Chloride Alkalosis

In addition, the physician with the aid of the clinical chemist, needs to calculate salt and water requirements for the newborn infant. Of prime importance is the determination of how much sodium bicarbonate is required to correct an acidosis, or in rare cases, how much ammonium chloride might be required to correct an alkalosis ( ). 

Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis. 

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. 

Now consider a psychiatric patient who presents with a pH of 7.50, a PaC02 of 20 mm Hg (2.7 kFh), an HC03 of 16 mEq/L (mmol/L), a sodium concentration of 140 mEq/L (mmol/L), and a chloride level of 103 mEq/L (mmol/L). Because this person is alkalemic, the low PaC02 is the primary disturbance and represents respiratory alkalosis. If this disturbance is a chronic respiratory alkalosis with metabolic compensation, the expected AHC03 is 0.4 x APaC02 (in millimeters of mercury) or 0.4 x 20, which is 8 mEq/L (mmol/L). As such, the predicted HC03 concentration should be 24 mEq/L (mmol/L) [normal] - 8 mEq/L (mmol/L) [expected compensation] or 16 mEq/L (16 mmol/L). 

Acid-base disturbances associated with PN usually are related to the patient s underlying condition(s). However, acid-base abnormalities may develop as a result of changes in chloride or acetate concentrations in PN admixtures. Because acetate is converted to bicarbonate in the body, excessive acetate salts in PN can lead to metabolic alkalosis excessive chloride salts in PN can lead to metabolic acidosis. PN should not be used to... 

Serum electrolytes can be altered secondary to respiratory alkalosis. Serum chloride is usually increased serum potassium, phosphorus, and ionized calcium are usually decreased. 

The metabolic component of mixed respiratory and metabolic alkalosis should be corrected by administering sodium and potassium chloride solutions. The respiratory component should be treated by readjusting the ventilator or by treating the underlying disorder causing hyperventilation. 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

When hypokalemia is associated with alkalosis, use potassium chloride. When acidosis is present, use the bicarbonate, citrate, acetate, or gluconate potassium salts. 

Metabolic alkalosis Potassium depletion is usually accompanied by an obligatory loss of chloride resulting in hypochloremic metabolic alkalosis. Treat the underlying cause of potassium depletion and administer IV potassium chloride. 

Sodium chloride (normal saline)- 0.9% Sodium chloride (normal saline), which is isotonic, restores both water and sodium chloride losses. Other indications for parenteral 0.9% saline include Diluting or dissolving drugs for IV, IM, or subcutaneous injection flushing of IV catheters extracellular fluid replacement treatment of metabolic alkalosis in the presence of fluid loss and mild sodium depletion as a priming solution in hemodialysis procedures and to initiate and terminate blood transfusions without hemolyzing red blood cells. 

Losing chloride by vomiting or from continuous Gl suction receiving diuretics known to produce a hypochloremic alkalosis metabolic and respiratory alkalosis hypocalcemia in which alkalosis may produce tetany, hypertension, convulsions, or congestive heart failure (CHF) when sodium use could be clinically detrimental. 

Chloride loss Patients losing chloride by vomiting or Gl intubation are more susceptible to developing severe alkalosis if given alkalinizing agents. 

Contraindications Excessive chloride loss due to diarrhea, diuretics, GI suctioning, or vomiting hypocalcemia metabolic or respiratory alkalosis, HTN, CHF... 

Certain foreign compounds may cause the retention or excretion of water. Some compounds, such as the drug furosemide, are used therapeutically as diuretics. Other compounds causing diuresis are ethanol, caffeine, and certain mercury compounds such as mersalyl. Diuresis can be the result of a direct effect on the kidney, as with mercury compounds, which inhibit the reabsorption of chloride, whereas other diuretics such as ethanol influence the production of antidiuretic hormone by the pituitary. Changes in electrolyte balance may occur as a result of excessive excretion of an anion or cation. For example, salicylate-induced alkalosis leads to excretion of Na+, and ethylene glycol causes the depletion of calcium, excreted as calcium oxalate. 

Children with heart disease often require high-dose diuretic therapy, which can lead to hypochloremic metabolic alkalosis. There are limited data on the safety of acetazolamide in the treatment of hypochloremic metabolic alkalosis in children. In 28 patients, median age 2 (range 0.3-20) months who took acetazolamide 5 mg/kg for 3 days, there were no adverse events (36). There was no significant difference in any electrolyte concentration, except for serum HC03, which fell from 36 to 31 mmol/1, and serum chloride, which rose from 91 to 95 mmol/1. There was no change in urine output. Acetazolamide appears to be safe in very young patients when given for 3 consecutive days. 

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. 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

F7. Forbes, G. B., and Erganian, J. A., Parenteral administration of ammonium chloride for alkalosis of congenital Pyloric stenosis. A.M.A. J. Diseases Children 72, 649 (1946). 

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