Sodium Bicarbonate
Summary All Essential Benefits/Effects/Facts & Information Sodium bicarbonate (baking soda) is a supplement that provides dietary bicarbonate, which can increase serum levels of bicarbonate (normally produced by the kidneys) and subsequently buffer acid production in the body. The main mechanism of action of sodium bicarbonate is in negating the effects of acidosis. It provides benefits both in situations of chronic mild acidosis, commonly seen in metabolic ailments or during aging as kidney function slowly declines, and in exercise-induced acidosis. In athletes, the standard doses of sodium bicarbonate supplementation (200-300 mg/kg) tend to reliably benefit performance when failure on the exercise is associated with metabolic acidosis, aka “the burn.” Sports where failure occurs due to the cardiorespiratory system or due to force production by the central nervous system (e.g., single sprints or rowing in elite rowers) do not appear to reliably benefit from supplemental bicarbonate. Benefits of sodium bicarbonate can be observed with a single dose taken 60-90 minutes before exercise, but supplementation should be approached cautiously as it can cause gastrointestinal side effects if too much is taken at once or, if it’s consumed too rapidly. Additionally, 5 g of sodium bicarbonate taken daily appears to be somewhat effective in reducing acidosis induced by the diet or the aging process (although using potassium bicarbonate appears to be better), and therefore it may reduce the rate of bone loss over time in susceptible populations. There are mechanisms in place for sodium bicarbonate to be a fat-burning agent (it increases ketone production and lipolysis and causes a minor increase in metabolic rate), but these have not yet been linked to actual weight loss in tr Continue reading >>
Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis
Sodium bicarbonate in the critically Ill patient with metabolic acidosis Uso de bicarbonato de sdio na acidose metablica do paciente gravemente enfermo Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation. Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock. A acidose ltica um distrbio do equilbrio cido-base muito frequente em pacientes internados em unidades de terapia intensiva e est associado a um mau prognstico. Embora exista um acmulo substancial de evidncias de que nveis crticos de acidemia provocam inmeros efeitos adversos sobre o funcionamento celular, a utilizao de bicarbonato de sdio para o tratamento da acidose ltica em pacientes gravemente enfermos permanece alvo de controvrsias. Neste artigo, pretendemos: 1) analisar as principais diferenas entre as acidoses hiperclormicas e as acidoses orgnicas, com nion gap (AG) elevado, visando embasar a discusso sobre os fundamentos da terapia Continue reading >>
Sodium Bicarbonate Use
metabolic acidosis leads to adverse cardiovascular effects bicarbonate must be administered in a solution as sodium bicarbonate 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000mOsm/kg) goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) Urinary alkalinisation (salicylate poisoning) Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8) Severe pulmonary hypertension with RVF to optimize RV function Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues POINTS TO REMEMBER WHEN USING BICARBONATE it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate ensure adequate ventilation to eliminate CO2 pro Continue reading >>
Sodium Bicarbonate Injection
Sodium bicarbonate is a systemic alkalinizing agent. It most often is administered IV in the treatment of metabolic and respiratory acidosis. Sodium bicarbonate is also used in the acute treatment of hyperkalemia, although it should be kept in mind that this represents palliative treatment for this condition. Sodium bicarbonate is sometimes used for urinary alkalinization. Despite being a highly effective antacid, sodium bicarbonate is rarely used for the chronic treatment of peptic ulcer disease because it can be absorbed and can affect systemic acid-base balance. Sodium bicarbonate was in use prior to 1938 and approved by the FDA at its inception. Mechanism of Action: After oral administration, sodium bicarbonate neutralizes hydrochloric acid in the stomach, forming sodium chloride, carbon dioxide, and water. Excess bicarbonate ions are absorbed in the small intestine. Thus, all of a dose of exogenous sodium bicarbonate eventually reaches the extracellular fluid, and a mild alkalosis can result. This usually is corrected quickly by the renal system in patients with normal renal function. After IV administration, sodium bicarbonate dissociates to bicarbonate ions, which constitute the conjugate base portion of the body's extracellular buffer system (bicarbonate/carbonic acid buffer). Administration of sodium bicarbonate will restore acid-base balance in patients with metabolic or respiratory acidosis; however, metabolic alkalosis can result from the use of sodium bicarbonate. Excess bicarbonate ions that result from the administration of sodium bicarbonate are excreted in the urine, alkalizing the urine. This alkalization decreases renal absorption and increases the clearance of certain drugs, intoxicants, weak acids, and blood pigments. Pharmacokinetics: Sodium bicar Continue reading >>
