Bicarbonate hyperkalemia

Treatment depends on degree of hyperkalemia and presence/severity of signs and symptoms (sometimes irrespective of actual serum potassium level). Mild 5.5-6 mEq/L—furosemide and sodium polystyrene sulfonate. Moderate 6.1-7 mEq/L—insulin, glucose, sodium bicarbonate,... 

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. 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

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. 

Rapid correction of hyperkalemia requires administration of drugs that shift potassium intracellularly (e.g., insulin and dextrose, sodium bicarbonate, or albuterol). 

Potassium bicarbonate is used in cosmetics, foods, and oral pharmaceutical formulations, where it is generally regarded as a relatively nontoxic and nonirritant material when used as an excipient. However, excessive consumption of potassium bicarbonate or other potassium salts may produce toxic manifestations of hyperkalemia. 

Renal Tubular Acidoses, Types I and II These syndromes are predominantly characterized by loss of bicarbonate because of decreased tubular secretion of (distal or type I RTA) or decreased reabsorption of HCO3 (proximal or type II RTA). Because the major urine-acidifying power of the kidneys rests in the distal tubules, the proximal and distal RTAs may be differentiated by measurement of urine pH. In proximal RTA, urine pH becomes <5.5, whereas in distal RTA the distal tubules are compromised and urine pH is >5.5. When distal RTA is associated with obstructive nephropathy, sickle cell disease, or systemic lupus erythematosus, hyperkalemia may... 

Hyperkalemia History of renal failure, diabetes, recent dialysis, dialysis fistulas, medications Calcium chloride, insulin, glucose, sodium bicarbonate, sodium polystyrene sulfonate, dialysis... 

Recommendations for sodium bicarbonate vary (from class 1 to class in) depending on the clinical situation. Sodium bicarbonate use is acceptable for patients with known, preexisting hyperkalemia (class 1), preexisting bicarbonate-responsive acidosis (class 11a), overdoses of tricychc antidepressants (class 11a), and to aUcalinize the urine in aspirin and other drug overdoses (class 11a). In addition, sodium bicarbonate may be of benefit in intubated and ventilated patients with along arrest interval (class 11b). Sodium bicarbonate may be harmful in hypercarbic acidosis, and patients with this condition should not receive it (class IH). 

Major functions of the distal nephron include the regeneration of bicarbonate, the excretion of acid (hydrogen ion), the secretion of potassium, and the reabsorption of water. Damage to this portion of the nephron may present as significant acidemia and either hypo-or hyperkalemia, depending on the mechanism of injury. For example, amphotericin B produces small pores in the luminal membrane of distal tubular cells. These pores allow small molecules such as potassium to leak out the molecules are then wasted in the urine. Consequently, amphotericin B nephrotoxicity is characterized by hypokalemia secondary to renal potassium wasting. ATN is associated with urinary sediment characterized by the presence of tubular cells, coarse granular casts, and rarely, RBC casts. 

In patients with Stage 3 or higher CKD, the use of aUcalinizing salts, such as sodium bicarbonate or citrate/citric acid preparations, is useful to replenish depleted body bicarbonate stores. Sodium bicarbonate tablets are manufactured in 325- and 650-mg strengths (a 650-mg tablet contains 7.7 mEq sodium and 7.7 mEq bicarbonate). Shohl s solution and Bicitra contain 1 mEq/mL of sodium and the equivalent of 1 mEq/mL of bicarbonate as sodium citrate/citric acid. Citrate is metabolized in the liver to bicarbonate, and citric acid is metabolized to CO2 and water. Polycitra, which contains potassium citrate, (1 mEq/mL of sodium, 1 mEq/mL of potassium, and 2 mEq/mL of bicarbonate) should not be used in patients with severe CKD since hyperkalemia may result. 

End-stage renal disease (ESRD) patients who present with severe hyperkalemia, or with cardiac manifestations of hyperkalemia, should undergo immediate hemodialysis. Dialysis is the most rapid means of lowering potassium compared to bicarbonate, epinephrine, or insulin plus glucose therapy. Other forms of dialysis can be performed (e.g., peritoneal dialysis or continuous renal replacement therapy), although they appear to be less effective means to acutely lower an elevated serum potassium. ... 

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). 

Under normal circumstances, potassium bicarbonate poses no health threat to humans. Excess potassium in the body may result in a condition known as hyperkalemia, characterized by tingling of the hands and feet, muscle weakness, and temporary paralysis. Such a condition is very rare when potassium bicarbonate is used in normal amounts. 

Treat hyperkalemia (see p 37), if greater than 5.5 mEq/L, with sodium bicarbonate (1 mEq/kg), glucose (0.5 g/kg IV) with insulin (0.1 U/kg IV), or sodium polystyrene sulfonate (Kayexalate, 0.5 g/kg PO) Do not use calcium it may worsen ventricular arrhythmias. Mild hyperkalemia may actually protect against tachyarrhythmias. 

If the acidosis causing the hyperkalemia is extreme, bicarbonate may be administered to restore acid-base balance. If other electrolyte imbalances are noted, the appropriate treatment (e.g., chloride replacement) should be implemented. Care should be taken when providing supplements for electrolyte replacement. Electrolyte and acid-base levels should be monitored carefully to prevent overtreatment and additional electrolyte imbalance or alkalosis. 

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