [A-]) (2) where A- is negatively charged non-volatile weak acid. Missing or excess charges are attributed to abnormal [strong acid] or [strong base], and [A-]WB is computed using actual, as opposed to effective, [Hb]. This problem has been adequately addressed in arterial blood by standard [BE]WB ([SBE]WB), by assuming that effective [Hb] in vivo is approximately one third of that in vitro. However, it is not clear whether this assumption is sufficiently accurate to examine arteriovenous differences. A second and related problem with using [BE] to detect (a-v) differences is the magnitude of change in Hb buffering in vivo during O2 desaturation. Desaturation renders Hb a stronger weak acid buffer, i.e. increases its effective pK value. Consequently, [HCO3-]p is greater at any given PCO2, creating the appearance of a larger [BE]WB, whereas [strong acid] or [strong base] has not changed. This artifact can be corrected using the "O2 desaturation transform factor," which is 0.19 mM delta g [HbO2].dl-1 in vitro. In vivo, however, the magnitude of the O2 desaturation transform factor might be different. An alternative approach to acid-base analysis is strong ion difference (SID) where a strong ion is one that is always dissociated in physiologic solution. [SID] can usually be approximated as: [Na+] + [K+] - [Cl-] - [La-]. Although [BE] does not equal [SID], a change in [BE] must always accompany a change in [SID], and vice-versa. While the [SID] approach is tedious, and often unnecessarily so, [SID] ca |