Treatment Of Metabolic Acidosis In Patients With Ckd
Treatment of Metabolic Acidosis in Patients With CKD We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Treatment of Metabolic Acidosis in Patients With CKD Wei Chen, MD and Matthew K. Abramowitz, MD, MS Metabolic acidosis is a common complication of chronic kidney disease and believed to contribute to a number of sequelae, including bone disease, altered protein metabolism, skeletal muscle wasting, and progressive GFR loss. Small trials in animal models and humans suggest a role for alkali therapy to lessen these complications. Recent studies support this notion, although more definitive evidence is needed on the long-term benefits of alkali therapy and the optimal serum bicarbonate level. The role of dietary modification should also be given greater consideration. In addition, potential adverse effects of alkali treatment must be taken into consideration, including sodium retention and the theoretical concern of promoting vascular calcification. This teaching case summarizes the rationale for and the benefits and complications of base therapy in patients with chronic kidney disease. Index Words: metabolic acidosis, chronic kidney disease, bicarbonate, alkali therapy Metabolic acidosis is associated with many of the complications of chronic kidney disease (CKD), including bone disease, muscle protein catabolism, and progressive glomerular filtration rate (GFR) loss. The Kidney Dialysis Outcomes Quality Initiative (KDOQI) guideline Continue reading >>
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Sodium Bicarbonate Dosage
If acid-base status is available, dosages should be calculated as follows: 0.2 x weight (kg) x base deficit. HCO3 (mEq) required = 0.5 x weight (kg) x [24 - serum HCO3 (mEq/L)]. Moderate metabolic acidosis: 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. Severe metabolic acidosis: 90 to 180 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. If acid-base status is not available, dosages should be calculated as follows: 2 to 5 mEq/kg IV infusion over 4 to 8 hours; subsequent doses should be based on patient's acid-base status. Moderate metabolic acidosis: 325 to 2000 mg orally 1 to 4 times a day. One gram provides 11.9 mEq (mmoL) each of sodium and bicarbonate. Usual Adult Dose for Diabetic Ketoacidosis Although sodium bicarbonate is approved for the treatment of metabolic acidosis, data have shown that the use of this drug may be harmful in certain clinical settings such as lactic acidosis, acidosis with tissue hypoxia, uremia, severe cardiac dysfunction or arrest, and diabetic ketoacidosis. Most experts only allow for its use when tissue perfusion and ventilation are maximized and the arterial pH is 7.1 or lower. If sodium bicarbonate is used to treat diabetic ketoacidosis, the initial dosage is 50 mEq sodium bicarbonate in 1 L of appropriate IV solution to be given once. Insulin therapy may obviate the need for bicarbonate therapy since it will promote glucose utilization and decrease the production of ketoacids. Usual Adult Dose for Urinary Alkalinization 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour. 325 to 2000 mg orally 1 to 4 times a day. O Continue reading >>
Metabolic Acidosis Treatment & Management
Approach Considerations Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>
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[calculation Of The Dose Of Sodium Bicarbonate For Correcting Metabolic Acidosis In Surgery With Circulation Arrest And Deep Hypothermia].
Anesteziol Reanimatol. 1997 Nov-Dec;(6):23-6. [Calculation of the dose of sodium bicarbonate for correcting metabolic acidosis in surgery with circulation arrest and deep hypothermia]. Dement'eva II , Rotman EV , Maba EN , Charnaia MA , Zolicheva NIu , Bogorad IV . The study was aimed at detecting the factors which determine the amount of 7% sodium bicarbonate solution needed to correct metabolic acidosis in patients subjected to repair surgery on the aorta involving long arrest of circulation under conditions of deep hypothermia. The total dose of 7% sodium bicarbonate solution was calculated as the sum of volumes of this solution needed to neutralize certain concentrations of underoxidized metabolites and BE. Accumulation of acid metabolites in tissues is caused by ineffective compensation of energy expenditure during warming of a patient after circulation arrest and deep hypothermia. After reperfusion injury to tissues, the release of these metabolites into the blood and further neutralization are appreciably slower during such operations than during other cardiovascular bypass interventions. That is why the routine method for calculating the dose of 7% sodium bicarbonate solution for correcting metabolic acidosis is not adequate in cases with abnormal body temperature. Estimation of the dose with consideration for venous blood temperature and pO2 is more correct. An algorithm of calculation is proposed. Continue reading >>
Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology
0.25-0.50 mmol/kg/hour. Continuous IV infusion. Doses needs to be individualised and titrated according to response and to adverse effects (e.g. hypernatraemia) Not recommended for hypercapnia or hypernatraemic states. Caution in infants with renal impairment. Caution in preterm infants. Rapid infusion of hypertonic NaHCO3 has been incriminated in the pathogenesis of intraventricular haemorrhage in preterm infants. Sodium bicarbonate is the alkali most frequently employed for correction of metabolic acidosis. The drug is well absorbed from the gastrointestinal tract. Between 20-50% of an orally administered dose can be recovered in the form of expired carbon dioxide. The apparent bicarbonate space has been estimated to be 74% of body weight (range of 37-134%). Thus calculations of bicarbonate dosage are based on an apparent volume of distribution of 0.3 to 0.6 L/kg. Bicarbonate is rapidly metabolised to carbonic acid which rapidly dissociates into water and carbon dioxide. The carbon dioxide is excreted via the lungs. Venous irritation, soft tissue injury at the site of IV injection. Increased vascular volume, serum osmolarity, serum sodium. Continue reading >>
Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis
The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>
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Sodium Bicarbonate (sodium Bicarbonate 5% Injection): Side Effects, Interactions, Warning, Dosage & Uses
Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection may be indicated in the treatment of metabolic acidosis which can occur in severe renal disease, uncontrolled diabetes , circulatory insufficiency due to shock , anoxia or severe dehydration, extracorporeal circulation of blood and severe primary lactic acidosis . Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection is further indicated in the treatment of certain drug intoxications, including barbiturates, in poisoning by salicylates or methyl alcohol, and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of blood pigments. Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection may also be indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. As directed by a physician. Dosage is dependent upon the age, weight and clinical condition of the patient as well as laboratory determinations. For mild acidosis, the usual dosage is 1 to 2 mEq per kg of body weight, administered slowly. For more severe acidosis, 2 to 5 mEq per kg of body weight may be administered over a 4 to 8 hour period. Subsequent therapy is dependent on the clinical response of the patient. In emergencies, 300 to 500 mL of the 5% Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection should or administered as rapidly as is possible without overalkalinizing the patient. Generally, to avoid overalkalinizing a patient whose own body mechanisms for correcting metabolic acidosis may be maximally stimulated, only 1/3 to 1/2 of the calculated dose is administered as rapidly as indicated by the patient's cardiovascular and fluid balance status. The serum pH and bicarbonate concentration should then be redetermined. Parenteral drug products should be Continue reading >>
Intravenous Sodium Bicarbonate
Robin Gross, William Peruzzi, in Critical Care Medicine (Third Edition) , 2008 Intravenous sodium bicarbonate (NaHCO3) solution is an appropriate intervention for reversing metabolic acidemia, provided that lung and cardiac function are adequate. NaHCO3 solution adds HCO3 to the blood only after the CO2 load inherent in the NaHCO3 solution is eliminated by the lungs. When NaHCO3 solution is administered to a patient with acute ventilatory failure (respiratory acidosis), the Paco2 usually increases, and pH decreases because the CO2 load cannot be eliminated. As illustrated in Figure 14-8, low cardiac output may be a limiting factor in CO2 excretion. When NaHCO3 solution is administered to a patient with very poor cardiac output, the venous blood shows a paradoxical respiratory acidosis. When NaHCO3 is administered intravenously to correct severe metabolic acidemia, it is essential to quantify the abnormality as a guide to therapy. A simple way to calculate the amount of bicarbonate to administer is: mmol HCO3 = base deficit (mmol/L) ideal weight (kg) 0.25 (L/kg) where 0.25 represents the volume of distribution of the bicarbonate. It is generally prudent to administer one half to one third of the calculated deficit, obtain another ABG sample in 5 minutes, and re-evaluate. In Pocket Companion to Brenner and Rector's The Kidney (Eighth Edition) , 2011 In cases of intractable shock, metabolic acidosis may persist despite volume expansion and improved oxygen delivery. Intravenous bicarbonate is often used in this setting in an attempt to improve cardiac function. However, decreased cardiac contractility in the setting of lactic acidosis may be partially due to hypoxemia, hypoperfusion, or sepsis, and establishing the direct effects of the low pH is difficult. Many patients t Continue reading >>
