Metabolic acidosis sodium bicarbonate

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Metabolic Effects. Severe metabolic acidosis with high anion gap and hyperglycemia was reported in humans after acute poisoning with endosulfan (Blanco-Coronado et al. 1992 Lo et al. 1995). In five of the six cases reported by Blanco-Coronado et al. (1992), the metabolic acidosis was corrected with gastric lavage with activated charcoal and intravenous sodium bicarbonate and diazepam. No further information regarding metabolic effects in humans after exposure to endosulfan was located. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Sodium bicarbonate administration for cardiac arrest is controversial because there are few clinical data supporting its use, and it may have some detrimental effects. Sodium bicarbonate can be used in special circumstances (i.e., underlying metabolic acidosis, hyperkalemia, salicylate overdose, or tricyclic antidepressant overdose). The dosage should be guided by laboratory analysis if possible. 

Metabolic and/or respiratory acidosis should be assessed by ABG measurements to determine pH, Pa02, PaC02, and HC03. If pH is less than 7.2, secondary to metabolic acidosis, sodium bicarbonate should be given. 

Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis. Therapeutic options include sodium bicarbonate and tromethamine. 

Less urgent forms of metabolic acidosis - Sodium bicarbonate injection may be added to other IV fluids. The amount of bicarbonate to be given to older children and adults over a 4- to 8-hour period is approximately 2 to 5 mEq/kg, depending on the severity of the acidosis as judged by the lowering of total CO2 content, blood pH, and clinical condition. Initially, an infusion of 2 to 5 mEq/kg over 4 to 8 hours will produce improvement in the acid-base status of the blood. 

Secondly, i.v. sodium bicarbonate is given for correction of the metabolic acidosis. Hemodialysis may be used in very serious cases. 

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. 

The pH-buffering of extracellular fluid depends in part on the carbon dioxide/ bicarbonate equilibrium so that the intake of sodium bicarbonate is followed by a brief alkalosis and an increased excretion of sodium carbonate in the urine. Depending on its carbonate concentration, the pH of the urine may rise to 8.07. Large doses (80—100 g/day) of sodium bicarbonate were needed if the pH of stomach contents was to be maintained at 4 or over in patients with duodenal ulcers8. Oxidation of organic anions in the body to carbon dioxide and water permits the use of sodium citrate, lactate or tartrate instead of sodium bicarbonate. In an analogous manner the ingestion of ammonium chloride induces a brief acidosis as a result of the metabolic conversion of ammonia to urea and lowers the pH of the urine. 

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

Acid-base disturbance. Alkalosis or mixed alkalosis/ acidosis need no specific treatment. Metabolic acidosis is treated with sodium bicarbonate, which alkalinises the urine and accelerates the removal of salicylate in the urine (see p. 97). 

The enzyme carbonic anhydrase facilitates the reaction between carbon dioxide and water to form carbonic acid, which then breaks down to hydrogen (H" ) and bicarbonate (HCOj") ions. This process is fundamental to the production of either acid or alkaline secretions and high concentrations of carbonic anhydrase are present in the gastric mucosa, pancreas, eye and kidney. Because the number of available to exchange with Na" in the proximal tubule is reduced, sodium loss and diuresis occur. But HCOg reabsorption from the tubule is also reduced, and its loss in the urine leads within days to metabolic acidosis, which attenuates the diuretic... 

A 12-month-old girl, weighing 10 kg, developed metabolic acidosis after taking 500-1250 mg of acetazolamide (26). The maximum base deficit recorded was 11.6. She was treated with sodium bicarbonate and recovered completely. 

A woman developed a severe metabolic acidosis and coma after taking nalidixic acid 28 g (14). She was given sodium bicarbonate 600 mmol and developed a respiratory alkalosis with secondary tetany. She recovered consciousness 9 hours later and the acid-base disturbance resolved after 60 hours. 

An 11-year-old boy with refractory partial epilepsy who had been taking topiramate 300 mg/day for 13 months developed hyperventilation. He had a hyperchloremic metabolic acidosis with partial respiratory compensation. The hyperventilation and acidosis resolved after the administration of sodium bicarbonate and reduction of the dose of topiramate. 

Therapeutically, potassium bicarbonate is used as an alternative to sodium bicarbonate in the treatment of certain types of metabolic acidosis. It is also used as an antacid to neutralize acid secretions in the gastrointestinal tract and as a potassium supplement. 

Therapeutically, sodium bicarbonate may be used as an antacid, and as a source of the bicarbonate anion in the treatment of metabolic acidosis. Sodium bicarbonate may also be used as a component of oral rehydration salts and as a source of bicarbonate in dialysis fluids. 

Around 60-70% of the filtered sodium is usually reabsorbed in the proximal tubule therefore, acetazolamide could be expected to have a rather potent diuretic effect. However, it produces rather modest diuresis because most of the excess sodium leaving the proximal tubule can be reabsorbed in the more distal segments of the nephron. Furthermore, its diuretic action is progressively diminished by the development of hyperchloremic metabolic acidosis caused by the loss of bicarbonate ions into the urine (Martinez-Maldonado Cordova 1990, Rose 1989, 1991, Wilcox 1991). In humans, the primary indication for acetazolamide (as a diuretic agent) is the treatment of edema with metabolic alkalosis. 

Sodium bicarbonate (8.4%, 5% and 1.25% (isotonic)) has been advocated for the correction of metabolic acidosis in horses (Table 17.7) (Divers 1998, Johnson 1995). However, the cause of the... 

Hyperchloremia is rare in horses but may occur in renal tubular acidosis (Ziemer et al 1987, Trotter et al 1986) and severe colitis. In the absence of hypernatremia, hyperchloremia results in a metabolic acidosis (Corley Marr 1998). It should be treated with 5% dextrose if accompanied by hypernatremia and with sodium bicarbonate if severe and accompanied by a low or normal plasma sodium concentration (Schaer 1999). 

There is no specific antidote. Supportive care should be instituted for all patients with history of serious boric acid exposure. Substantial recent ingestions may benefit from administration of activated charcoal. Fluid and electrolyte balance, correction of acid/base disturbance, and control of seizures are essential to therapy. Hemodialysis has been successfully used to treat acute boric acid poisoning. Sodium bicarbonate may be used for any metabolic acidosis. 

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