Sodium Bicarbonate - Scientific Review on Usage, Dosage, Side Effects. Sources and Structure. Introduction. Sodium bicarbonate (commonly referred to as either 'Bicarb' or simply as Baking Soda. Sodium bicarbonate (as well as potassium bicarbonate) are approved for human consumption by the FDA with a GRAS rating. Sodium bicarbonate (baking soda) is a generally recognized as safe food additive. Biosynthesis and Regulation. Beyond the kidneys having a role in excreting excess hydrogen (H+) ions and reabsorbing bicarbonate into the blood (and controlling acidity via controlling what molecules get urinated). Due to a preservation of bicarbonate after a certain point and buffering help from the bones, acidosis is associated with mineral loss from bones. Bicarbonate secretion can also occur in pretty much all sections of the gastrointestinal tract, and forms a barrier between the stomach and intestines (in the duodenum) to protect the intestines from the acidity of the stomach. Structure and Properties. ![]() ![]() Dissolving sodium bicarbonate into a beverage and leaving it overnight (in the fridge) does not appear to hinder the ability of this supplement to increase blood bicarbonate levels. Absorption and Intestines. It has been confirmed that the consumption of food alongside sodium bicarbonate reduces gastrointestinal side effects relative to the same dose taken on an empty stomach, and serum increases of bicarbonate appear to be highest when coingested with food. Serum. When 3. 00mg/kg sodium bicarbonate is given to recreationally active males at rest (4. ![]() Secure video or text chat with a doctor anywhere, anytime, 24/7 - get prescriptions, referrals, second opinions and more. Or get trusted answers and tips from tens of. ![]() ![]() L liquid), there is an increase in blood bicarbonate and p. H within 3. 0 minutes which plateus at 6. Excretion. Bicarbonate excretion in the kidneys is mediated by a variety of transports including the Cl- dependent class (AE1- 3, short for Anion Exchange), the NA+ dependent class (NBC1,3, and 4 with NBC2 being a splice variant of NBC3. Memory and Cognition. Acid sensing channels on neurons are known to be involved in synaptic plasticity, learning, memory, pain, and neurodegeneration. Bioenergetics. The exercise- induced changes in energy production (normally almost exclusively provided by glucose at nonfasted rest. Despite theoretically preserving the percentage of glucose used relative to lactate during exercise (there is normally a shift to lactate from glucose with exhaustive exercise), supplementation bicarbonate does not appear to have this trait. Blood Flow. Metabolic acidosis is known to reduce cerebral blood volume, as the blood vessels are sensitive to hydrogen ions. Panic Disorders. It has been observed that, in response to a flashing checkerboard test, the increase in brain lactate was exacerbated in persons with panic disorders relative to controls. However, both an increase and decrease of acidity are able to induce panic attacks in those with panic disorders and it is unlikely that sodium bicarbonate has a therapeutic role in this regard (instead, it is possible sodium bicarbonate can actually exacerbate symptoms)3. Exercise- induced Neurotransmitters. It appears that . Absorption. In menopausal women given mineral water with or without added bicarbonate (1,0. Baking Soda For Weight Loss. Some of them are home made weight loss solutions such as the baking soda for weight loss solution. Sodium bicarbonate also known as. Sodium Bicarbonate* Urea* Weight Loss/physiology* Substances. Carbon Radioisotopes; Sodium Bicarbonate; Urea; Creatinine. Can Sodium Bicarbonate cause Weight Loss? Weight Loss is #33 concern. Sodium bicarbonate is increasingly used in dentifrice and its presence appears to be less abrasive to enamel and. L water) alongside a standardized test meal was noted to reduce postprandial lipidemia over 7 hours (peak value reduced 1. AUC reduced by 1. Cholesterol and Lipoproteins. The state of metabolic acidosis is known to promote LDL oxidation due to shortening the lag phase of oxidation, which is theoretically a pro- artherosclerotic event. Is theoretically beneficial for LDL oxidation in persons with metabolic acidosis (ie. Blood Pressure. Polymorphisms of the sodium bicarbonate transporter SLC4. ![]() The Synthesis of Sodium Bicarbonate. Suppose I expect a loss of 75% when producing Sodium Bicarbonate via the Solvay.A5 (NBC4. Chronic Obstructive Pulmonary Disease. Chronic obstructive pulmonary disease (COPD) is a cardiac condition associated with severe limitations on physical exertion, and supplementation of the standard dose of sodium bicarbonate (3. COPD. Insulin Resistance. Among adults without diabetes, lower serum bicarbonate concentrations appear to be correlated with a higher risk for insulin resistance. Supplementation of bicarbonate does not appear to indiscriminately benefit insulin resistance, however. Fat Mass and Obesity. Mechanisms. It is fairly established that