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Intracellular potassium shifts to the extracellular fluid in hyperkalemia associated with acidosis. Serum potassium concentration rises about 0.7 meq/L for every decrease of 0.1 pH unit during acidosis. Potassium movement out of cells occurs primarily in metabolic acidosis due to the accumulation of minerals such as NH4Cl or HCl. The inability of the chloride anion to permeate the cell membrane results in the transcellular exchange of H+ for K+. Metabolic acidosis from organic acids (keto acids and lactic acid) does not induce hyperkalemia. Unlike the minerals, these organic acids easily permeate cell membranes and retard Na+-K+ ATPase. The hyperkalemia frequently observed in diabetic ketoacidosis is not due to the acidosis but to a combination of the hyperosmolality (the intracellular K+ concentration of the dehydrated cell increases and K+ diffuses extracellularly) and deficiencies of insulin, catecholamines, and aldosterone. In the absence of acidosis, serum potassium concentration rises about 1 meq/L when there is a a total body potassium excess of 50–200 meq/L. However, the higher the serum potassium concentration, the smaller the excess necessary to raise the potassium levels further.
Trimethoprim is structurally related to amiloride and triamterene, and all three drugs inhibit renal potassium excretion. Serum potassium levels rise progressively over 4–5 days in patients treated with standard or high-dose trimethoprim (combined with sulfamethoxazole or dapsone), especially if they have concurrent renal insufficiency (creatine ± 1.2 mg/dL). Over one-half of inpatients taking this drug have potassium levels over 5 meq/L and 20% have severe hyperkalemia (> 5.5 meq/L). The potassium concentration returns to baseline after drug discontinuation.
Causes of hyperkalemia in AIDS include adrenal insufficiency, hyporeninemic hypoaldosteronism, renal failure, and drugs such as pentamidine and trimethoprim.
The elevated K+ concentration interferes with normal neuromuscular function to produce weakness and flaccid paralysis; abdominal distention and diarrhea may occur. Electrocardiography is not a sensitive method for detecting hyperkalemia, since nearly half of patients with a serum potassium level greater than 6.5 meq/L will not manifest electrocardiographic changes. When electrocardiographic changes of hyperkalemia occur, the ECG reflects impaired conduction by peaked T waves of increased amplitude, atrial arrest, widening of the QRS, and biphasic QRS–T complexes. The heart rate may be slow; ventricular fibrillation and cardiac arrest are terminal events.
First confirm that the elevated level of serum K+ is genuine. Potassium concentration can be measured in plasma rather than in serum to avoid leakage of potassium out of cells into the serum of the blood sample in the course of clotting, which may be matched in thrombocytosis. Treatment consists of withholding potassium and giving cation exchange resins by mouth or enema. Sodium polystyrene sulfonate, 40–80 g/d in divided doses, is usually effective. Emergent treatment of hyperkalemia is indicated if cardiac toxicity or muscular paralysis is present or if the hyperkalemia is severe (serum potassium > 6.5–7 meq/L) even in the absence of electrocardiographic changes. Insulin plus 10–50% glucose (5–10 g of glucose per unit of insulin) may be employed to deposit K+ with glycogen in the liver, and Ca2+ may be given intravenously as an antagonist ion. Transcellular shifts of potassium can also be mediated by b2-adrenergic stimulation. Albuterol, a nebulized b2 agonist, is effective in decreasing serum potassium in patients on hemodialysis. For such patients, nebulized albuterol can reduce serum K+ 0.5–1 meq/L within 30 minutes after administration, and this effect is sustained for at least 2 hours. Albuterol and insulin are probably equally efficacious in lowering potassium in uremic patients, and the hypokalemic effects of coadministration of the two drugs (with glucose) are additive and appear not to be a hazard. Sodium bicarbonate can be given intravenously as an emergency measure in severe hyperkalemia; the increase in blood pH results in a shift of K+ into cells. Hemodialysis or peritoneal dialysis may be required to remove K+ in the presence of protracted renal insufficiency. Therapy of the precipitating event proceeds concurrently.
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