Citric acid/potassium bicarbonate/sodium bicarbonate Disease Interactions

Alkalinizing agents containing sodium can induce sodium and water retention and result in hypernatremia, hypokalemia, hyperosmolality, edema and aggravation of congestive heart failure. Therapy with sodium- containing alkalinizing agents should not be used in patients with hypernatremia or fluid retention. Clinical monitoring of acid/base balance and electrolytes prior to, during, a following completion of therapy with alkalinizing agents is recommended.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Alkalinizing agents act as proton acceptors and/or dissociate to provide bicarbonate ions. Elimination of bicarbonate is decreased in patients with renal impairment and can result in metabolic alkalosis. Symptoms of metabolic alkalosis include hyperirritability or tetany, arrhythmia, and/or seizures (altered pH = altered calcium), or lactic acidosis due to impaired oxygen release. Therapy with alkalinizing agents should be administered with extreme caution in patients with compromised renal function. Clinical monitoring of renal function, acid/base balance and electrolytes is recommended.

Hypokalemia in patients with metabolic or respiratory alkalosis should generally be treated with potassium chloride rather than an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate), since alkali therapy may exacerbate the condition. In addition, hypochloremia may accompany alkalosis, which is best treated with potassium chloride. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.