a reduction in p. H (increasing acidity) is associated with a reduction of lipolysis. Although there is a fair bit of evidence from dialysis and animal models, only one study in otherwise healthy persons has noted that oral sodium bicarbonate is able to increase the metabolic rate by 9. Ketosis. Bicarbonate is of interest for ketosis diets (commonly employed by overweight persons to lose body fat) as ketosis diets are met with a benign but predictable decrease in blood p. H which is effectively negated with supplemental bicarbonate. Despite an increase in serum p. H, sodium bicarbonate failed to reverse the diet- induced decline in performance on a 9. VO2 cycling test. ![]() ![]() ![]() ![]() Lactate Production. Lactate and lactic acid form a balance within the body, where lactate may dissociated into lactic acid plus a free hydrogen ion in order to acidify (decrease p. H) tissues. Sodium bicarbonate supplementation reliably increases lactate concentrations in serum following short exhaustive exercise (such as sprints, rowing, and weight lifting). It is possible that this may be reversed with prolonged aerobic exercise. Although most studies measure serum lactate, intramuscular lactate (via biopsy) has been noted to be increased and to a degree of 7. Converse to the influence of sodium bicarbonate, ingestion of acidifying compounds (ammonium chloride) can decrease intramuscular p. H. Studies that measure glycogen utilization note a significant increase in the rate of utilization (1. This is seen during high intensity exercises only (above the lactate threshold) and is likely due to increased glycogen utilization. Hypertrophy. It has been noted that both acute. There are no interventions currently assessing proteolysis rates in persons with acidosis given bicarbonate to normalize p. H7. 3. Mechanisms. Bicarbonates main mechanism of action is an attenuation of cellular acidosis (acidosis refers to an increase in acidity that is the result of metabolic processes) and is effective in the exercising muscle in this regard. Studies conducted in humans have confirmed that the exercise- induced decrease in p. H is attenuated with acute loading of 0. H) in trained athletes. This is thought to either attenuate the decline in muscle contractions (directly sequestering acidity) or by preserving muscle oxygenation. Sodium bicarbonate ingestion is able to alter the slow phase of pulmonary VO2 (p. VO2) kinetics (for anaerobic exercise, highly associated with muscle energy turnover. Sodium bicarbonate may be able to prolong energy metabolism in muscle cells during exercises associated with lactic acid production thought to be related to the intracellular buffering component, with uncertain and possibly no benefit to exercise not associated with lactic acid. Neuromuscular Interactions. A study using submaximal cycling (to induce fatigue) and then later testing force conduction velocity in the muscle of participants noted that the decline in force production seen in placebo (from the submaximal cycling) was abolished with supplemental sodium bicarbonate at 3. Resistance Exercise. In a simulated judo test (judo tends to have 1. Special Judo Fitness Test (SJFT. Rowing and Cycling. In well trained cyclists subject to a 4 minute cycle test, both acute loading of 0. VO2 max (1. 2- 2%). However, during repeated sprints (doing the short sprint multiple times) there does appear to be more trials which note benefit than null effects. For a 3km time trial in trained cyclists, time to complete the trial is reduced by 1. It may be beneficial in some individuals (some reports are positive while other studies that note overall no benefit note a few responders) but it is not an overly reliable intervention. Sprinting and Swimming. Supplementation of sodium bicarbonate at 3. L powerade) 6. 5 minutes before sprint testing in elite rugby players failed to improve performance despite increasing serum bicarbonate. It seems the longer the run is conducted, the more likely that sodium bicarbonate is beneficial. In swimmers (competitive but not elite) given 3. Timing and Dosage. Most trials investigating the acute usage of sodium bicarbonate at 3. The dosage range of 2. Studies that compare acute dosing (3. Benefits still appear to exist if sodium bicarbonate is loaded but then not taken for up to 2 days. Bone Metabolism and the Skeleton. Mechanisms. Chronic low- grade metabolic acidosis has a known degratory effect on bone tissue as evidenced by the alteration in phosphate. Protein losses from bone appear to be enhanced in experimentally induced acidosis in research animals. There may be too much acid production relative to bicarbonate in a diet excessive in sodium, and possibly in older individuals with declining kidney function. Potassium bicarbonate at 3. Potassium bicarbonate appears to be significantly more protective than sodium bicarbonate, which may be due to potassium also inherently being osteoprotective while sodium is an independent risk factor for bone mineral