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Severe metabolic acidosis is defined by a pH < 7.2 with HCO3- < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces multiple complications such as resistance to the action of catecholamines, pulmonary vasoconstriction, impaired cardiovascular function, hyperkalemia, immunological dysregulation, respiratory muscle fatigue, neurological impairment, cellular dysfunction, and finally, it contributes to multisystemic failure. Intravenous NaHCO3 buffers severe acidemia, preventing the associated damage and gains time while the causal disease is corrected. Its indication requires a risk-benefit assessment, considering its complications. These are hypernatremia, hypokalemia, ionic hypocalcemia, rebound alkalosis, and intracellular acidosis. For this reason, therapy must be "adapted" and administered judiciously. The patient will require monitoring with serial evaluation of the internal environment, especially arterial blood gases, plasma electrolytes, and ionized calcium. Isotonic solutions should be preferred instead of hypertonic bicarbonate. The development of hypernatremia must be prevented, calcium must be provided for hypocalcemia to improve cardiovascular function. Furthermore, in mechanically ventilated patients, a respiratory response similar to the one that would develop physiologically, must be established to be able to extract excess CO2 and thus avoid intracellular acidosis. It is possible to estimate the bicarbonate deficit, speed, and volume of its infusion. However, the calculations are only for reference. More important is to start intravenous NaHCO3 when needed, administer it judiciously, manage its side effects, and continue it to a safe goal. In this review we address all the necessary elements to consider in the administration of intravenous NaHCO3, highlighting why it is the best buffer for the management of severe metabolic acidosis.

Introduction: Metabolic acidosis (MA) is a common complication of chronic kidney disease (CKD) and is associated with numerous adverse effects, which is why its correction is highly recommended. Oral sodium bicarbonate is the current treatment of choice., Objectives: To describe the prevalence of MA in advanced CKD patients and to determine the clinical and biochemical characteristics associated with its successful correction., Material and Methods: Retrospective, observational cohort study in adult patients with CKD stage 4-5. The inclusion criteria were: not being treated with alkali therapy at the time of inclusion, and to have at least three consecutive glomerular filtration rate (GFR) measurements and biochemical parameters during a minimum follow-up period of 3 months. Incident patients with serum bicarbonate<22 mEq/l were included in the follow-up study and treated with oral sodium bicarbonate. Correction was considered successful when more than half of the samples and the mean bicarbonate levels during individual follow-up were≥22 mEq/l., Results: The study group consisted of 969 patients (age 65±14 years, 507 males) with a mean GFR of 14.8±4.5ml/min/1.73 m 2 . At baseline, 530 patients (55%) had serum bicarbonate<22mEq/l. They were treated with sodium bicarbonate and followed for 15 months. Satisfactory correction of MA was only achieved in 133 patients (25%). By multivariate logistic regression analysis, the main characteristics of patients with adequate control of MA were: age (OR=1.03; 95% CI 1.01 - 1.05), baseline GFR (OR=1.07; 1.02 - 1.12), and treatment with proton-pump inhibitors (OR=1.61; 95% CI 1.06 - 2.44). Patients who achieved successful correction of MA showed slower CKD progression (-1.67±3.71 vs -4.36±4.56ml/min/1.73 m 2 /year, P<.0001), and lower average serum potassium concentration (5.1±0.5 vs 5.3±0.5, P<.0001) than those who did not. However, there were no differences in the hospitalisation or mortality rate., Conclusion: MA is a common complication of advanced CKD but difficult to manage with current therapies. Due to the significant potential benefit of controlling MA, new, more effective therapies should be further researched., (Copyright © 2019 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Background: Being born preterm implies comorbidities, among them the risk of intraventricular hemorrhage (IVH). The use of sodium bicarbonate has been linked to the presence of IVH. The main purpose of this study was to determine if the infusion of sodium bicarbonate during the first 24 hours increases the risk of IVH in preterm infants., Methods: Our study is a cohort; we analyzed the files of 160 patients and divided them into two groups: one in which sodium bicarbonate was not used and another in which it was; this latter group was subdivided into two considering if the use was therapeutic of prophylactic., Results: In our total group of patients 10 % presented IVH; had a mean weight of 1500 g and 31 weeks of gestational age. The incidence of IVH was identical between both groups, although patients in which bicarbonate was used were more premature, unstable, and in worse clinical conditions., Conclusions: Our data indicate the need of large scale studies to determine if the clinical benefits of the use of sodium bicarbonate outweigh the risk of IVH.