Sodium Bicarbonate In Severe Metabolic Acidosis
Sodium Bicarbonate in Severe Metabolic Acidosis Sodium Bicarbonate in Severe Metabolic Acidosis Aka: Sodium Bicarbonate in Severe Metabolic Acidosis No evidence that Sodium Bicarbonate improves outcomes Treat acidosis with ventilation and perfusion Documented severe Metabolic Acidosis associated with: Diabetic Ketoacidosis with Arterial pH <6.9 Adequate ventilation and perfusion are critical V. Dosing: Adults (if arterial pH <6.9 to 7.0) Sodium Bicarbonate 1 amp (50 meq or 100 mmol) Dose full bag or 400 cc of 50 meq if pH <6.9 Dose half bag or 200 cc of 25 meq if pH 6.9 - 7.0 If arterial pH <6.9 on recheck in 2 hours Solution should contain <0.5 meq/ml bicarbonate Sodium should be <155 meq/L (NS concentration) Every bicarb ampule contains 2000 meq/L Sodium Limit infusion rate to <1 meq/kg/hour bicarbonate Example: 20 kg child with arterial pH <6.9 Maximum replacement is 40 meq bicarbonate Contains 40 meq Na + 38 meq Na = 78 meq Na Sodium concentration is 156 meq/L (same as NS) Limit this 20 kg child's rate to 20 meq/hour Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Sodium Bicarbonate in Severe Metabolic Acidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window Continue reading >>
Sodium Bicarbonate: Indication, Dosage, Side Effect, Precaution | Mims.com Malaysia
Adult : PO Urine alkalinisation Up to 10 g/day in divided doses w/ sufficient fluid intake. Chronic metabolic acidosis 4.8 g/day as needed. Dyspepsia 1-5 g when needed. IV Severe metabolic acidosis By slow inj of a hypertonic soln 8.4% or by continuous infusion of a weaker soln, usually 1.26% . Adult: By slow inj of a hypertonic solution of up to 8.4% (1000 mmol/L), or by continuous infusion of a weaker solution, usually 1.26% (150 mmol/L). For correction of acidosis during advanced cardiac life support procedures, 50 ml of an 8.4% solution may be given. Elderly: Dosage adjustments may be required. Adult: Doses providing 57 mmol (4.8 g sodium bicarbonate) or more daily as required. Elderly: Dosage adjustments may be required. Adult: To prevent development of uric-acid renal calculi in the initial stages of uricosuric therapy for hyperuricaemia in chronic gout: Up to 10 g daily in divided doses, to be taken with a liberal amount of fluid. Elderly: Dosage adjustments may be required. Category C: Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the foetus. Increases toxicity of amphetamines, ephedrine, pseudoephedrine, flecainide, quinidine and quinine. Decreases effects of lithium, chlorpropamide and salicylates due to increased clearance. May affect the absorption of certain drugs due to raised intra-gastric pH. Description: Sodium bicarbonate raises blood and urinary pH by dissociation to provide bicarbonate ions, which neutralises the hydrogen ion concentration. It also neutralises gastric acid via production of carbon dioxide. Durat Continue reading >>
Sodium Bicarbonate Deficit Calc
In all cases, the primary goal in treating metabolic acidosis is to focus on reversal of the underlying process causing the acidosis. Examples: (1) Renal failure: dialysis if needed. (2) Alcoholic ketoacidosis: fluids, electrolytes, thiamine, folic acid. (3) Sepsis/shock: volume resuscitation, vasopressors, etc. (4) Salicylate intoxication: IV fluids, alkalinization of the urine, .... If there is a severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) correct with sodium bicarbonate. Sodium bicarb is also useful if the acidosis is due to inorganic acids (especially if renal disease is present). However, when the acidosis results from organic acids (lactic acid, acetoacetic acid, etc) the role of bicarbonate is controversial. In most cases of DKA or severe lactic acidosis the administration of sodium bicarbonate does not decrease mortality even when the acidosis is severe. In sum, sodium bicarbonate should be reserved for severe cases of acidosis only (pH <7.2 and serum bicarbonate levels <10-12 meq/L). This can be accomplished by adding 1 to 3 ampoules of sodium bicarb to D5W or 1/2NS. IV-push administration should be reserved for cardiac life support and not metabolic acidosis. Sodium bicarbonate administration: It is recommended that 50% of total deficit be given over 3 to 4 hours, and the remainder replaced over 8-24 hours. The usual initial target ((desired HCO3- concentration): 10 - 12 mEq/L, which should bring the blood pH to ~7.20. The subsequent goal is to increase the bicarbonate level to 15 meq/L over the next 24 hours. Replace 50% over 3 to 4 hours and the reminder over 24 hours. Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than 4 to 8 mEq/L over 6 to 12 hours to avoid the risks of over-alkalinization (paradoxical CNS acidosis; decr Continue reading >>