losses. A high vegetable diet (high in potassium) with a concomitant reduction in sodium intake may maximize the benefits of sodium bicarbonate on bone health. Dental Health and Hygiene. Chewing gum with bicarbonate added to it is able to increase salivary p. H (reduced acidity) without significantly influencing salivary flow rates. Although not fully demonstrated, a possible reduction in bad breath may result following usage of oral products with a sodium bicarbonate content. Usage in Disease States. Metabolic Acidosis. Metabolic acidosis is a condition that is characterized by a drop in serum bicarbonate (usually seen as the consequence of metabolic acidosis) that has both an acute and lethal component (usually induced by drugs, not in the realm of dietary supplements to address and is a clinical issue) and a chronic and mild component. Sodium Bicarbonate - FDA prescribing information, side effects and uses. Sodium Bicarbonate Injection, USP is a sterile, nonpyrogenic, hypertonic solution of Sodium Bicarbonate (Na. HCO3) in water for injection for administration by the intravenous route as an electrolyte replenisher and systemic alkalizer. Solutions are offered in concentrations of 7. See table in HOW SUPPLIED section for contents and characteristics. Solutions in the Ansyr. When smaller doses are required, the unused portion should be discarded with the entire unit. Sodium Bicarbonate, 8. Na+ and HCO3. Sodium Bicarbonate, USP is chemically designated Na. HCO3, a white crystalline powder soluble in water. Water for Injection, USP is chemically designated H2. O. The syringe is molded from a specially formulated polypropylene. Water permeates from inside the container at an extremely slow rate which will have an insignificant effect on solution concentration over the expected shelf life. Solutions in contact with the plastic container may leach out certain chemical components from the plastic in very small amounts; however, biological testing is supportive of the safety of the syringe material. Ansyr. Sodium (Na+) is the principal cation of the extracellular fluid and plays a large part in the therapy of fluid and electrolyte disturbances. Plasma concentration is regulated by the kidney through acidification of the urine when there is a deficit or by alkalinization of the urine when there is an excess. Bicarbonate anion is considered . Normally a ratio of 1: 2. In a healthy adult with normal kidney function, practically all the glomerular filtered bicarbonate ion is reabsorbed; less than 1% is excreted in the urine. Indications and Usage for Sodium Bicarbonate. Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Sodium Bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate- protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium Bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Treatment of metabolic acidosis should, if possible, be superimposed on measures designed to control the basic cause of the acidosis – e. But since an appreciable time interval may elapse before all of the ancillary effects are brought about, bicarbonate therapy is indicated to minimize risks inherent to the acidosis itself. Vigorous bicarbonate therapy is required in any form of metabolic acidosis where a rapid increase in plasma total CO2 content is crucial – e. Contraindications. Sodium Bicarbonate Injection, USP is contraindicated in patients who are losing chloride by vomiting or from continuous gastrointestinal suction, and in patients receiving diuretics known to produce a hypochloremic alkalosis. Warnings. Solutions containing sodium ions should be used with great care, if at all, in patients with congestive heart failure, severe renal insufficiency and in clinical states in which there exists edema with sodium retention. In patients with diminished renal function, administration of solutions containing sodium ions may result in sodium retention. The intravenous administration of these solutions can cause fluid and/or solute overloading resulting in dilution of serum electrolyte concentrations, overhydration, congested states or pulmonary edema. Extravascular infiltration should be avoided, see ADVERSE REACTIONS. Precautions. General. Do not use unless solution is clear and the container or seal is intact. Discard unused portion. The potentially large loads of sodium given with bicarbonate require that caution be exercised in the use of Sodium Bicarbonate in patients with congestive heart failure or other edematous or sodium- retaining states, as well as in patients with oliguria or anuria. See table in HOW SUPPLIED section for amounts of sodium present in solutions. Caution must be exercised in the administration of parenteral fluids, especially those containing sodium ions, to patients receiving corticosteroids or corticotropin. Potassium depletion may predispose to metabolic alkalosis and coexistent hypocalcemia may be associated with carpopedal spasm as the plasma p. H rises. These dangers can be minimized if such electrolyte imbalances