Introduction: The correction of metabolic acidosis caused by renal failure is achieved by adding bicarbonate during dialysis. In order to avoid the precipitation of calcium carbonate and magnesium carbonate that takes place in the dialysis fluid (DF) when adding bicarbonate, it is necessary to add an acid, usually acetate, which is not free of side effects. Thus, citrate appears as an advantageous alternative to acetate, despite the fact that its acute effects are not accurately known., Objective: To assess the acute effect of a dialysis fluid containing citrate instead of acetate on acid-base balance and calcium-phosphorus metabolism parameters., Material and Methods: A prospective crossover study was conducted with twenty-four patients (15 male subjects and 9 female subjects). All patients underwent dialysis with AK-200-Ultra-S monitor with SoftPac® dialysis fluid, made with 3 mmol/L of acetate and SelectBag Citrate®, with 1 mmol/L of citrate and free of acetate. The following were measured before and after dialysis: venous blood gas monitoring, calcium (Ca), ionic calcium (Cai), phosphorus (P) and parathyroid hormone (PTH)., Results: Differences (p<0.05) were found when using the citrate bath (C) compared to acetate (A) in the postdialysis values of: pH, C: 7.43 (0.04) vs. A: 7.47 (0.05); bicarbonate, C: 24.7 (2.7) vs. A: 27.3 (2.1) mmol/L; base excess (BEecf), C: 0.4 (3.1) vs. A: 3.7 (2.4) mmol/L; corrected calcium (Cac), C: 9.8 (0.8) vs. A: 10.1 (0.7) mg/dL; and Cai, C: 1.16 (0.05) vs. A: 1.27 (0.06) mmol/L. No differences were found in either of the parameters measured before dialysis., Conclusion: Dialysis with citrate provides better control of postdialysis acid-base balance, decreases/avoids postdialysis alkalaemia, and lowers the increase in Cac and Cai. This finding is of special interest in patients with predisposing factors for arrhythmia and patients with respiratory failure, carbon dioxide retention, calcifications and advanced liver disease., (Copyright © 2015. Published by Elsevier España, S.L.U.)

The critically ill patient, during the natural course of the disease often presents acid-base disturbances acidosis being the most common metabolic problem. Sodium bicarbonate has been used, for its correction but due to complications its use is restricted. In the present experimental study, mixed race dogs were artificially induced metabolic acidosis with in chloride acid. Arterial and venous blood gases were determined. Afterwards 0.1N sodium hydroxide was administered in the same amount statistically demonstrating modifications, in the pH values, as well as an excess of arterial and venous base which indicates the possibility of using this substance in humans to correct metabolic acidosis.

To verify whether there is a state of phosphate depletion in dehydrated infants with diarrhea and whether phosphate administration affects recovery from metabolic acidosis, two groups of infants were studied. All were males, from 1 to 7 months old, and in good nutritional state. The control group was treated with a standard regimen of I.V. fluids initially, followed by feedings of a diluted milk formula starting on the 2nd day of treatment. The study group, in addition to this standard regimen, received sodium phosphate (Na2HPO4/Na2HPO4, 4:1, pH 7.4), initially by the I.V. route and thereafter orally with the feedings, at the dose of 2mM/kg/day. During the first 6 days of treatment, daily electrolyte (Na, K, Ca, Mg. Cl and P) and nitrogen balances were recorded. Hydrogen ion excretion (NH4 + TA--HCO3) was determined daily. Clinical findings and course were similar in the two groups. No untoward effects were observed with phosphate administration. In the control group, P balance was negative during all the periods and losses were in excess of those expected from nitrogen losses, thus suggesting a state of depletion. In the P-treated group however, P retention was not demonstrated in the first 2 days, finding a not suggestive of a P depleted state. Linear regressions between both daily and cumulative balances of P-nitrogen-free and Ca indicated a close correlation, thus suggesting that these two ions are mobilized concommitantly.

The study included ten patients with severe metabolic acidosis (pH under 7.0) and clinical signs of shock. In four of them assisted ventilation was indicated as an urgency. In the other six patients assisted ventilation was used since the beginning, simultaneously with reposition of blood volume and administration of sodium bicarbonate. There were much better results with the latter management, with faster correction of the acidosis, without any complications and good survivorship.

Considering the disparity of criteria regarding the use of sodium bicarbonate in the management of infants with diarrhea, dehydration and metabolic acidosis, a prospective study was done in 25 infants (13 managed without and 12 with bicarbonate) where it was demonstrated; a) The use of bicarbonate does not lead to a more rapid correction of the metabolic acidosis. b) Bicarbonate should not be used in patients with serum bicarbonate levels of 5 mEq/1. or over. c) Patients with dehydration and metabolic acidosis show hyperglycemia that returns to normal when the dehydration is corrected. This fact is of great interest because these children should not be considered nor managed as diabetics.