Bicarbonate, loss

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. 

Determine etiology (bicarbonate loss or nonvolatile acid gain)... 

Metabolic acidosis Hyperchloremic, nonanion gap, metabolic acidosis is associated with topiramate treatment. This metabolic acidosis is caused by renal bicarbonate loss because of the inhibitory effect of topiramate on carbonic anhydrase. Generally, topiramate-induced metabolic acidosis occurs early in treatment, although cases can occur at any time during treatment. Bicarbonate decrements usually are mild to moderate rarely, patients can experience severe decrements to values below 10 mEq/L. Conditions or therapies that predispose to acidosis may be additive to the bicarbonate lowering effects of topiramate. If metabolic acidosis develops and persists, consider reducing the dose or discontinuing topiramate. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase-independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. Nevertheless, carbonic anhydrase inhibition causes significant bicarbonate losses and hyperchloremic metabolic acidosis. Because of this and the fact that HCO3" depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, the diuretic efficacy of acetazolamide decreases significantly with use over several days. 

CAIs alter renal function primarily by inhibiting carbonic anhydrase in the proximal tubule, which results in decreased bicarbonate reabsorption. The net effect of the renal actions of acetazolamide therapy is alkaliniza-tion of the urine and metabolic acidosis. Metabolic acidosis results from the initial bicarbonate loss and persists with continued acetazolamide use. Moderate metabolic acidosis develops in most patients. Reabsorption of bicarbonate independent of carbonic anhydrase prevents severe acidosis. Initially, acetazolamide produces diuresis, but urinary output decreases with the development of metabolic acidosis. In addition, decreased urinary citrate excretion follows acetazolamide therapy and has been attributed to the metabolic acidosis it produces. A high urinary pH and low urinary citrate concentration are conducive to precipitation of calcium phosphate in both the renal papillae and the urinary tract. 

The finding of a hyperchloremic metabohc acidosis in a patient without evidence of gastrointestinal bicarbonate losses and with no obvious pharmacological cause should prompt suspicion of an RTA. The presence of suggestive clinical (e.g., nephrocalcinosis in dRTA) or biochemical (e.g., hypophosphatemia and hypouricemia as a result of proximal tubular wasting in pRTA) features should also be considered. 

In hyperchloremic metabolic acidosis, bicarbonate losses from the ECF are replaced by chloride and the SAG remains normal. This decrease in bicarbonate results from losses from the gastrointestinal tract, dilution of bicarbonate in the ECF space by the addition of sodium chloride solutions, or the addition of chloride-containing acids to the ECF. Common causes of metabolic acidosis with an increased or a normal SAG are listed in Table 51-5. 

Gastrointestinal pathology should be treated to reduce ongoing bicarbonate losses, and factors that exacerbate RTA should be treated. If acidemia persists, alkali therapy should be instituted, with the goal of normalization of blood pH. The loading dose (LD) of alkali to initially correct the acidemia can be calculated as follows ... 

In patients with chronic metabolic acidosis because of gastrointestinal bicarbonate losses, maintenance therapy should provide sufficient alkali to replace ongoing bicarbonate losses. The magnitude of this replacement is variable and may be substantial (>10 mEq/kg per day). In addition, associated losses of other electrolytes, such as potassium and magnesium, may need to be replaced (see Chap. 50). 

The decreased clearance of waste materials results in a buildup of waste in the blood. Blood urea nitrogen (BUN) and creatinine are two end products of protein and muscle metabolism. In addition to waste buildup, electrolyte and acid buildup and bicarbonate loss may be noted, leading to imbalances. Supplemental cleansing of the Wood through dialysis— use of an artificial kidney (hemodialysis) or the peritoneal membrane (peritoneal dialysis) to filter blood—may be performed until renal function is restored. 

Reactions of Picric Acid, (i) The presence of the three nitro groups in picric acid considerably increases the acidic properties of the phenolic group and therefore picric acid, unlike most phenols, will evolve carbon dioxide from sodium carbonate solution. Show this by boiling picric acid with sodium carbonate solution, using the method described in Section 5, p. 330. The reaction is not readily shown by a cold saturated aqueous solution of picric acid, because the latter is so dilute that the sodium carbonate is largely converted into sodium bicarbonate without loss of carbon dioxide. 

This product is sufficiently pure for the preparation of phenylacetic acid and its ethyl ester, but it contains some benzyl tso-cyanide and usually develops an appreciable colour on standing. The following procedure removes the iso-cyanide and gives a stable water-white compound. Shake the once-distilled benzyl cyanide vigorously for 5 minutes with an equal volume of warm (60°) 60 per cent, sulphuric acid (prepared by adding 55 ml. of concentrated sulphuric acid to 100 ml. of water). Separate the benzyl cyanide, wash it with an equal volume of sa+urated sodium bicarbonate solution and then with an equal volume of half-saturated sodium chloride solution- Dry with anhydrous magnesium sulphate and distil under reduced pressure. The loss in washing is very small (compare n-Butyl Cyanide, Section 111,113, in which concentrated hydrochloric acid is employed). 

Caustic soda is removed from the carbonate—bicarbonate solution by treating with a slight excess of hard-burned quicklime (or slaked lime) at 85—90°C in a stirred reactor. The regenerated caustic soda is separated from the calcium carbonate precipitate (lime mud) by centrifuging or rotary vacuum filtration. The lime mud retains 30—35% Hquid and, to avoid loss of caustic soda, must be weU-washed on the filter or centrifuge. Finally, the recovered caustic solution is adjusted to the 10% level for recycle by the addition of 40% makeup caustic soda. 

Tubercles are mounds of corrosion product and deposit that cap localized regions of metal loss. Tubercles can choke pipes, leading to diminished flow and increased pumping costs (Fig. 3.1). Tubercles form on steel and cast iron when surfaces are exposed to oxygenated waters. Soft waters with high bicarbonate alkalinity stimulate tubercle formation, as do high concentrations of sulfate, chloride, and other aggressive anions. 

Under conditions of water loss and poor waterside control, it is fairly common for iron sludges and foulants formed elsewhere to settle in the boiler. Trying to identify the source of this problem is complicated when the transport of soluble iron salts such as ferrous bicarbonate Fe(HC03)2 into the boiler takes place. A further complication occurs... 

Hyperchloremic (nonanion gap) metabolic acidosis ° Consumption/loss of bicarbonate... 

Mg < 1 mEq/L) depletion (renal ammoniagenesis, renal H+ losses, and stimulate renal bicarbonate reabsorption)... 

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. 

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