are appropriately treated prior to or concomitantly with bicarbonate infusion. Laboratory Tests. The aim of all bicarbonate therapy is to produce a substantial correction of the low total CO2 content and blood p. H, but the risks of overdosage and alkalosis should be avoided. Hence, repeated fractional doses and periodic monitoring by appropriate laboratory tests are recommended to minimize the possibility of overdosage. Drug Interactions. Additives may be incompatible; norepinephrine and dobutamine are incompatible with Sodium Bicarbonate solution. The addition of Sodium Bicarbonate to parenteral solutions containing calcium should be avoided, except where compatibility has been previously established. Precipitation or haze may result from Sodium Bicarbonate/calcium admixtures. NOTE: Do not use the injection if it contains precipitate. Additives may be incompatible. Consult with pharmacist, if available. When introducing additives, use aseptic technique, mix thoroughly and do not store. Pregnancy: Teratogenic Effects. Pregnancy Category C. Animal reproduction studies have not been conducted with Sodium Bicarbonate. It is also not known whether Sodium Bicarbonate can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Sodium Bicarbonate should be given to a pregnant woman only if clearly needed. Pediatric. Rapid injection (1. L/min) of hypertonic Sodium Bicarbonate Injection, USP solutions into neonates and children under two years of age may produce hypernatremia, a decrease in cerebrospinal fluid pressure and possible intracranial hemorrhage. The rate of administration in such patients should therefore be limited to no more than 8 m. Eq/kg/day. A 4. 2% solution may be preferred for such slow administration. In emergencies such as cardiac arrest, the risk of rapid infusion must be weighed against the potential for fatality due to acidosis. Geriatric. Clinical studies of Sodium Bicarbonate Injection, USP did not include sufficient numbers of subjects aged 6. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy. Adverse Reactions. Overly aggressive therapy with Sodium Bicarbonate Injection, USP can result in metabolic alkalosis (associated with muscular twitchings, irritability, and tetany) and hypernatremia. Inadvertent extravasation of intravenously administered hypertonic solutions of Sodium Bicarbonate have been reported to cause chemical cellulitis because of their alkalinity, with tissue necrosis, ulceration or sloughing at the site of infiltration. Prompt elevation of the part, warmth and local injection of lidocaine or hyaluronidase are recommended to reduce the likelihood of tissue sloughing from extravasated I. V. 0. 9% sodium chloride injection intravenous may be given; potassium chloride also may be indicated if there is hypokalemia. Severe alkalosis may be accompanied by hyperirritability or tetany and these symptoms may be controlled by calcium gluconate. An acidifying agent such as ammonium chloride may also be indicated in severe alkalosis. See WARNINGS and PRECAUTIONS. Sodium Bicarbonate Dosage and Administration. Sodium Bicarbonate Injection, USP is administered by the intravenous route. In cardiac arrest, a rapid intravenous dose of one to two 5. L syringes (4. 4. Eq) may be given initially and continued at a rate of 5. L (4. 4. 6 to 5. 0 m. Eq) every 5 to 1. H and blood gas monitoring) to reverse the acidosis. Caution should be observed in emergencies where very rapid infusion of large quantities of bicarbonate is indicated. Bicarbonate solutions are hypertonic and may produce an undesirable rise in plasma sodium concentration in the process of correcting the metabolic acidosis. In cardiac arrest, however, the risks from acidosis exceed those of hypernatremia. In less urgent forms of metabolic acidosis, Sodium Bicarbonate Injection, USP may be added to other intravenous fluids. The amount of bicarbonate to be given to older children and adults over a four- to- eight- hour period is approximately 2 to 5 m. Eq/kg of body weight – depending upon the severity of the acidosis as judged by the lowering of total CO2 content, blood p. H and clinical condition of the patient. In metabolic acidosis associated with shock, therapy should be monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics and cardiac rhythm. Bicarbonate therapy should always be planned in a stepwise fashion since the degree of response from a given dose is not precisely predictable. Initially an infusion of 2 to 5 m. Eq/kg body weight over a period of 4 to 8 hours will produce a measurable improvement in the abnormal acid- base status of the blood. The next step of therapy is dependent upon the clinical response of the patient. If severe symptoms have abated, then the frequency of administration and the size of the dose may be reduced. In general, it is unwise to attempt full correction of a low total CO2 content during the first 2. Owing to this lag, the achievement of total CO2 content of about 2.
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