PubMed · 15658320
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Akira Suwabe. 2004. [Base excess and buffer base].. https://pubmed.ncbi.nlm.nih.gov/15658320/
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It has been suggested that hyperventilation and the disproportionate increase in VCO2 versus VO2 above the ventilatory threshold (V(TH)) in ramp exercise are due to the production of nonmetabolic CO2 in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a approximately 1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2 is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2 produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2 flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2 production in muscle (no nonmetabolic CO2 is produced in tissues); (4) the CO2 flow to the lungs, which should not be confused with VCO2 at the mouth, does not increase at a faster rate above than below V(TH). The disproportionate increase in VCO2 at the mouth above V(TH) is due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body.
The present study was designed to determine the changes in serum sodium, anion gap, different antioxidants and free radicals in preeclamptic patients and control subjects. Serum sodium, chloride, bicarbonate, calcium, potassium and magnesium were estimated and anion gap was determined in 100 proteinuric hypertensive and 100 normotensive pregnant women. Mean serum sodium, chloride and bicarbonate level (133.26 +/- 13.1, 104.97 +/- 11.37, and 22.01 +/- 4.66 mEq/l, respectively) were significantly higher in proteinuric hypertensive women as compared to controls (125.85 +/- 10.4, 101.90 +/- 6.3, 19.34 +/- 3.21 mEq/l, respectively) whereas anion gap level (6.28 +/- 16.147) was nonsignificantly higher in proteinuric hypertensive as compared to normotensive (4.61 +/- 11.84). Total serum sodium concentration increases in preeclamptic subjects, the exact distribution of serum sodium in various compartments of the body are not clear and correlation of serum sodium and anion gap with proteinuria is also not known. The levels of different antioxidants were decreased in preeclamptic patients as compared to the controls while the level of free radicals elevated in preeclamptic subjects as compared to controls. In our study, anion gap level was found to be rather non-significantly higher in proteinuric hypertensive women as compared to normotensive women.
In non-emergency medical departments such as internal medicine sampling of arterial blood and analysis for acid-base status is not routinely performed. Peripheral venous blood is routinely taken but interpretation of its acid-base status is difficult. This paper presents a method for calculation of arterial acid-base and blood gas status from measurements in peripheral venous blood combined with a pulse oximeter measurement of arterial saturation. The use of the method has been illustrated using the data of three patients with different acid-base, haemodynamic, and metabolic conditions. The sensitivity of the method has been tested for measurement errors including venous blood acid-base and blood gas status and pulse oximetry; errors due to physiological assumptions including the values of RQ and strong acid production at the tissues; and errors due to air bubbles in the blood. Errors due to these effects are relatively insignificant except for errors in calculated arterial PO(2), particularly when SpO(2) is greater than 97%; and errors when the change in base excess across the sampling site due to strong acid production is greater that 1.3 mmol/l.